The present state of passive (linear and non-linear) and active techniques for hearing protection in the military environment is reviewed. Solutions which allow to protect the ear from large continuous and high-level impulse noises while preserving the operational abilities of the personnel (detection, localization, communication...) are emphasised.

This review will briefly examine evidence supporting the hypothesis that sound causes changes in cochlear blood flow, intracochlear oxygen levels, and the morphology of cochlear blood vessels. A survey of the literature shows that traditional histopathological studies provided such evidence and that decreased cochlear blood flow can be demonstrated and measured by laser Doppler flowmetry and by direct observation of cochlear microvessels. Oxygen levels also decline and possibly to a greater degree than blood flow. There is also evidence that in certain circumstances sound can increase blood flow. Reduced blood flow, or reduced oxygenation, is critically important in an organ system with high energy needs like the cochlea. Therefore, a second hypothesis, that sound-induced reduction in CBF represents a functional ischemia, will be explored in examining the relevance of traditional ischemia/reperfusion models to cochlear damage. It is found that reactive oxygen species (free radicals and oxidizing ions) are present in sound-induced hearing loss and thus there is evidence that an ischemia/reperfusion type of injury occurs during loud sound exposures.

Some research suggests that young children may be relatively more susceptible to noise­ induced hearing loss (NIHL) than adults, and that the unique noise footprint associated with military jet aircraft is particularly damaging to hearing. This pilot study looked for evidence of NIHL in adults who have been exposed to military jet noise in early childhood, while living in Married Quarters on active RAF fast jet stations. Many Married Quarters lie within 70 dB(A) Leq contours, fewer in 83 dB(A) Leq contours. A cross-sectional pilot study was under­taken to examine the hypothesis that military jet noise exposure early in life is associated with raised hearing thresholds.

Studies have shown that in order for sound to affect the vestibular end organs in the inner ear, very high intensities are required. Furthermore, in patients with noise induced hearing loss, vestibular signs, if present, are subclinical. In order to study possible auditory-vestibular interactions in a more controlled fashion, using physiological sound intensities, the present study used short latency vestibular evoked potentials (VsEPs) to impulses of angular (15,000°/sec ² , risetime 1.5 msec) and linear (3-5 g, rise time 1.5 msec) acceleration were used to study the possible effects of sound on peripheral vestibular function in rats. Four different paradigms were used: a - an intense (135 dB pe SPL) click stimulus was presented 5 msec before the linear acceleration impulse and the VsEP to 128 stimuli were recorded with and without this click stimulus. There was no effect of the preceding intense click on the first wave (reflecting end organ activity) of the linear VsEP. b - 113 dB SPL white noise "masking" was presented while the VsEPs were elicited. A 10-20% reduction in the amplitude of the first VsEP wave was seen during the noise exposure, but 5 minutes after this exposure, there was almost complete recovery to pre-exposure amplitude. c - 113 dB SPL noise was presented for one hour and VsEPs were recorded within 15 minutes of cessation of the noise. The auditory nerve-brainstem-evoked response showed a temporary threshold shift while there was no effect on the VsEP. d - 113 dB SPL white noise was presented for 12 hours per day for 21 consecutive days. Auditory nerve-brainstem-evoked responses and vestibular (VsEPs) function were studied one week after the conclusion of the noise exposure. Auditory function was severely permanently depressed (40 dB threshold elevation and clear histological damage) while the amplitude of wave 1 of the VsEP was not affected. It seems therefore that even though intense noise clearly affects the cochlea and may have a "masking" effect on the vestibular end organs, the intensities used in this study (113 dB SPL) are not able to produce a long-term noise induced vestibular disorder in the initially normal ear. These differences between the response of the cochlear and vestibular end organs to noise may be due to dissimilarities in their acoustic impedances and/or their electrical resting potential.

In spite of the differences in the nature of the insult, the hearing loss from ototoxic drugs and noise exposure share a number of similarities in cochlear pathology. This paper explores the common factors between noise-induced hearing loss and ototoxicity by experimentally manipulating cochlear glutathione (GSH). In the first experiment, chinchillas were treated with a drop of saline (50 µl) on the round window of one ear and a drop of buthionine sulfoximine (BSO, 50 µl of 200 mM) on the other ear. BSO is a drug that blocks GSH synthesis and it was hypothesized that GSH-depressed ears would be more vulnerable to noise. Six hours after treatment, the animals were exposed to a 105 dB 4 kHz octave band noise for 4 hours, then a second dose of BSO was applied 2 hours later. The BSO treated ears showed more temporary threshold shifts and reduced GSH staining at day 4 post exposure, but there was no BSO effect in terms of greater permanent threshold shift (PTS) or hair cell loss. In the second experiment, chinchillas were pretreated with BSO and 3 days later were given either a single dose of carboplatin (25 mg/kg i.p.), a double dose (day 3 and 7) or only BSO. Chinchillas that received BSO and the double dose of carboplatin had significantly greater loss of inner and outer hair cells than the carboplatin chinchillas. In addition, the BSO and carboplatin chinchillas also had larger decreases in evoked response amplitudes suggesting that GSH depletion potentiated the ototoxicity of carboplatin. These results are discussed in terms of the role of reactive oxygen species in creating hearing loss and the potential protective role of glutathione.