The Effect of Sonar on Human Hearing

The lowest audible SPL for a human diver with normal hearing is about 67 dB re 1 μPa, with greatest sensitivity occurring at frequencies around 1 kHz (Fothergill et al., 2001).

Dolphins and other toothed whales are renowned for their acute hearing sensitivity, especially in the frequency range 5 to 50 kHz (Mooney et al., 2009). Several species have hearing thresholds between 30 and 50 dB re 1 μPa in this frequency range. For example the hearing threshold of the killer whale occurs at an rms acoustic pressure of 0.02 mPa (and frequency 15 KHz), corresponding to an SPL threshold of 26 dB re 1 μPa (Simon et al., 2005). By comparison the most sensitive fish is the soldier fish, whose threshold is 0.32 mPa (50 dB re 1 μPa) at 1.3 kHz, whereas the lobster has a hearing threshold of 1.3 Pa at 70 Hz (122 dB re 1 μPa) (Patek & Oakley 2003).

It’s evident as high levels of underwater sound create a potential hazard to marine and amphibious animals as well as to human divers (Steevens et al., 1999). Recently, for these reasons, guidelines for exposure of human divers and marine mammals to underwater sound are reported by different organizations: human divers exposed to SPL above 154 dB re 1 μPa in the frequency range 0.6 to 2.5 kHz are reported to experience changes in their heart rate or breathing frequency, diver aversion to low frequency sound is dependent upon sound pressure level and center frequency (Fothergill et al., 2009; Steevens et al., 1999).

The potential for active sonar to impact on a species is dependent on the ability of the species to hear the sound. Species hear sounds over different frequencies ranges, and the efficiency of sound detection varies markedly with frequency. Additionally, species behavioural responses to a detected sound may vary according to the sensitivity of the species to disturbance and what activities the animals are engaged in at the time.

Determination of potential impact on a species must therefore include estimation of the ability of the species to detect the sound, and the likelihood of disturbance to critical activities such as feeding or parental protection of juveniles.

In order to further understand these pathophysiological mechanisms, recent experiences examined post-mortem and studied histopathologically different marine animals (Ziphius cavirostris, Mesoplodon densirostris and Mesoplodon europaeus) after exposure to midfrequency sonar activity: no inflammatory or neoplastic processes were noted, and no pathogens were identified. Macroscopically, whales had severe, diffuse congestion and haemorrhage, especially around the acoustic jaw fat, ears, brain, and kidneys. Gas bubble-associated lesions and fat embolism were observed in the vessels and parenchyma of vital organs. In vivo bubble formation associated with sonar exposure that may have been exacerbated by modified diving behaviour caused nitrogen supersaturation above a threshold value normally tolerated by the tissues (as occurs in decompression sickness). Alternatively, the effect that sonar has on tissues that have been supersaturated with nitrogen gas could be such that it lowers the threshold for the expansion of in vivo bubble precursors (gas nuclei). Exclusively or in combination, these mechanisms may enhance and maintain bubble growth or initiate embolism. Severely injured whales died or became stranded and died due to cardiovascular collapse during beaching. These injures are apparently induced by exposure to mid-frequency sonar signals and particularly affects deep, long-duration, repetitive-diving species like whales ( Fernández et al., 2005 ).

Recent reports show the presence of gas and fat emboli in marine animals during exposure to naval sonar ( Tyack, 2006 ).These reports suggest that exposure to sonar sounds may cause a decompression-like syndrome in deep-diving whales either by changing their normal diving behaviour or by a direct acoustic effect that triggers bubble growth ( Tyack, 2006 ). The latter scenario would, however, only seem to happen for animals with 100–223% supersaturated tissues within tens of meters from a sonar where the received levels exceed 210 dB re 1 μPa ( Tyack, 2006 ). Nonetheless, the geographical pattern of strandings suggests that animals are impacted at ranges significantly greater than those required for acoustically driven bubble growth, implying that the observed pathologies may follow from a behavioural response that has adverse physiological consequences ( Tyack, 2006 ).

Pathologies related to effects of pressure are well known among human divers, but marine mammals appear to have developed adaptations to avoid most mechanical and physiological effect. The hazard of bubble formation during decompression is best known for humans breathing compressed gases, but empirical studies and theoretical considerations have shown that breath-hold divers can develop supersaturation and possible decompression-related problems when they return to the surface. Supersaturation has not been measured during normal diving behaviour of wild marine mammals but rather in specially designed experiments performed by trained subjects ( Tyack, 2006 ).

Furthermore, subtle behavioural changes are also associated with sonar exposure. Animals that prolong apnea must optimize the size and use of their oxygen stores, and must deal with the accumulation of lactic acid if they rely upon anaerobic metabolism ( Popper et al., 2007 ).

These data show as repeated exposures are necessary to generate effects. It’s evident as the effects of sound on marine animals could potentially include increased stress, damage to organs, the circulatory and nervous systems; long-term effects may alter feeding and reproductive patterns in a way that could affect the fish population as a whole. In the limited existing research on the effects of sound on marine animals hearing and behavior, different scientists have discovered that exposure to some very loud sounds, such as seismic air guns, can produce no effect, or result in a range of effects from temporary hearing loss to more lasting damage to the haircells of marine animal' inner ears. But it is hard to say that effects on one species indicate that another species will be affected in the same way by the same signal.

Exceptions may be if the sonar signals are rapidly repeated (which is unlikely due to overlap of returning echoes) or if oceanographic conditions are such that sound levels do not attenuate regularly over short distances (i.e. less than several 100 m) and thus remain intense. Perhaps such a situation could occur with multiple sonar sources over steep bathymetric conditions ( Mooney et al., 2009 ).

However, the animal would still need to remain within a close range long enough to receive al level of exposure that would induce auditory threshold shifts, a potentially unlikely situation: all scenarios entail the subject being relatively close to the sonar source for a ‘prolonged’ duration ( Mooney et al., 2009 ).

The animal would then have to maintain at most that distance for the approximate 2–2.5 min of operating the sonar to receive a level of exposure of near 214 dB;

Assuming a usual sound attenuation rate of 6 dB per doubling of distance, the dB level used in high frequency sonar would be the received level approximately 40 m from the sonar source, a distance that can be considered ‘close’ with respect to naval ships;

The exposure to high frequency sonar (200-214 dB re 1 μPa) can determinate an hearing shifts of the marine animal: in particular recent report show as these data also imply that the animal must be very close to the source and/or exposed repeatedly in a short period time ( Mooney et al., 2009 ):

Although these evidences, recent studies showed the absence of side effects on marine animals: the sensory tissue of the inner ears did not show morphological damage even several days post-sound exposure; similarly, gross- and histopathology observations demonstrated no effects on nonauditory tissues ( Popper et al., 2007 ).

Changes in the distribution, abundance, or productivity of important marine mammal prey species and subsequent decreases in both individual marine mammal survival and productivity and in population size and productivity. These changes in prey species possibly could be caused both directly and indirectly by the low-frequency sonar transmissions: for example, transmissions conceivably could kill or impair development of the eggs and larval forms of one or more important marine mammal prey species; they might also disrupt feeding, spawning, and other vital functions or cause shifts in distribution patterns of certain important prey species and make some prey species more vulnerable to disease, parasites, and being eaten by other predators.

Disruption of feeding, breeding, nursing, acoustic communication and sensing, or other vital behavior and, if the disruption is severe, frequent, or long lasting, possible decreases in individual survival and productivity and corresponding decreases in population size and productivity;

Introduction of new types of military sonar, such as low-frequency system, should proceed with caution; the low-frequency sounds produced by the systems will travel much farther than the mid-frequency sonar sounds currently causing concern ( Salami et al., 2010 ). However, at low powers, sonar can protect marine mammals against collisions with ships.

However, these hypotheses typically lack controlled experimental conditions to best evaluate potentially deleterious noise effects. Thus, the actual mechanisms that may be initiated by sonar exposure, which could actually result in multi-species strandings, have yet to be empirically supported.

High-powered sonar transmitters can kill marine animals. In the Bahamas in 2000, a trial by the US Navy of a 230 decibel transmitter in the frequency range 3 to 7 kHz resulted in the beaching of sixteen whales, seven of which were found dead. The Navy accepted blame in a report published in the Boston Globe on 1/1/2002. Continued emission of noise can increase the damage, due to the “habituation” to a familiar sound to which it is difficult to react more strongly ( Sypin, 2008 ). The “habituation” is known as being provoked by continued acoustical stimuli, reducing the hearing sensitivity to high-level sounds; the hearing sensitivity may be regulated at both conductive (stapedial reflex) and sensorineural levels (adaptation) ( Sypin, 2008 ).

These temporally and spatially overlapping events seem to indicate that high-intensity sonar may instigate some marine mammal strandings. Recent work has suggested that sonar exposure could induce a variety of effects in marine mammals including changes in dive profile, acoustically induced bubble formation or decompression sickness ( Salami et al., 2010 ).

Some marine animals, such as whales and dolphins, use echolocation systems similar to active sonar to locate predators and prey. It is feared that sonar transmitters could confuse these animals and cause them to lose their way, perhaps preventing them from feeding and mating. Recent articles report findings to the effect that military sonar may be inducing some whales to experience decompression sickness (and resultant beachings) ( Parsons et al., 2008 ).

It has been suggested that overexposure to noise could induce permanent physiological damage and deleterious behavioural alterations. For these reasons: there has been growing concern that the noise humans have introduced into the sea might disrupt the behaviour of marine mammals ( Salami et al., 2010 ).

Marine mammals are of particular concern regarding the effects of noise as they typically have sensitive underwater hearing and they use sound for important activities such as communicating, orienting and finding prey.

Modern ships generate enough noise from their engines and propellers to have reduced the range over which whales can communicate. The low frequency noise from ships travels so well in the ocean that it has raised the noise levels ten to one hundred times compared to a century ago ( Stocker, 2004 ).

We can usually see things that are miles away, but if you have ever snorkelled, you know that vision is limited to a few tens of meters underwater. Vision is the best way to sense distant objects in air, but sound is the best way to sense objects that are far away under the sea. Low frequency sounds can travel hundreds of miles in the right conditions. When mammals entered the ocean tens of millions of years ago, they evolved mechanisms to sense objects by listening for echoes from their own sounds, and to use sound to communicate over long distances.

In terrestrial habitats, increasing sound levels have been shown to induce various effects across taxa including behavioural changes, temporary physiological alterations and permanent anatomical damage. While it is apparent that anthropogenic noise may affect marine animals, we know relatively less about the actual causes or mechanisms of these effects.

5.2. Effects of sonar on human hearing

Relying on one’s hearing it is extremely difficult to orientate oneself under water. Because of the high speed of sound under water, it is perceived by both ears virtually simultaneously and the orientation error may be possible. Bad orientation under water is also due to the prevalent bone conductivity. Sufficient audial orientation is possible to be acquired only after systematic training. The diving suit isolates the human ear from the surrounding water medium. That is why sound waves penetrate the helmet and the layer of air but reach the eardrum partly absorbed and scattered. In this case, sound perception through air conductivity is insignificant.

However, while diving without a helmet, which is possible in warm water, sound is perceived just like in the air. If the rubber helmet fits tightly, sound is well perceived because of bone conductivity – sound waves are transmitted through the bones of the human skull. With no helmet, a diver can hear very well, with a rubber helmet – fairly well, and with a metal one – very bad.

The development of underwater technology commonly results in a noisy working environment for commercial divers (Tindle & Deane, 2005). Also, the increasing use of active low-frequency sonar by submarines and ships raises the risk of accidental exposure to low frequency underwater sounds. While hearing conservation programs based on recognized risks from measurable sound pressure levels exist to prevent occupational hearing loss for most normal working environments, there are no equivalent guidelines for noise exposure underwater.

The Threshold Limit Values (TLVs) represent conditions under which it is believed that nearly all workers may be repeatedly exposed without adverse effect on their ability to hear and understand normal speech. For Threshold Limit - Ceiling Values (TLV-C) the concentration should not be exceeded during any part of the working day (ACGIH, 1998).

In particular the “American Conference of Governmental Industrial Hygienists (ACGIH)” has established permissible ultrasound exposure levels. These recommended limits (set at the middle frequencies of the one-third octave bands from 10 kHz to 50 kHz) are designed to prevent possible hearing loss caused by the subharmonics of the set frequencies, rather than the ultrasonic sound itself. These TLVs represent conditions under which it is believed that nearly all workers may be repeatedly exposed without adverse effect on their ability to hear and understand normal speech. Previous TLVs for frequencies in the 10 kHz to 20 kHz range, set to prevent subjective effects, are referenced in a cautionary note below. The 8-hour time-weighted average (TWA) values are an extension of the TLVs for noise, which is an 8-hour TWA of 85 dBA for sound below 10 kHz. The ceiling values may be verified by using an integrating sound level meter with slow detection and 1/3 octave bands. All instrumentation should have adequate frequency response and should meet the specifications of ANSI S1.4-1983 and International Electrotechnical Commission (IEC) 804 (ACGIH, 1998).

Measuring any source suspected of producing sound at levels exceeding the ACGIH recommended limits requires the use of a precision sound level meter, equipped with a suitable microphone of adequate frequency response, and a portable third-octave filter set. Consult with the Assistant Regional Administrator for Technical Support for guidance (ACGIH, 1998).

TVLs for Ultrasound One-third Octave-Band Level Measure in Air in dB

Re:20 μ Pa; Head in Air Measure in Water in dB

Re:20 μ Pa; Head in Water Mid-Frequency ofThird-Octave Band (kHz) CeilingValues 8-hour TWA Ceiling Values 10 105A 88A 167 12.5 105A 89A 167 16 105A 92A 167 20 105A 94A 167 25 110B -- 172 31.5 115B -- 177 40 115B -- 177 50 115B -- 177 63 115B -- 177 80 115B -- 177 100 115B -- 177 Table 1. (ACGIH, 1998)

Different studies highlighted as behavioural and memory disturbances, intellectual impairment, depression, and other long-term neuropsychiatric changes are well known in professional divers: these symptoms are probably caused by repeated focal ischemia due to intravascular gas bubbles and hyalinosis of the walls of small blood vessels (Reul et al., 1995). The lesions were predominantly in the subcortical white matter and basal ganglia, suggesting a vascular pathogenesis (Reul et al., 1995).

Other studies highlight as diving puts the inner ear at risk. Inner ear barotrauma and inner ear decompression can lead to permanent sensorineural hearing loss, tinnitus and vertigo (Klingmann et al., 2004).

Inner ear barotrauma is related to pressure changes in the middle and inner ear. Barotrauma refers to tissue damage that occurs when a gas-filled body space (e.g., lungs, middle ear) fails to equalize its internal pressure to accommodate changes in ambient pressure. The behaviour of gasses at depth is governed by Boyle’s law: the volume of a gas varies inversely with pressure. During descent, as ambient pressure increases, the volume of gas-filled spaces decreases unless internal pressure is equalized. If the pressure is not equalized by a larger volume of gas, the space will be filled by tissue engorged with fluid and blood. This process underlies the common “squeezes” of descent that affect the middle ear, external auditory canal, mask, sinuses and teeth. Barotrauma of the inner ear during descent develops when middle ear clearing fails and the eustachian tube is blocked and locked (Klingmann et al., 2004). Under these conditions, the raised intracranial pressure brought about by forceful efforts to equalize pressure might be transmitted to the inner ear through a patent cochlear aqueduct. These pressure forces may cause rupture of Reissner’s or the basilar membrane and/or labyrinthine window fistula with consequent impairment of inner ear functions (Klingmann et al., 2004). Symptoms often occur during ascent when expanding air in the middle ear is forced through a round window membrane fistula into the inner ear. The resulting gas bubble in the labyrinth expands during ascent and replaces the perilymph fluids. Barotrauma of the inner ear during ascent is a result of a blocked eustachian tube with air expanding in the middle ear forcing the tympanic membrane into the auditory canal. As a result, the oval window membrane is dislocated into the middle ear and the round window membrane is forced into the inner ear with increasing tension on both membranes (Klingmann et al., 2004). When there is an abrupt pressure equalization, either because of a tympanic membrane rupture or because the blocked eustachian tube releases the increased middle ear pressure, the oval and round window membranes snap back to their original position causing a pressure wave running through the inner ear.

Whether uneventful scuba diving in the absence of a decompression incident is a risk factor for cochlear disorders is a matter of debate. Most studies of diving associated hearing loss reveal an association with occupational noise exposure.

Different reports showed as divers exposed to high levels of underwater sound can suffer from dizziness, hearing damage, somnolence, lightheadedness inability to concentrate or other injuries to other sensitive organs, depending on the frequency and intensity of the sound. This may include neurological symptoms such as blurred vision, lightheadedness, vibratory sensations in hands, arms and legs, and tremors in upper extremities (Fothergill et al., 2009; Steevens et al., 1999).

Most reports of diving injury have concentrated on acute injuries rather than chronic disability e.g. deafness. Hence, while many divers reported aural symptoms, few attributed them to diving. It is possible that repeated hyperbaric exposure among very experienced divers may be responsible for their aural symptoms, despite the lack of an obvious acute injury for many. The cause(s) of the aural disorders described above are unknown. Different authors have reported that hearing loss in divers may be due to external ear canal obstruction, tympanic membrane perforation, middle ear disorders and sensorineural hearing damage (Taylor et al., 2006). However, aural barotrauma is the most likely cause (as it is a relatively common occurrence). It is known that the strain exerted upon the tympanic membrane (TM) and middle ear from minor barotrauma results in reversible impairment of the recoiling capacity of the TM elastic fibrils. It has been postulated that, if this barotrauma is repeated over lengthy periods, the TM changes could become irreversible (Taylor et al., 2006). Hence, hearing loss is a possible outcome (Taylor et al., 2006).

Sub-clinical brain and inner ear injury may offer an alternative explanation. Different authors found that divers had significantly more hyper-intense lesions of the sub-cortical cerebral white matter (on MRI) compared to controls (Taylor et al., 2006): these authors concluded that long term recreational diving may cause central nervous system degeneration even if diving incidents have not occurred. The exact mechanism of this degeneration remains unclear although paradoxical gas embolism, through a patent foramen ovale, has been postulated (Taylor et al., 2006).

However, the association between diving and hearing loss, in the absence of clinically apparent diving injury, may not be as clear cut. Therefore, the effect of acoustic trauma or potential harmful effects of increased pressure and partial pressures of breathing gases cannot be differentiated. In fact the following well-recognized factors can affect the inner ear in divers: inner ear decompression sickness, noise, and potentially chronic effects of the breathing gases.

A number of studies have compared the hearing threshold in professional divers (Klingmann et al., 2004):

In 1961 in a group of 62 Royal Navy divers and submarine escape training instructors, a high-frequency hearing loss was found in most of the divers. However, these divers had been exposed to gunfire and machinery noise during their naval careers, and noise could not be excluded as the causative mechanism.

An intriguing finding was a prevalence of 60% of hearing impairment in a group of abalone divers who had not been exposed to noise. These divers, however, had been subjected to an extraordinary compression decompression stress by a mean history of 6 years of diving with an average diving depth of 15 to 20 m during 4 hours on 100 days per year. The divers with recognizable hearing loss in that study remembered having barotrauma in the past. Therefore, residual damage after diving accidents may mask putative chronic effects of breathing air under hyperbaric conditions. In addition, hearing thresholds found in divers were compared with thresholds of controls from a different study.

One hundred sixty-four professional Norwegian divers were subdivided into different age groups and hearing thresholds were compared with a standard population from Norway. Young divers were found to have better hearing compared with the reference group, and with increasing age this difference decreased. The authors claimed that hearing deteriorates faster in professional divers with increasing age. These results were confirmed when 116 divers were reexamined 5 years later. Noise at work and barotrauma were thought to contribute to the rapid deterioration of hearing in the professional divers.

It is postulated that the human hearing range is reduced from 130 dB in air to 55 to 60 dB in water. The reduction causes the diver to be less resistant to noise underwater because acoustic energy underwater does not resolve as fast as in air. In addition, sawing, drilling, and grinding underwater may give rise to noise levels of 90 to 105 dB, and noise from the air stream venting inside underwater helmets can reach average noise levels of 93 to 99.5 dB. Most of the studies examined professional divers who had been exposed to gunfire or other noise at work. Noise was likely the main cause of the altered pure-tone thresholds (Molvaer & Albrektsen, 1990; Molvaer & Lehmann 1985).

This interpretation is supported by the fact that puretone thresholds of divers who had been exposed to noise underwater are similar to those obtained from control subjects who had been exposed to noise on land. In a cross-sectional study, auditory function was compared in Norwegian construction divers and workshop workers. Both groups had been exposed to noise, and divers had less hearing impairment at low frequencies (0.25 and 0.5 kHz) (Skogstad et al., 1999).

Another study from Skogstad et al examined 54 occupational divers at the beginning of their diving career and 3 years later. That study subdivided the divers into groups of low exposure (100 dives in 3 years) and high exposure (100 dives in 3 years). Skogstad and coworkers did not find a statistically significant difference for both ears combined between both groups (Skogstad et al., 2000).

One should expect that divers with high exposure to diving should have poorer hearing levels because they have more contact with breathing gases under increased ambient pressure and work longer underwater and therefore spend more time in a noisy environment. However, the low exposure group might have worked in a noisy environment, too, when they were not underwater (Klingmann et al., 2004).

These findings are confirmed by the data of Benton, who examined 281 commercial divers. He investigated the audiometric records of a group of United Kingdom professional divers, all of whom had been examined by an approved medical examiner. All divers underwent a hearing test between 1989 and 1992 and had a minimum of 5 years of diving experience. The divers were divided into 7 age groups ranging from 25 to 60 years. The median hearing level thresholds were compared with the predicted values for otologically healthy individuals, the comparison revealed that the median hearing threshold values of the divers lay between the predicted median and predicted upper quartile values (Klingmann et al., 2004). Within the older group (40 years), the median and predicted median values of the divers were similar. The author postulated that these results show as the divers had no impairment of the inner ear function compared with a non diving control group.

This short revision of the literature highlights that the data on the effect of marine noise on diver are few and sometimes in contrast. However it's important to remember that, although different injuries (dizziness, hearing damage, etc) have been reported, the single most important issue related to diver safety resulting from low frequency sonar is that of disorientation due to vestibular stimulation. Whilst exposure to sonar transmissions below a level necessary to cause disorientation can give rise to temporary hearing threshold shifts, these are considered operationally acceptable for diving operations over limited periods (Salami et al., 2010).

This effect of sonar on diver is related to its duration too: studies on marine animals have demonstrated that changes in hair bundle density paralleled changes in hair cell nucleus density, indicating that entire hair cells disappeared after noise exposure; the inner ear damage is characterized by a permanent threshold elevation after an exposure to white noise ranging in intensity from 130 to 170 dB re 1 μPa for 24 h (Salami et al., 2010; Smith et al., 2006).

Although there are differences among the ears of different species, the basic processes of hearing are the same between marine and terrestrial mammals. For this reason, some of the previous considerations can be applied on humans (Salami et al., 2010; Popper & Fav, 2000).

In particular we had done a personal experience on ten male divers with normal hearing; the divers were exposed to active sonar of the Italian Navy for more than 100 exposures, each of at least 1-h duration, in the course of 6 months (Salami et al., 2010): all the subjects have been exposed to active sonar of the Italian Navy (Hull MF), at a frequency of 7.5 kHz and an intensity of 230 dB re 1 μ Pa. All the divers have had more than 100 exposures of at least 1 h, for six months, in the winter time (from October to April). The diver was exposed to the sonar at a constant depth of 3 m and at a distance from the sonar reducing progressively from 300 to 30 m. Each subject was instructed to stop the exposure in case of pain, tinnitus, vertigo, or hearing loss.

Before, at the end, and six months after the end of noise exposures, all the divers underwent the following instrumental examinations: pure-tone audiometry, Carhart test, Peyser test, thresholds of discomfort test (TDT), tympanometry, transient evoked otoacoustic emissions (TEOAE) with linear click emission, distortion product otoacoustic emissions (DPOAE), and auditory brainstem response (ABR) by MK 12-ABR (Amplifon—Italy) (Chapman & Ellis, 1998).

At the end of the exposure, the absence of TEOAE and DPOAE was observed in all the divers, the positive Peyser and TDT tests, observed in 7/10 and 10/10 divers, and the worsening of the mean air and bone audiometric thresholds, especially at the 4,000 and 8,000 frequencies, highlights the pathophysiologic features of continued and intense sound stimulation of the cochlea (Chapman & Ellis, 2008).

The injuries occur first in the first row of the outer hair cells, then in the inner hair cells, and subsequently in the second and third rows; the temporary threshold shift, at the Peyser test, observed in 9/10 of the divers, shows the presence of an auditory adaptation to the noise and underlines the risk of increasing the hearing damage: it is well established that a single exposure to a severe sound can result in direct mechanical damage to the delicate tissues of the peripheral auditory apparatus, including components of the middle ear (tympanic membrane, ossicles) and inner ear (organ of Corti); in contrast, regular exposure to less intense, but still noisy sounds, involves the insidious destruction of inner-ear components that eventually and unavoidably leads to an elevation in hearing levels.

The results of the TDT test confirm the correlation between the acoustic reflex threshold and the loudness discomfort level for people with hearing damage (Olsen, 1999).

Following a noise exposure, the hearing damage could also be due to the loss of the protective effect of the efferent fibres, perhaps mediated by the lateral olivocochlear neurons that synapse beneath the inner hair cells (Attanasio et al., 1999).

The transitory auditory injury observed in our test group may also be related to the hyperbaric work environment: oxygen toxicity is a problem in diving and can have fatal consequences in the water; past experiences made on divers, highlighted the significant presence of hearing disturbances and disorientation, and demonstrated changes of the Central Nervous System in hyperbaric conditions (Cakir et al., 2006).

Experiences done on animals (guinea pig) showed that repeated hyperbaric exposures that were considered to be safe did cause damage to the cochlear system (Zheng & Gong, 1992). These modifications are characterised by: alterations in the metabolism and in the concentration of neurotransmitters; block of intercellular oxidation processes; accumulation of carbon dioxide.

At the last control, the complete recovery observed in all the divers shows the temporary negative effects of repeated and lasting exposure to active sonar (Hull MF) and demonstrates the absence of permanent noise-induced hearing loss in divers exposed to active sonar (Salami et al., 2010).

The frequencies used in sonar are above the human hearing threshold (Gong et al., 2010; Kane et al., 2010): as because the power of ultrasonic sonar rapidly falls off with distance, a safe operating distance is 10 meters or greater. Diving may be conducted around this type of sonar provided the diver does not stay within the sonar focus beam. None of the above avoids the need for positive safety measures to be adopted when divers are working on or very close to sonar sources which are inactivated. The possibility of accidental activation must be precluded.

Since physical damage and impairment of the auditory system is caused both by high peak pressure and energy flux, safety limits for sound exposure should include both a maximum received energy fluid level and a maximum received peak–peak pressure level (impulse noise can have very high peak sound levels, but carry very little energy) (Madesen, 2005).

As different studies give only basic instructions governing hearing conservation and noise abatement, while they do not address exposure to waterborne sound, the instructions should provide field guidance for determining safe diving distances from transmitting sonar.

Sonar with an intensity level of about 230 dB re 1 μ Pa may cause on divers: slight visual-field shifts (probably due to direct stimulation of the semicircular canals), fogging of the face plate, spraying of any water within the mask, and other effects. In particular in the presence of long sonar pulses (one second or longer), depth gauges may become erratic and regulators may tend to free-flow. Different divers experienced these phenomena during controlled research report that while these effects are unpleasant, they are tolerable. Similar data are not available for un-hooded divers but visual-field shifts may occur for these divers at lower levels. If divers need to be exposed to such conditions, they must be carefully briefed and, if feasible, given short training exposures under carefully controlled conditions.

As the probability of physiological damage increases markedly with sound pressurese increase, fully protected divers must not be exposed to intensity level superior to 215 dB re 1 μPa for any reason.

A distinction is made between in-water hearing and in-gas hearing (Tompkins, 2007):

in-water hearing occurs when the skull is directly in contact with the water, as when the head is bare or covered with a wet-suit hood.

in-gas hearing occurs when the skull is surrounded by gas as in the MK 21 diving helmet.

In-water hearing occurs by bone conduction—sound incident anywhere on the skull is transmitted to the inner ear, bypassing the external and middle ear. In gas hearing occurs in the normal way—sound enters the external ear canal and stimulates the inner ear through the middle ear.

For these reasons, if the diver is helmeted, it’s necessary to use greater distance from the sonar source.

It’s also important to identify the type of diving equipment: wet-suit un-hooded, wet-suit hooded, helmeted; wet-suit hooded diver can safely get closer to a sonar source. If the type of sonar is unknown, start diving at 600–3,000 yards, depending on diving equipment (use greater distance if helmeted), and move in to limits of diver comfort.

Helmeted divers experience reduced sensitivity to sound pressure as depth increases.

The sonar presents different effect on divers, according to the intensity (low, medium, high):