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Estimates of blast injury and acoustic traumazones for marine mammals from underwater explosions
Darlene R. Ketten
Department of Otology and Laryngology, Harvard Medical School, Boston, Massachusetts, 02114,U.S.A. Email: [email protected]
Summary
The physical parameters of two underwater detonations of Class A explosives (TNT derivatives with fast rise-time waveforms) are analyzed for their potential to induce blast injuryand acoustic trauma in marine mammals. Anatomical differences between marine and landmammal ears that may affect the incidence and severity of acoustic trauma and the basicconcepts of temporary versus permanent threshold shifts are summarized. Overpressurecalculations are combined with experimental data from the literature to calculate theoreticalzones for acute trauma, permanent hearing loss, and temporary threshold shifts for midwater explosions at two charge weights.
Key words: blast injury, threshold shift, ship shock, Cetacea, acoustic trauma
Introduction
This paper is a theoretical overview. In it, thephysical parameters of two hypotheticalhazards, large and small underwater explosions, are outlined and analyzed for theirpotential interactions with marine mammalears. For the last decade, there has beengrowing concern about the effects of manmade sounds in the oceans. These concernsare timely, and more stringent reviews areunderway of many activities that couldacoustically impact marine life. However, atthe moment, we have no direct experimentalevidence or controlled measures of energylevels that induce blast or acoustic trauma inmarine mammals.
How labile is the ear of any marine mammalspecies? Given that marine mammals arehighly aural animals, we expect serious im-
pact from even minor acoustic trauma. Thealternative view argues that highly prizedresources, including' sensory systems, aregenerally well protected. To date, there is nodefinitive study of temporary or permanentthreshold shifts in any marine mammal. Pinniped and cetacean ears provide an interesting functional paradox: they are essentiallyland mammal ears immersed in a biologically rich but acoustically harsh environment.As marine mammals evolved from landmammals, their ears coupled a terrestrialblueprint to extensive adaptations for rapidpressure changes and large concussiveforces. On one hand, they have basicallyacoustically fragile land mammal ears. Onthe other hand, they evolved in a high noiseenvironment, and some adaptations; e.g.,those that prevent inner ear barotrauma,may deter noise and shock trauma. Little isknown on the effects of intense sounds and
Sensory Systems of Aquatic Mammals (1995)R.A. Kastelein, J.A. Thomas and P.E. Nachtigall (editors)De Spil Publishers, Woerden, The Netherlands ISBN 90-72743-05-9
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concussive forces on hearing in water forvirtually any species. Evidence from humandivers is largely anecdotal and often contradictory. There are few audiograms for marine mammals and no published data ontemporary or permanent threshold shifts.Thus, at this stage, there are no direct measures of underwater acoustic trauma for anymarine mammal and detailed descriptionsof the ear are available for fewer than 20% ofcetacean and pinniped species.
The "experiment" presented here is not, inany sense, a definitive analysis of marinemammal acoustic hazards, nor is it an expert opinion on trauma. Rather, it providesan overview of the physiologic aspects ofacoustic trauma and a discussion of the relevance and limitations of currently available data (primarily from land mammalears) for predicting the effects of man-madesounds on marine mammals. The scope islimited to two tangible impacts: shockwave and acoustic trauma from blast zones.The values calculated are impact estimatesonly and are largely speculative. Conservative estimates of the zones of potential lethal, sublethal, transitional, and low to zeroimpacts are extrapolated from arbitrarycharge weights, published anatomical andphysiological data on blast injury, and related anatomical data on marine mammalears. It does not attempt to assess any of thepossible, equally grave, but subtle, effectssound can have; e.g., disruption of communication, breeding behaviour, or navigation. Regrettably, there is little direct factual evidence that can be brought to bear onany of these issues. In essence, this experiment is directed not at addressing a single,well defined question but at construing ourcurrent, relatively small volume of knowledge into a more coherent form for objective discussion of potential marine acousticimpacts.
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Materials and methods
The following model assesses the theoreticalhazards of impulse pressures and peak overpressures that marine mammals may encounter within a 15 km radius of multi- tonnage mid-water explosions. The specific detonations addressed are 1200 lbs (544 kg) and10000 lbs (4535 kg) charges of Class A explosives commonly used in inshore and offshore industrial and military activities(DOC, 1993; Ketten et al., 1993; Czaban et al.,1994; Reeves and Brown, 1994). Class A explosives are TNT-derivative water-gel compounds that generate complex, fast-rise timeimpulse waveforms. Detonation velocitiestypically range 4,000 - 10,000 m/sec. The twocharge weights chosen for this model spanthe conventional range used in demolition,construction, and live-fire military testing(DOC, 1993, Ketten et al., 1993). Several simplifying assumptions are made in the model:1. detonation occurs at ~ 100m depths.2. bottom depth is ~ 20 times the detonation
depth.3. the bottom is thick sediment with no dis
cernible terrain.
A charge depth < 5% total water depth islargely a practical constraint. Given theseassumptions, the pressure spread is spherical for 100 m, becoming planar as surfaceinfluences emerge. This model more closelyapproximates military ship shock trials thannear shore industrial activity. In- and nearshore explosions imply multiple irregularinfluences; e.g., bottom topography, artificial structures, etc., that rapidly distort thewave front and produce complex cancellation-enhancement patterns.
Ship shock trials are widely accepted procedures for live-fire testing of new or existingship designs. Because they are highly regulated test procedures, they provide con-
Estimates of blast injury and acoustic trauma zones
trolled measures of a ship's ability to withstand a near-miss underwater explosion,and, as a consequence, also provide empirical data (Czaban et al., 1994) which, in thispaper, act as controls for theoretical estimates from ideal models.
sound into neural impulses. Although marine mammal ears clearly follow the landmammal blueprint, they have both grossand microscopic, aquatic-related adaptations at all auditory system levels (Ketten,1992, 1993).
Results
Charge parameters in this model are basedon published manufacturer's standards forHBX-l, a common ship shock test explosivein North American trials (DOC 1993; Reevesand Brown, 1994):
Marine mammal earsThere are three essential parts to the mammalian auditory periphery: 1) an outer earwhich captures sound, 2) a middle ear whichfilters and amplifies, and 3) the inner ear(cochlea) which is a band-pass filter andelectro-mechano-chemical transducer of
Model analyses include calculated pressuresand overpressures at eight arbitrary distances, ranging 1 to 10,000 m from thesource, and estimated distances from thesource for five zones that cover major stagesof blast injury and trauma. These stages aredesignated lethat sublethal with permanentthreshold shifts, temporary to permanentthreshold shift transitions, and minimal tozero injury transitional zones. Related datafrom previous studies are presented in anoverview of marine mammal hearing and ina brief summary of known factors for acoustic trauma and blast injury in mammals.
External (outer ear) canal adaptations rangefrom extreme (possibly dysfunctional) inCetacea to broad, essentially terrestriat airadapted canals in the true-eared seals andmustelids. Four outer ear adaptations arecommon to all cetaceans: there are no pinnae, no air-filled external canals, no encapsulated pneumatized areas, and exceptionally dense temporal bones. These appear tobe correlated largely with locomotion anddiving; Le., pinnae would provide hydrodynamic drag, and thin-walled, air-filled, bonychambers would be a liability in rapid, deepdives. However, these adaptations are mostderived in echolocating cetaceans, wherethey subserve an acoustic function (Ketten,1992). In odontocetes, the external ear canalsare completely occluded by wax and debris,ending in a blind pouch that does not contactthe middle ear. The temporal bones are suspended by ligaments in a peribullar sinusfilled with a spongy mucosa. This ligamentmucosa complex isolates the ear from bonysound conduction and aligns the middle earcavity with two orthogonat specialized fattychannels. Anatomical and behavioral studies suggest these discrete fatty tubes are lowimpedance sound channels (Brill et al., 1988;Ketten, 1992 for review). Mysticetes similarly have occluded external canals, but explicit tissue channels to the ear have not beenidentified. Pinniped and mustelid ears areless derived than cetacean. The external pinnae are reduced or absent. Ear canal diameter and closure mechanisms vary widelyin pinnipeds, and the exact role of the canalin submerged hearing has not clearly beendetermined.
HBX-l1,200/10,000 lbs(544/4,535 kg)(non-sequential)1,344/11,200 lbs(609/5,080 kg)8,800 m/sec
ExplosiveCharge Weights
TNT equivalents(HBX factor = 1.12)Detonating velocity
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D.R. Ketten
As in the external ear, most middle ear adaptations in marine mammals appear to berelated to diving. The dense-walled middleear cavity in whales is lined with a thick,distensible corpus cavernosum which mayregulate middle ear cavity volume or pressure. The Eustachian tube in both seals anddolphins is broad, fibrous, and resists collapse, thereby assuring rapid middle earequalization and decreasing the probabilityof implosive injury or middle ear barotrauma. Ossicular configurations and stiffnesscharacteristics are highly species-specificand therefore may reflect frequency specializations.
As in other mammals, whale inner ears arefluid-filled membranous labyrinths thathouse two sensory organs: a three-ringedvestibular system (for balance) and a spiralcochlea (for hearing). The vestibular systemis exceptionally small in whales and dolphins, and vestibular innervation is reducedproportionately; i.e., < 10% of cetacea VIIIth nerve fibers are vestibular, compared to40% in most mammals (Gao and Zhou, thisvolume). Vestibular down-sizing may be acorollary of fused cervical vertebrae inwhales, or alternatively, a valuable adaptation for rapid, continuous rotations in water.Maculae are present, implying that geotacticand linear acceleration cues at least are perceived.
Dolphin, baleen whale, and seal inner earshave the same general format as other mammalian ears (Fig. 1a); i.e., a fluid-filled, tripartate spiral with a resonating membranesupporting mechano-sensory receptors(Ketten, 1992; Ketten, 1993). Mammalianbasilar membranes are essentially tonotopicbivariate resonators built of repeated, relatively uniform modules. The range of thestiffness and mass of these modules in eachear determines the range of cochlear reso-
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nances and therefore the hearing limits ofthat ear. Because all mammalian basilarmembranes have a similar cellular structure,most interspecific differences in stiffnessand mass are determined largely by thickness and width distributions along themembrane's length. Highest frequencies areencoded in the base of the spiral where themembrane is narrow and stiff. Progressivelylower frequencies are encoded as the membrane becomes broader and more pliant towards the spiral apex. The primary soundtransducer is the Organ of Corti (Fig. 1b), anarray of hair cells with stereocilia that aredeflected when the basilar membrane is deformed by a pressure wave.
Membrane distortions depend on the interaction of intensity-frequency distributionsof incoming sounds with the resonancecharacteristics of the basilar membrane. In aresponsive membrane region, as the ciliabend, graded chemical changes in the haircells produce a depolarization in the auditory nerve, and impulses coding spectraland temporal patterns of the sound are sentto the brain. The absolute range of frequencies encoded by the ear varies naturally foreach species according to its average distribution pattern of inner ear stiffness andmass characteristics. Some mammals hearwell into the ultrasonic range (> 20 kHz);others, into the infrasonic «50 Hz) (Fay,1988). In addition to differences in absoluterange, species vary in their sensitivity ateach frequency band. Species ranges arefixed by basic structure; however, acuity varies widely by individual according to thehealth or integrity of the ear.
Specializations in marine mammal ears relate not only to extended frequency-intensity ranges, but also to the differences inacoustic power and transmission characteristics for waterborne versus airborne sound.
Estimates of blast injury and acoustic trauma zones
A. X~SECTION OF COCHLEA
SpiralGanglion
B, COCHLEAR DUCTspiral
ligament
Figure 1. Schematized marine mammal inner ear (a) and details of the cochlear duct (b) containing the Organ ofCorti (OC) which is the cochlear structure most directly and frequently impacted by sound. (Sc =scala; M =media;V = vestibuli; T = tympani; sp = spiral prominence)
The odontocete inner ear, like that of bats, isprimarily adapted for echolocation; the dolphin is capable of producing, perceiving,and analyzing ultrasonics. These ears haveexceptional frequency discrimination abilities but are comparatively poor at perceiving lower frequency sounds (Au, 1993). Balaenid ears are adapted to the other end ofthe spectrum; i.e., they hear poorly over 20kHz but are probably exceptionally acute atfrequencies in the 10-100 Hz range (Ketten,1992; 1993). Some cetaceans produce sourcelevels as high as 180 to 220 dB re 1 f.lPa(Richardson et al., 1991; Wursig and Clark,1993; Au, 1993). Pinnipeds are equally variable. Some, like the high-frequency harbour
seal (Phoca vitulina), are effectively - acoustically - sea-going cats; others, like the aptlynamed elephant seal (Mirounga angoustirostris), appear to have low to infrasonic adapted ears (Ketten, pers obs.).
In summary, marine mammals are acoustically diverse with wide variations not onlyin ear anatomy but also in hearing range andsensitivity. Both mysticetes and odontocetesappear to use soft tissue channels for soundconduction to the ear, which may decreasereceived acoustic power. Whale middle andinner ears are most heavily modified structurally from those of terrestrial mammals inways that accommodate rapid pressure
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changes. The end-product is an acousticallysensitive ear that is simultaneously adaptedto sustain moderately rapid and extremepressure changes, and appears capable ofaccommodating acoustic power relationships several magnitudes greater than in air.It is possible that these special adaptationscoincidentally may provide protectivemechanisms that lessen the risk of injuryfrom high intensity noise, but no behavioural or psychometric studies are availablewhich directly address this issue.
Noise traumaFor this discussion, sound-related trauma isdivided into two simplistic divisions: lethaland sublethal impacts. Lethal impacts arethose that result in the immediate death orserious debilitation of the majority of animals in or near an intense source; i.e., profound injuries from shock wave or blast effects. Lethal impacts are not, technically,pure acoustic trauma; they are discussed atthe end of this section. Sublethal impacts inwhich a hearing loss is caused by exposuresto perceptible sounds are correctly termedacoustic or noise derived trauma. In thesecases, some sound parameters exceed theear's tolerance; i.e., auditory damage occursfrom metabolic exhaustion or over-extension of one or more ear components. In somecases, sublethal impacts may ultimately beas devastating as lethal impacts, causingdeath through impaired foraging or predator detection, but they do not carry the immediate, broad devastation of a blast injury.
To determine whether an animal is subject tohearing loss from a particular sound requires understanding how its hearing sensitivity interacts with that sound. Basically, ifyou can hear a noise, at some level it candamage your hearing by causing decreasedsensitivity. The minimal level at which asound is perceived is the threshold.
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If an individual requires a significantly greater intensity (than the species norm) to perceive a particular frequency, there is a hearing deficit marked by a threshold shift.Noise induced threshold shifts are a moderately well investigated phenomenon for airadapted ears (Lehnhardt, 1986; Lipscomb,1978; Richardson et al., 1991 for detailed reviews). Any noise at sufficient levels willsignificantly shift hearing thresholds, but allnoises at the same levels do not cause equivalent shifts. The important issue is whetherthe impact produces a recoverable (TTS Temporary Threshold Shift) or permanent(PTS - Permanent Threshold Shift) loss.
Major research efforts have been directed atunderstanding the relationships of frequencies, intensities, and duration of exposuresin producing damage; that is, what sounds,at what levels, for how long, or how oftenwill produce temporary versus permanenthearing loss. A comprehensive discussion ofthe complexities involved in TTS versus PTSis not possible in the scope of this paper.Excellent reviews of noise trauma mechanisms are available in Lehnhardt (986);Miller et aI. (987); and Liberman (990). Only the briefest, and therefore necessarily simplistic, introduction is given here. Two fundamental effects are generally accepted:1. for pure tones, the loss centers around the
incident frequency.2. for all tones, at some balance of noise
level and time, the loss is irreversible.
TTS may be broad or punctate, according tosource characteristics, subject hearing sensitivity, and relative health of the ear impacted. The majority of studies have been conducted with cats and rodents, using relatively long duration stimuli (> 1 hr) and midto low frequencies 0-4 kHz) (Lehnhardt,1986). The extent and duration of suchthreshold shifts generally are proportional
Estimates of blast injury and acoustic trauma zones
to the extent of inner ear damage. Virtuallyall studies show that losses from short tomoderate term, narrowband stimuli « 1 hr,CF ± 2 kHz) are centered around the peakspectra of the stimulus and are largely recoverable although recoverability is strongly influenced by individual sensitivity of thesubject (Henderson et a!., 1983; Miller et a!.,1987). Histologic data from impacted earsshowed very discrete, localized cell damageat short-duration exposures progressing towidespread lesions with increasing intensity and bandwidth (Liberman, 1987). Recoverable (TTS) to non- recoverable (PTS) losseswere characterized by a progression fromsimple stereocilia fatigue to loss of hair cellbodies to broadening patches of strial, ligament, and neuronal degeneration.
In the typical air-adapted ear, a pure tonewith an intensity 80 dB (re 20 IlPa) higherthan the normal minimum response threshold for that frequency is generally sufficientfor stereocilia and hair cell damage. Mostdamaged cells will recover from this impact,but repeated exposures compound the insult. Recovery periods can vary from hoursto weeks among individuals. This findingled to the current allowable limit of 90 dB re20 IlPa for human workplace exposures(Lehnhardt, 1986); i.e., a 90 dB limit for allsignals reduces the probability of encountering a broadband signal with components 2':80 dB over threshold at the most sensitivefrequency range (500-5000 Hz) for humans.
Repeated exposures to TTS level stimuliwithout adequate recovery periods can induce permanent, acute threshold shifts(PTS). Liberman (1987) showed that losseswere directly correlated with levels of damage to hair cell stereocilia, the hair cell bodies, stria vascularis, the spiral ligament, andnerve fibers. The duration of a thresholdshift, is correlated with both the length of
time and the intensity of exposure. This doesnot, however, mean that TTS and PTS aresimply gradations of the same damagemechanisms. A major complication in anyTTS versus PTS comparison is that signalrise- time and duration of peak pressure aresignificant factors in PTS. If the exposure isshort, hearing is recoverable; if long, or has asudden, intense onset and is broadband,hearing, particularly in the higher frequencies, can be permanently lost. Experimentally, PTS is induced in air with multi-hourexposures to narrowband noise. In humans,PTS typically results accidentally from protracted, repeated intense exposures (continuous occupational background noises) orsudden onset of intense sounds (repeatedgun fire). Sharp rise-time signals have beenshown also to produce broad spectrum PTSat lower intensities than slow onset signalsboth in air and in water (Lipscomb, 1978;Lehnhardt, 1986; Liberman, 1987).
TTS has been produced in humans with underwater sound sources at levels of 150 - 180dB re 1 IlPa for frequencies between 700 5600 Hz (Smith and Wojtowicz, 1985; Smithet al., 1988). These intensities are similar tothose that induce TTS in air in humans because: a) intensity is a power ratio that depends on sound speed and density of themedium and b) the absolute value dependson the reference pressure used. The following calculations illustrate this difference:
1= pv = p2/epIail- = p2j(340 mlsee)(O.0013 glee)Iwata = p2j(1530 mlsee)(1.03 glee)
where I = intensity, v = vibration velocity, p= sound pressure, c = the speed of sound inthat medium, p = the density of the medium.Appropriate comparisons can be made interms of acoustic power (W1m2); however,in many texts the reference pressures will be
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D.R. Ketten
dB re 20 /-lPa for airborne sound versus dB rel/-lPa for in-water thresholds. Ears are essentially sound energy difference detectors. Ifan auditory percept depends on the samelevel of intensity in air and in water, theunderwater sound level that will produce anequivalent sensation must be 61.5 dB greaterthan its airborne counterpart; i.e., 150 dB re 1/-lPa "" 90 dB re 20 /-lPa.
Blast injurySimple, intensity related loss is not synonymous with blast injury. Blast injuries can bedivided into three groups based on the severity of the symptoms:
1. MILD - RecoveryPain, vertigo, tinnitus, hearing loss, tympanic tears
2. MODERATE - Partial lossOtitis media, tympanic membrane rupture, tympanic membrane hematoma, serum or blood in middle ear, dissection ofmucosa
3. SEVERE - Permanent loss or deathOssicular fracture or dislocation, round/oval window rupture, CSF leakage intomiddle ear, cochlear and saccular damage.
Moderate to severe losses result most oftenfrom blasts, extreme intensity shifts, andtrauma in which explosions or blunt cranialimpacts cause sudden, massive systemicpressure increases and surges of circulatoryor spinal fluid pressures (Schuknecht, 1993).Hearing loss in these cases results from aneruptive injury to the inner ear; i.e., with therarefactive wave of a nearby explosion, cerebrospinal fluid pressures increase and theinner ear window membranes blowout dueto massive surges in the inner ear fluids.
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Inner ear explosive damage frequently coincides with fractures in the bony capsule ofthe ear or middle ear bones and with ruptureof the eardrum. Although technically a pressure induced injury, hearing loss and theaccompanying gross structural damage tothe ear are more clearly thought of as theresult of the inability of the ear to accommodate the sudden, extreme pressure differentials and over-pressures from the shockwave.
At increasing distance from the blast, theeffects of the shock wave lessen. Eventhough there is no overt tissue damage, milddamage with some permanent hearing lossoccurs (Burdick, 1981, in Lehnhardt, 1986).This type of loss generally is called anasymptotic threshold shift (ATS) because itderives from a saturation effect. Like TTS,the hair cells are damaged, but as in any PTS,no recovery takes place. Because ATS depends on complex interactions of rise- timeand waveform, not simply intensity at peakfrequency, asymptotic hearing losses typically are broader and more profound thansimple PTS losses.
There is no well-defined single criterion forsublethal ATS (Roberto et al., 1989), but eardrum rupture, which is common to all stagesof blast injury, has been moderately wellinvestigated. Rupture per se is not synonymous with permanent loss; eardrum ruptures have occurred at as little as 2.5 kPaoverpressure. However, the incidence oftympanic membrane rupture is strongly correlated with distance from the blast (Kerrand Byrne, 1975). As frequency of ruptureincreases, so does the incidence of permanent hearing loss. In zones where > 50%tympanic membrane rupture occurred, 30%of the victims had long-term or permanentloss.
Estimates of blast injury and acoustic trauma zones
Recent experimental work showed thatweighted sound exposure level is a morerobust predictor of permanent loss thanpeak pressure (Patterson, 1991). Data withweighted levels are rare; overpressure dataare more common and are highly correlatedwith received levels (Roberto et al., 1989).Table 1 summarizes the experimental resultson overpressures associated with> 50% rupture. The data indicate complex and fast risetime sounds cause ruptures at lower overpressures than slow rise-time waveforms,and smaller mammals are injured by smalleroverpressures than larger animals. Of theanimals listed, sheep and pigs have ears anatomically closest to those of whales andseals. The air-based data for pigs and sheepimply that overpressures> 70 kPa are needed to induce 100% tympanic membrane rupture. However, cross-study comparisonsand extrapolations are risky because of radically different experimental conditions aswell as differences in power transmission inair and water.
Data available for submerged terrestrial andaquatic vertebrates imply that lower pressures in water than in air induce serioustrauma (Myrick et al., 1989; Richardson et al.,1991). For submerged terrestrial mammals,lethal injuries occurred at overpressures>55 kPa (Yelverton, 1973, in Myrick et al.,1989; Richmond et aI., 1989). In a blast studyin Lake Erie using Hydromex, a TNT-derivative explosive, the overpressure limit for100% mortality for fish was 30 kPa (McAnuffand Booren, 1976), suggesting overpressures between 30 and 50 kPa are sufficientfor a high incidence of severe blast injury.Minimal injury limits in both land and fishstudies coincided with overpressures of 0.5to 1 kPa.
Marine mammal blast injuriesVery few reports of blast induced trauma inmarine mammals detail injuries to the headregion. Bohne et al. (1985) reported on innerear damage in Weddell seals (Leptonychotesweddelli) that survived blasts, but they didnot have access to exposure levels or numberof exposures per animal. Scattered reports ofopportunistic examinations of animals exposed to large blasts include one on sea otters (Enhydra lutris) with extensive traumafrom nuclear explosions (cited in Richardson et al., 1991). The study concluded thatpeak pressures of 100-300 psi were invariably lethal.
Recently, several humpback whales (Megaptera novaeangliae) exposed to TOVEX blastswere shown to have severe blast injuries(Ketten et al., 1993; Lien et al., 1993). TOVEX,like Hydromex, is a TNT clone explosivesimilar to HBX-1 with an average detonationvelocity of 4,500 m/sec. Received levels inthe whales could not be calculated with confidence; however, the charge weights associated with the injuries ranged between 1700to 5000 kg. The animals died within threedays of the blasts, and the extent of the injuries implied they were close to the blastsite. Mechanical trauma in these ears included round window rupture, ossicular chaindisruption, bloody effusion of the peribullarspaces, dissection of the middle ear mucosawith pooled sera, and bilateral periotic fractures (Fig. 2). These observations are consistent with classic blast injuries reported inhumans, particularly with victims near thesource who had massive, precipitous increases in cerebrospinal fluid pressure andbrain trauma. There was no evidence of shipcollision or prior concussive injury in thesewhales, and no similar abnormalities werefound in ears from humpback whales notexposed to blasts.
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D.R. Ketten
Figure 2. A three-dimensional reconstruction from CT scans of an ear from a humpback whale (Megaptera71oveae71gliae) with blast injuries shows multiple fractures throughout the periotic, which are consistent withintracochlear blood. Blood, serum, and cellular debris of both intra- and extra-cochlear origin filled the middle earand surrounding peribullar region (reproduced with permission, Ketten et aI., 1993).
Table 1. Peak overpressures producing 50% tympanic membrane rupture (Phillips et aI., 1989; Richmond et aI.,1989; Bruins and Carwood, 1991)
Species
Sheep (Ovis spp.)
Pig (Sus spp.)Dog (Canis familiaris)
Monkey (Macaca mulatta)
Human (Homo sapiens)Rabbit (Sylvilagus spp.)
Guinea Pig (Cavia porcella)
400
Peakpressure
(kPa)
16575-12915278205296103172138-17257-34564155115
Waveform
Fast-rising, reflected shockComplexComplexFast-rising, reflected shockComplexSmooth-risingStaticFast-rising, reflected shockFast-rising, incident shockFast-rising, incedent shockComplexFast-rising, incident shockComplexFast-rising, incident shock
Estimates of blast injury and acoustic trauma zones
Discussion and conclusions
The few data points available for blast trauma in marine mammals indicate that external and middle ear structural adaptations in cetaceans and pinnipeds that mayminimize barotrauma do not provide immunity to blast trauma. Considering tli.esimilarities of seal and whale ears to landmammal ears, it is not surprising that explosions, and the resulting intense transientsound field and shock wave, produce bothblast injury and asymptotic acoustic trauma in marine animals. More important,even though the whale ear is a fluid-tofluid coupler, all marine mammals retainedan air-filled middle ear, which makes themsubject to all ranges of compressive-rarefactive blast injury.
The level of impact from blasts depends onboth an animal's location and, at outerzones, on its sensitivity to the residual noise.Important factors for trauma from explosivesources are the following:
1. Topography2. Proximity of ear to the source3. Anatomy and health of ear4. Charge weight and type5. Rise time6. Overpressure7. Pressure and duration of positive pres
sure phase
In the specified model, topographic effectsare minimal. The bottom is effectively nonreflective; therefore, with a 100 m detonation, surface reflections are the primary interference source.
The health of individual ears that may beimpacted cannot be estimated in advance. Itis reasonable to assume an average distribution.
HBX-1 has a rapid detonation velocity (8800m/sec), a relatively long peak pulse (5 to 10msec), and a complex waveform. It is effectively an instantaneous onset, high peakpressure, broad spectrum blast. Therefore,the explosive front and acoustic signature ofthe proposed charges (1200 and 10000 lbs)are likely to cause equivalent damage to allspecies in the target area; i.e., individualhearing ranges and thresholds are largelyirrelevant. High impedances and reflectionsat the air-sea boundary make calculations ofreceived levels for surface animals unreliable, but it is possible that some individualsabove or at the boundary layer will be partially protected.
Overpressure is based on a scaled distancenormalized to charge weight in TNT equivalents (Bruins and Cawood, 1991) and is calculated as:
Z = s/m1/3
PoverlkPIl) = (11.3/z-186/z2+19210/z3)(101.3)
Poverlps;) = PoverlkPIl) /6.9
where Z =scaled distance; s =distance (cm);m = charge mass (g) in TNT equivalents;PoverlkPa) = overpressure (kPa);Poverlps;) = overpressure (psi).Peak pressure (psi) is calculated using astandard algorithm (Czaban et al., 1994):
P = (8.22)(103) [W033/s]1-15
where W = weight (kg) in TNT equivalentsand s = distance from source (m).
Table 2 compares these calculations for theoretical maximal pressures and overpressures with semi-empirical peak pressure data reported by Czaban et al. (1994) forHBX. Under stable field conditions, there is
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D.R. Ketten
Table 2. Pressure level estimates at the charge depth contour (100 m) for 1200 lb and 10000 lb HBX charges withsimultaneous detonations (dB and measured maximum pressure data excerpted from Czaban et al., 1994)
-1200 II:> Charge-
Distance dB Maximum Theoretical Scaled Overpressure Overpressure(m) pressure pressure distance (psi) (kPa)
(psi) (psi)
1 257 95700.0 96121.8 1.18 167753.13 1157496.5710 233 6790.0 6804.9 11.85 164.17 1132.75100 206 481.0 481.8 118.48 1.38 9.52500 188 75.5 75.7 592.42 0.27 1.891000 180 34.0 34.1 1184.83 0.14 0.964500 164 5.99 6.0 5331.75 0.03 0.215000 162 5.4 5.4 5924.17 0.03 0.1910000 155 2.4 2.4 11848.34 0.01 0.10
-10000 II:> Charge-
1 263 216000.0 216577.0 0.58 1426284.83 9841365.3410 237 15300.0 15332.5 5.82 1381.99 9535.76100 211 1080.0 1085.5 58.15 3.49 24.08500 193 170.0 170.5 290.77 0.55 3.811000 185 76.8 76.8 581.53 0.28 1.934500 168 13.6 13.6 2616.89 0.06 0.445000 167 12.1 12.1 2907.65 0.06 0.3910000 159 5.4 5.4 5815.31 0.03 0.20
no significant difference between the empirical and theoretical values for peak pressurefor either charge weight.
Although multiple parameters are associated with both lethal and sublethal effects,studies of lethal or compulsory injury zonesfor fast-rise time, complex waveforms agreeon baseline criteria: 30-50 kPa peak overpressure in water and/or> 180 dB re 20 IlPain air (240 dB re 1 IlPa in water) (McAnuffand Booren, 1976; Yelverton and Richmond,1981; Phillips et al., 1989: Richmond et al.,1989; Myrick et ai., 1989). Given the pressuredistributions calculated for HBX-l detonations at 100 m, the 100% lethal impact zonelimits for a 1200 lb source are between 40 m(absolute minimum -land mammal) and 300m (conservative estimate based on otter psidata).
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For a 10000 lb charge, the equivalent minima-maxima limits for the killing ground is70 m to 800 m. Figures 3 and 4 illustrates thevariables that are most relevant to these limitestimates. For either charge, within 100 m ofthe source, death would likely be immediateor would follow in days as a result of concussive brain damage, cranial fractures, hemorrhage, etc. for the majority of animals. Forthe remainder, permanent, profound deafness from massive inner ear trauma wouldseriously impair the animal's ability to survive (Lehnhardt, 1986; Bruins and earwood,1991; Ketten et al., 1993; Schuknecht, 1993).
The criteria for differentiating PTS or ATSzones from TTS are less clear. The transitional lethal zones in which serious sublethalinjury predominates are estimated as 100500 m (1200 lb) and 150-900 m (10000 lb).
Estimates of blast injury and acoustic trauma zones
overpressure (kPa) 1200 Ibs
l!!I - overpressure (kPa) 10000 Ibs
and even minimal injury is rare (Yelvertonand Richmond, 1981; Smith et al., 1985, 1988;Myrick et al., 1989; Roberto et al., 1989).Therefore, between 1-10 km of the source thepotential for any acoustic impact drops precipitously (Figs. 3 and 4). Because intensitydecays exponentially, 5 km is a reasonablyestimate of a safe outer limit for the 10000 lbcharge for minimal, recoverable auditorytrauma versus 2 km for the 1200 lb charge.Figure 4 provides a schematic of all of thezones extrapolated from the data outlined.
403
100
Distance (m)1 0
100% lethalo~- for
mammalsfish .__. ... _.__
~~ 1000(/)/l)..a...~ 100o
Figure 3. Overpressures at the 100 m depth contour are plotted for each charge weight versus distance from source.The gray vertical bars show the differences in distance from source for the outer edge of 1200 vs 10000 lb chargezones based on the following categories: 100% lethal overpressure for submerged land mammals (57 kPa) and100% lethal overpressure for fish (30 kPa).
Beyond 500 meters and 900 m, the relativeincidence of PTS to TTS largely depends onindividual susceptibility. That is, the variables that will determine TTS vs PTS arehighly species dependent and the animalsare sufficiently mobile that no global, permanent division of these intermediate zoneswill be correct.
There is general consensus in the literatureon the criteria for assigning an outer limit tothe mild/moderate TTS zone. Generally, 515 psi is accepted as the value at which TTS
D.R. Ketten
LI ,,1200 los. psi
ll1l 10000 Ibs. psi
100% lethalrange for otters
300 psi 100 psiQ)...~ 1000IIIl!!0..
100
0:'
1 0 100
Distance (m)1000
50% TMruptlire
Figure 4. Peak pressures at the 100 m depth contour are plotted for each charge weight versus distance from source.The gray vertical bars show the differences in distance from source for the outer edge of 1200 vs 10000 lb chargezones based on reported pressures for 100% mortality in otters (Enhydra lutris) from blast and minimal peakpressure for 50% incidence of eardrum rupture,
It must be recalled here that these conclusions are highly speculative. They dependlargely on limited anatomical comparisons.Depending upon its actual, and currentlyunknown, function, the same specializedstructure in a marine ear could aggravate orameliorate the effects of blasts. For example,dolphins have soft tissue sound conductionpathways and fibro-elastic tissue beds thatacoustically isolate the inner ear. Either adaptation could significantly attenuate or enhance conduction of potentially damagingsounds. Without more explicit data, definitive guidelines for safe limits on underwa-
404
ter signals are not possible. Substantiallymore research is needed on all aspects ofmarine mammal hearing before wholly reliable estimates, much less solid answers, areavailable.
Acknowledgements
Moira Brown (East Coast Ecosystems), Randall Reeve, and Jan Czaban (NDHQ, Ontario) were instrumental in the creation of thisreport. Their assistance and encouragementare gratefully acknowledged, as is the coop-
Estimates of blast injury and acoustic trauma zones
>50%TTS ~
toNo Injury
"I
1 04
L. 'I
>50% TTSto ...~
No InjuryTransition
1200 Ib charge zones
10000 ib charge zones
Distance from source 1 000(m)10010
Figure 5. Impact zone summary for 1200 and 10000 lb charges. The 5 divisions shown represent distances from thesource in which a) 100% mortality is expected (lethal), b) permanent hearing loss is common and some mortality isexpected (sublethal), c) > 50% animals have some permanent hearing loss (all ranges of acoustic trauma), d) themajority of animals have temporary hearing loss but some permanent auditory damage will be found (transitionaltrauma), and e) little or no clinically detectable auditory damage (low impact). The zones are synthesized based onconservative extrapolations of data from fish, submerged terr~strial mammals, and humans.
eration of the Canadian National DefenseHeadquarters and Nodeco, Newfoundland.An early version of this paper was preparedat the request and with support from EastCoast Ecosystems, Quebec, and was submitted previously to Bio Acoustics. Original research on mysticete and odontocete ears andparticipation in this symposium was supported by Office of Naval Research contractsN00014-92-J-4000 and N00014-93-1-0940.
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