Tinnitus from the Latin word tinnire meaning ringing is the perception of sound within the human ear in the absence of corresponding external sound. The most common cause is noise induced hearing loss. Tinnitus may be induced by an acoustic trauma or a permanent noise in the workplace. In case that Tinnitus is induced by acoustic trauma the site of lesion is commonly the base of the cochlea. Tinnitus in the senile population is mostly accompanying presbycusis. Although the incidence of permanent tinnitus following noise exposure is high, little is published about this issue. In the current article we are aimed at studying the prevalence of tinnitus in Minoo and other manufactures.

NIHL occurs when too much sound intensity is transmitted into and through the auditory system and can be occur following a shot gun or the exposure to a moderately intense sound for a long period of time. NIHL caused by acoustic trauma refers to permanent cochlear damage from a one-time exposure to excessive sound pressure. This form of NIHL commonly results from exposure to high-intensity sounds such as explosions, gunfire, a large drum hit loudly and firecrackers.Meanwhile the sound intensity, duration of exposure and personal hearing thresholds as the effective factors in the amount of noise induced hearing loss should not be overlooked.  Since numerous investigations have been performed about intense sudden sound we will discuss it in detail in the current article.

Many researchers have reported that after the sound trauma, RNA and DNA in the outer hair cells and ganglion cells will decrease. Some scientists have also mentioned the mitochondrial enzyme deficits in cochlear cells. Sound stimulation will induce the decrease of enzyme activities which are effective in the process of energy production. This process happens because of the reduced ATP synthesis and in turn the damage to receptors due to energy disruption.  The moderate oxygen deficiency can also be considered as a potential factor in the amplitude changes of the potential of cochlear microphonic due to irrita6ing sounds. On the other hand, since the organ of corti is far from blood tissue, logically, Anaerobic Glycogen should be considered as the main factor in the metabolism of the organ of corti.In addition to that, there are evidences which demonstrate intense acoustical stimulation can increase Na+ and decrease K+ in endolymphatic fluid and a contrary effect in perylimphatic fluid in scala vestibule.

Method and Materials :this cross sectional descriptive and analytic survey was done at Golestan navy hospital in Tehran, between June 1998 and March 1999 on total of 69 male subject (104 ears, ) 50 acoustic trauma & 54 noise induced H.L) between 20 to 40 ears old.
Results:1- The mean acoustic reflex threshold at 1 kHz showed there is no significant difference between two groups.
2- The intensity elicited maximum reflex amplitude at 1 kHz didn&apost produce at a significant linear correlation with subject&aposs age and ear canal volume in both groups.
3- The intensity elicited maximum reflex amplitude in NIHL group wasn&apost shown a significant correlation with ear compliance and gradient.
4- The mean Intensity (SPL) elicited maximum reflex amplitude in NIHL group was more than mean intensity (SPL) in acoustic trauma group.
5- The mean intensity (SL) elicited maximum reflex amplitude in NIHL group was More than mean intensity (SL) in acoustic trauma group.
Conclusion: Acoustic reflex amplitude is reduced for subjects with NIHL compared with acoustic trauma subjects.