Abstract
To evaluate the safety of sonar exposure from a neurological perspective, the vulnerability of the central nervous system to underwater exposure with high-intensity, low-frequency sound (HI-LFS) was experimentally examined. Physiological, behavioral and histological parameters were measured in anesthetized, ventilated rats exposed to brief (5 min), underwater HI-LFS. Exposure to 180 dB sound pressure level (SPL) re 1 μPa at 150 Hz ( n = 9) did not alter acute cardiovascular physiology (arterial blood pH, pO 2, pCO 2, heart rate, or mean arterial blood pressure) from that found in controls ( n = 11). Rats exposed to either 180 dB SPL re 1 μPa at 150 Hz ( n = 12) or 194 dB SPL re 1 μPa at 250 Hz ( n = 12) exhibited normal cognitive function at 8 and 9 days after sound exposure. Evaluation of neurological motor function revealed a minor deficit 7 days after 180 dB SPL/150 Hz exposure that resolved by 14 days, and no deficits after 194 dB SPL/250 Hz exposure. No overt histological damage was detected in any group. These data suggest that underwater HI-LFS exposure may cause transient, mild motor dysfunction.
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