Dear All
We are happy to to announce the publication of our open access paper in Frontiers in 
Aquatic Physiology called "Estimated tissue and blood N2 levels and risk of 
decompression sickness in deep-, intermediate- and shallow diving toothed whales during 
exposure to naval sonar". (Kvadsheim, P. H., Miller, P. J. O., Tyack, P. L., Sivle, 
L. L. D., Lam, F.-P. A. and Fahlman, A. (2012). Estimated tissue and blood N2 levels and 
risk of in vivo bubble formation in deep-, intermediate- and shallow diving toothed 
whales during exposure to naval sonar. Frontiers in Physiology 3). For those that might 
be interested, the paper can be downloaded at the following link:
http://www.frontiersin.org/aquatic_physiology/10.3389/fphys.2012.00125/abstract

Sincerely,
Andreas

Abstract:
Naval sonar has been accused of causing whale stranding by a mechanism which 
increases formation of tissue N2 gas bubbles. Increased tissue and blood N2 
levels, and thereby increased risk of decompression sickness (DCS), is thought 
to result from changes in behavior or physiological responses during diving. 
Previous theoretical studies have used hypothetical sonar-induced changes in 
both behavior and physiology to model blood and tissue N2 tension (PN2), but 
this is the first attempt to estimate the changes during actual behavioral 
responses to sonar. We used an existing mathematical model to estimate blood 
and tissue N2 tension (PN2) from dive data recorded from sperm, killer, 
long-finned pilot, Blainville’s beaked and Cuvier’s beaked whales before and 
during exposure to Low- (1-2 kHz) and Mid- (2-7 kHz) frequency active sonar. 
Our objectives were; 1) to determine if differences in dive behavior affects 
risk of bubble formation, and if 2) behavioral- or 3) physiological responses 
to sonar are plausible risk factors. Our results suggest that all species have 
natural high N2 levels, with deep diving generally resulting in higher end-dive 
PN2 as compared with shallow diving. Sonar exposure caused some changes in dive 
behavior in both killer whales, pilot whales and beaked whales, but this did 
not lead to any increased risk of DCS . However, in three of eight exposure 
session with sperm whales, the animal changed to shallower diving, and in all 
these cases this seem to result in an increased risk of DCS, although risk was 
still within the normal risk range of this species. When a hypothetical removal 
of the normal dive response (bradycardia and peripheral vasoconstriction), was 
added to the behavioral response during model simulations, this led to an 
increased variance in the estimated end-dive N2 levels, but no consistent 
change of risk. In conclusion, we cannot rule out the possibility that a 
combination of behavioral and physiological responses to sonar have the 
potential to alter the blood and tissue end-dive N2 tension to levels which 
could cause DCS and formation of in vivo bubbles, but the actually observed 
behavioral responses of cetaceans to sonar in our study, do not imply any 
significantly increased risk of DCS.

--
Andreas Fahlman
Department of Life Sciences
Texas A&M- Corpus Christi
6300 Ocean Dr Unit 5892
Corpus Christi, TX 78412
Ph. +1-361-825-3489
Fax +1-361-825-2025
mail: andreas.fahl...@tamucc.edu
web: http://www.comparative-physiology.tamucc.edu/



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