seaquake induced injury in whales and dolphins

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Joints are the meeting points of two separate bones, held together and in place by connective tissues and ligaments. All of the joints in our bodies are surrounded by synovial fluid, a thick, clear liquid. When you stretch or bend your finger to pop the knuckle, you are causing the bones of the joint to pull apart. As they do, the connective tissue capsule that surrounds the joint is stretched. By stretching this capsule, you increase its volume. And as we know from chemistry class, with an increase in volume comes a decrease in pressure. So as the pressure of the synovial fluid drops, gases dissolved in the fluid become less soluble, forming bubbles through a process called cavitation. When the joint is stretched far enough, the pressure in the capsule drops so low that these bubbles burst, producing the pop that we associate with knuckle cracking.

It takes about 25-30 minutes for the gas to redissolve into the joint fluid. During this period of time, your knuckles will not crack. Once the gas is redissolved, cavitation is once again possible, and you can start popping your knuckles again.

Fluids boil not only when the temperature of the fluid gets too hot, but also when the pressure on the fluid gets too low. At an ambient sea level pressure of 14.7 psia (one bar) water will boil at 212°F. (100°C) If the negative phase (vacuum) of a seaquake pressure wave lowers the pressure in the water it will boil at a much lower temperature and conversely, if the pressure is raised by a passing positive phase of a seaquake wave, the water will not boil until the temperature gets much hotter. There are charts available to give you the exact vapor pressure for any temperature of water. If you fall below this vapor pressure the water will boil. As an example:

Fahrenheit	Centigrade	Vapor pressure lb/in2	Vapor pressure (Bar)
40	4.4	0.1217	0.00839
100	37.8	0.9492	0.06546
180	82.2	7.510	0.5179
212	100	14.696	1.0135
300	148.9	67.01	4.62

In general, seaquakes generate powerful hydroacoustic waves of alternating pressures. Each wave consist of a compression phase of high pressure followed by a tension phase (vacuum) of low pressure. During an encounter with a reverse thrusting seaquake in which the depth of water is less than 500 meters and the vertical motion in the seafloor is rapid, we estimate the level of pressure near the surface during the compression phase at ~50 pounds per square inch above the surrounding water pressure (230.75 dB re: 1 micro PA). The equal but opposite tension (vacuum) phase will thus reach a minus 50 pounds per square inch. Thus, our estimates indicate that a pod on the surface surprised by a potent seaquake would be subject to a range of changing pressure of ~100 pounds per square inch.

Seismic waves range from .01 to 150 cycles per second (hertz) with the average being somewhere near 7-8 hertz. A pod exposed to a potent seaquake in which the pressure changes came at 7 hertz would be forced to endure changes in ambient pressure equivalent to diving back and forth from the surface to 70 meters seven times per second.

Seawater will vaporize (boil) if its temperature gets too high just as it will also turn to vapor if the absolute pressure gets too low. At sea level, where the surrounding air pressure is ~15 pounds psi, seawater vaporizes (aka: cavitates or boils) when the temperature reaches ~100 degrees centigrade (~212 degrees F). If the surrounding pressure is suddenly decreased by the vacuum phase of a seaquake wave to about 5 psi, seawater will start to vaporize (aka: cavitate or boil) at room temperature.

Now put yourself in the place of the whale. Imagine your pod has just finished a one hour dive to 200 meters and your body is super-saturated with dissolved nitrogen. To get rid of this gas you must continuous breathe deeply on the surface for up to an hour. However, imagine that after about 5 minutes on the surface your pod is suddenly exposed to a potent series of pressure changes generated during a seaquake. The surrounding water pressure during the negative phase of the seaquake drops momentarily to a minus 50 pounds per square inch causing the nitrogen saturated in you flesh and blood to suddenly come out of solution and form hundreds of thousands of tiny bubbles. You are now suffering the bends and the only way to get rid of the bubbles is to dive back down to 200 meters and then re-surface at a very slow rate.

There's another problem. During the exposure to the changing pressures, the air contained in your head sinuses and middle ear cavities expanded and collapsed violently, rupturing the membranes surrounding these enclosed air pockets (see barotrauma below).

Cavitation implies cavities or holes in a liquid. These holes can also be described as bubbles; thus, cavitation/decompression sickness in diving mammals is an illness caused by the formation and collapse of bubbles in the animal's blood, tissues, and bones.

Houser et al. [2001] modeled the accumulation of nitrogen in the muscle of several cetacean species. The results suggested that tissue nitrogen supersaturation in certain cetaceans could be substantially higher than previously modeled. Slow descending/ascending and deep diving marine mammals, such as beaked whales and sperm whales, were predicted to accumulate the greatest amount of nitrogen during diving, e.g. the northern bottlenose whale was predicted to have tissue nitrogen saturations >300% ambient when surfacing from a typical series of dives. Greater accumulation would presumably result from longer and deeper dives. The results of Houser et al. indicate that if gas bubble growth in tissues can be triggered or driven by seaquake exposure along with exposure to man-made sources, beaked whales and other inhalation deep-diving marine mammals might experience increased risk to micro-bubble activation and growth under appropriate exposure conditions.

Crum and Mao (1996) noted that repeated exposures to sudden changes in pressure were not required to drive the growth of bubbles if tissues were sufficiently supersaturated. Rather, once bubble growth was initiated it would be supported through static diffusion and would continue in the absence of further exposure to seaquake pressure changes.

John Potter (mechanism for acoustic triggering--pdf file) concludes that sizeable bubbles may be created in a period of a few minutes by static diffusion, given sufficient supersaturation levels of 150-300% (typical of deep-diving marine mammals on surfacing) and destabilization of in vivo bubble nuclei. The accumulation and aggregation of such bubbles may be sufficient to cause emboli and high, localized pressures in tissues that could result in decompression sickness. If micro-bubbles can be destabilized, the impact is likely to be significant in highly gas supersaturated tissues rather than in mildly supersaturated tissues. Slow, deep diving marine mammals are therefore expected to be at greater risk of acoustically triggered micro-bubble growth. This is consistent with the observations of deep-diving marine mammals being selectively stranded after receiving moderate acoustic intensities loosely estimated to be in the region of 160-165 dB re 1 micro Pa (less than one pound per square inch).

Potter said, "Crum and Mao did not need to concern themselves with issues of stabilization since they were interested in exploring the conditions under which rectified diffusion might inflate micro-bubbles, whether in supersaturated tissues or not. Their results showed that rectified diffusion (unassisted by normal diffusion) would not be effective at inflating micro-bubbles below receive acoustic levels of 210 dB re 1 micro Pa or so (4.6 pounds per square inch). x x x SCUBA divers are advised against strenuous exertion during ascent from a dive and after prolonged and deep dives for this reason. One might expect that deep-diving marine mammals would also avoid excessively energetic manoeuvres during ascension through depths at which tissues become supersaturated as well as shortly after a deep dive sequence, observations that have anecdotally been observed. If micro-bubbles can be activated by physical activity, presumably by creating tensions in the tissues, could an acoustic pressure wave act in a similar manner? If so, one might expect vulnerable species to avoid vocalising strongly after deep-diving. This is not known and further research on such behavioural clues would be welcome.

If an acoustic source (seaquake) were to provide a destabilising force to micro-bubbles so that they become able to absorb gas by diffusion across their boundary walls, deep-diving marine mammals with highly super-saturated tissues would be expected to experience bubble growth, the degree of which should vary with the degree of saturation. Pain, disorientation and hemorrhaging (possibly causing vertigo and other vestibular dysfunction) known to occur under certain degrees of bubble formation and growth could then reasonably be expected to cause manifestations similar to that observed in decompression sickness. If experienced, it seems possible that such induce such animals to beach, and to exhibit the kind of injuries found in the Bahamas beached whales.

If there is a mechanism acting approximately in the way this paper suggests, this may explain part of the mystery as to why beaked whales appear to strand when exposed to ‘moderate’ levels of sound (160-165 dB). While it is true that other inhalation deep-diving marine mammals (such as Sperm whales) have not been observed to beach, this could simply be due to a difference in habitat and behaviour that makes their response more likely to result in sinking in deep water and not being seen.

This researcher suggest that beaked whales are more vulnerable to navy sonar simple because these signals peak their curiosity. It might be that beaked whales see navy sonar as a competitor and swim in too close to these units with the idea of defending their territory. For example, several thousand bottlenose dolphin were killed by GLORIA sonar in 1987 and 1988 when it was towed along the US Atlantic Coast in a seafloor mapping operation. GLORIA left the Atlantic Coast to tour European waters starting in 1988 and caused the deaths of hundreds of thousands of seals and dolphins. These defenseless animals were drawn to GLORIA out of curiosity and slaughter when the unit blast out a narrow 2-second beam of sound every 30 seconds. (GLORIA finally retires--thank GOD)

Tissue samples are still available. This researcher suggest that the pox marks and sleuthing skin noted in the dying animals was the result of cavitation damage from exposure at close range to GLORIA's 252 dB signal at 5,200 kilocycles. The viral and bacterial infections were all the result of failing immunity and were secondary to the acoustic slaughter.

During the tension phase of seaquake waves, when the pressure drops into the minus column (vacuum), the sea starts to boil and so does the blood and fluids inside the body of exposed whales.

The bone of whales would be especially vulnerable to the violently collapse and expansion of bubbles. For example, if a diving whale encountered pressure changes from a seaquake, the nitrogen dissolved in its bones and tissues would come out of solution and be subject to violent expansions and implosions leading to extreme microscopic trauma. This would be detected on post-mortem examinations as tiny pits or pockmarks in the bones.

Are the pit marks in the 100-year-old whale bone above really evidence of previous seaquake exposure? Older whales are more likely to have encounter repeated seaquakes, which agrees with the findings that the pit marks are more abundant in older whales and missing in the young. (more on cavitation damage in sperm whale bone)

The LF signal from military sonar and from seaquakes have a lot in common. In fact, whatever injury a whale would get from one he could get from the other since the trauma is the direct result of the alternating pressure waves, especially the vacuum phase.

Whale blood and seawater also have a lot in common. Besides having the same specific gravity and the same salt content, bubbles will form in both at about the same negative pressures.

When cavitation bubbles form inside capillaries, they appear to rip the blood vessels apart. Once bleeding begins, pools of blood are conducive to even more severe cavitation bubbles, which can lead to hematomas.

At the onset of cavitation, bubbles oscillate violently, undergoing initial explosive growth and subsequent rapid collapse. In the final phase of collapse, pressure and temperature inside the bubble can reach thousands of atmospheres and degrees Kelvin. This high temperature and pressure leads to the emission of light (sonoluminescence) and can cause bond dissociation in molecules, producing free radicals capable to react with biomedical species in the same way as those produced by ionizing radiation. Immediately after the bubble rebound, the high-pressure shock wave emanates from the bubble location and causes mechanical damage to the surrounding fluid, tissue and bone.

It is highly likely that most of the bubbles collapse asymmetrically in tiny blood vessels because there is limited "space" for them to undergo expansion. This is true, particularly, for the bubbles near vessel walls. The behavior of a violently pulsating bubble adjacent to a rigid wall was studied both numerically and experimentally. They found that wall-directed reentrant jet is formed in the later phase of the bubble collapse. The jets produced by bubbles induce the erosion of endothelia and, finally, hemorrhage. Hence, the greatest destruction of tissue and bone is made by violently collapsing bubbles.

The fact that a negative pressure wave from a seaquake creates a vacuum and establishes cavitation in the blood of the whales is unique in nature. Vacuums of high intensity give rise to the formation and oscillation of gas or vapor bubbles. It is precisely these cavitation bubbles that are responsible for hemolysis and hemorrhage. Cavitation inception is a threshold process and significantly depends on the presence of “nuclei” in the blood. The more the quantity of “nuclei”, the smaller the vacuum amplitude needed for cavitation inception. Like any natural liquid, blood has cavitation nucleation agents, and therefore any negative pressure can cavitate it.

Toothed whales and dolphins have a complex system of air sacs and sinuses, which vary in size and complexity. Membranes divide these sinuses into many small pockets, richly supplied with networks of blood vessels and surrounded by bone.

The blood vessels inside the sinus cavities have a unique function. On the surface they lay flat against the inside of the cavity wall, held in place by a large volume of air and oily foam. This air mixture easily compresses as the animal dives and would create a vacuum inside the cavity if it were not for the fact that blood begins to swell the blood vessels compensating for the reduction in the volume of the air/foam.

The deeper the whale dives, the more blood is held in these vessels. When the whale starts back to the surface, the air and oily foam begin to expand and pressure starts to build inside the sinuses forcing the blood out. In this fashion, along with some help from the Eustachian tube, pressure inside the sinuses is equalized to changing ambient pressure during a dive.

The weak point in the entire system, as applies to sudden changes in pressure, is the diameter of the bony channels through which the blood must flow in and out of the sinus cavity. The volume of blood that can be supplied and/or drained from the system is directly dependent on the size of these openings.

Within the confines of this theory, waves of alternating pressure from a seaquake, extended in time, alter the ambient pressure too drastically, too rapidly, and/or for too long, thereby altering the volume of air/foam mixture inside the sinuses too vigorously, exceeding the ability of blood to move in and out through this bony restrictions.

Once a blood vessel is ruptured inside these sinuses, the area fills with blood and no longer functions properly.

The volume of air in the enclosed air spaces of a diving mammal underwater is in direct relationship to the pressure in the water. If a seaquake momentarily quadrupled the pressure surrounding a pod of whales, the volume of air inside each animal's sinus cavities would be reduced to one-fourth of the previous volume. A moment later, when the negative phase of the wave passed over the pod, the air in their sinuses would rapidly expand to over four times previous volume and cavitation would occur in the blood stream and in the oily foam of the sinuses.

These extreme alterations in the volume, and in the conditions for cavitation, would continue for as long as the seaquake continued, or until the whales reached the surface and raised their heads out of the water.

The depth of the pod when it encounters these rapid pressure changes is also critical. If they are deep, where ambient pressure is much higher, the change in the volume of entrapped air is not as drastic as it would be if the whales were caught shallow. For example, a 75-psia pressure pulse would produce a 500% change in the volume of air spaces at 33 feet, but only a 33% change at 450 feet.

An injury resulting from such drastic changes in the volume of the air spaces within an animal's body is called barotrauma. This word is well known in the field of scuba diving, yet discussion of a barotrauma-like injury never appeared in scientific material dealing with marine mammals until the public confronted the US Navy over the danger from LFA sonar. Undeniable evidence that this system can kill marine animals emerged in March 2000, when strandings of four different species of whales and dolphins in the Bahamas coincided with a Navy battle group's use of LFA sonar in the area. All but one of the whales suffered hemorrhages in and around the middle ear, almost certainly the result of barotrauma.

Whales and dolphins are protected from lung barotrauma because their ribs are hinged, allowing this air space to collapse during any increase in pressure. Nor is there any damage caused by a sudden decrease in pressure since this space is open allowing any expanding air to be vented out the mouth. Neither would the flesh and bones of diving mammals be affected since this part of their anatomy is mostly water allowing the pressure to travel through the body and back into the water without much fuss. But air spaces within the whale's head are a different story.

Even minor barotrauma and/or cavitation trauma would prevent the animals from diving thus disrupting their ability to feed. The degree of injury, and thus how long feeding would be disrupted, would vary depending on the intensity of the pressure waves and the depth of the pod when exposed.

Not all pressure-related injuries would be fatal. Pods have probably survived many encounters with seaquakes throughout their long lives. They likely recover if they find food on the surface or regain the ability to dive within a week or so. However, if they do not return to actively feeding within a few weeks, they would soon reach a point of no return where recovery would be impossible due to severe stress, failing immunity, parasitic invasion, shark attack, malnutrition, and dehydration. The outlook for a pod that has slipped past this point of no return is to either end their lives in a shark's belly or on a beach.

D. L. Miller, “A review of the ultrasonic bioeffects of microsonation, gas-body activation, and related cavitation-like phenomena,” Ultrasound in Med. & Biol. 13, 443 – 470 (1987).

J. S. Allen and R. A Roy, "Dynamics of gas bubbles in viscoelastic fluids. I. Linear viscoelasticity," J. Acoust. Soc. Am. 107, 3167 - 3178 (2000)

G. L. Chahine, "Cavitation dynamics at microscale level," J. Heart Disease 3, 102 - 116 (1993)

W.-S. Chen, P. P. Chang, T. J. Matula, and L. A. Crum “Correlations between UCA-destruction-induced bioeffects and inertial cavitation dose,” J. Acoust. Soc. Am. 107, 2814 (2000)

L. A. Crum and Yi Mao “Acoustically enhanced bubble growth at low frequencies and its implications for human diver and marine mammal safety” Journal of the Acoustical Soc. Am. pp. 2898-2907, 99 (5) (1996)

D.S Houser, R. Howard and S. H. Ridgway “Can diving-induced tissue Nitrogen supersaturation increase the chance of acoustically driven bubble growth in marine mammals?” Jnl Theor. Biol. 213 pp 183-195 (2001)

L. A. Frizzell, "Biological effects of acoustic cavitation," in Ultrasound: its chemical, physical, and biological effects, edited by K. S. Suslick (VCH Publishers, New York, 1988), pp. 287 - 303

K. Sato, Y. Tomita, and A. Shima, "Numerical analysis of a gas bubble near a rigid boundary in an oscillatory pressure field," J. Acoust. Soc. Am. 95, 2416 - 2424 (1994)