Cochlear pathology due to noise exposure were investigated by chiefly experimental approaches. Among a variety of the experimental procedures were predominantly employed optical microscopy and scanning and transmission electron microscopy for morphological examination and evoked response audiometry. Experimental animals used were guinea-pigs and mice. They were exposed to pure tone of 500, 2, 000 and 4, 000Hz with 110-120 dB SPL for various durations from 10 minutes to 15 days consecutively, or to a shock sound. Immediately and in different periods of time within 2 months after the completion of the exposure, the cochlea was examined and the extent of the lesions ranging initial sign to advanced degeneration was minutely clarified. Besides, it was demonstrated that the immature cochlea is less affected by sound injury while vulnerability of the mature cochlea is much intensified by concomitant medication with aminoglycoside drugs. Changes in auditory function were studied by evoked response auditometry at the stage in which no morphological change was found, and, as a result, a transient increase in amplitude of the course of recovery from the sound injury.
The pathology of cochlear sensory cells has been studied by light microscopy, phase contrast microscopy and transmission electron microscopy, but the study on the acoustic trauma of the sensory hairs are seldom. With guinea pigs exposed to pure tone of 500-4, 000Hz and white noise (80-135dB SPL) for 1-4 hours the damage of the cochlear sensory hairs was studied by scanning electron microscopy. The results are summarized as follows. The sensory hair damage such as bleb formation, derangement of sensory hairs, break-off of hair tips, fusion and loss of sensory hairs due to intense auditory stimulation appeared markedly at an early stage. The site of the most marked hair damage coincided with the response area of respective frequency in the case exposed to pure tone, namely, when exposed to 4, 000Hz it was found at the lower portion of the second turn, with 2, 000Hz at the middle of the second turn, with 1, 000Hz at the lower part of the third turn, and with 500Hz at the middle of the third turn. Some difference could be observed in the hair damage pattern of different rows, i.e. when exposed to 4, 000Hz or 2, 000Hz, the damage was remarkable in the inner row hair cells such as the inner hair cells and the first row outer hair cells, and when exposed 1, 000Hz or 500Hz, the damage to the outer row hair cells such as the third outer hair cells was striking, namely, there was difference in the hair cell damage patterns: one when exposed to the frequencies over 2, 000Hz and the other below 1, 000Hz. In the case exposed to white noise the center of the damage located in the lower part of the second turn coinciding to the 4, 000Hz response area, where the greater was the damage in the inner row hair cells, showing the damage pattern similar to that at 4, 000Hz.
Prevention of noise induced hearing damage is assuming great importance and this study was performed to uncover the relations between NITTS and NIPTS. NITTSs were examined after exposing cats to wide and narrow bands of noise for increasing durations. NITTS audiogram showed that hearing loss was greatest at the highest frequency of bands of noise at the shorter exposure, however, there was a progressive high frequency loss at the longer exposure. The growth curves of NITTSs were almost linear with logarithmic exposure time. However, the curves at 16kHz showed an accelerated rate for the narrow band noise. The growth rate was smaller at 1kHz than the ones at 2, 4, 8, and 16kHz. On the occurrence of NIPTS, the NITTS curve had a distinct acceleration at growth rate following a saturation or a slight acceleration. Curiously enough, NIPTS did not necessarily appear at the frequencies of the distinct acceleration.
Sound pressure amplifying function of the external ear was measured by using a probe tube microphone as the ratio of sound pressure at the tympanic membrane to field sound pressure at the position of the helix of the pinna. The maximum ratio was found as much as 28 to 21dB at frequencies of 2, 500 to 3, 000Hz in four persons with normal hearing. The frequency of this maximum ratio corresponded with the resonance frequency of the air contained in the external ear as a horn calculated from its dimension because the resonance frequency varied with individual variation of the dimension of the external ear in the tested persons. This maximum ratio was found to increase vibration amplitude of the tympanic membrane as much as this ratio in dB when the ratio of sound pressure at the tympanic membrane to field sound pressure was measured at the threshold of the same person. Therefore, this maximum peak of sound pressure amplifying function of the external ear was expected to cause a distinct dip in an audiogram of aural fatigue after exposing the ear of the tested person to an intensive white noise of flat spectrum of 87.5±2.5dB produced by a loud speaker. The maximum dip in a detailed audiogram of aural fatigue was found to be about a half octave higher than the resonance frequency of the external ear which had been measured by a probe tube microphone. Moreover, C5 dip appeared when the detailed audiogram was replotted exclusively according to the test tones of a clinical audiometer. It was concluded that the sound pressure amplifying function of the external ear at the resonance was the cause of C5 dip in acoustic trauma.
Standard pure tone audiometry and high frequency audiometry were conducted on 404 workers who work at a paper mill where the noise level is over 80 phone (A). Out of 404 subjects, 87 (20%) were formed having C5-dip. Out of the 87 C5-dip cases, 24 indicated C5-dip in one side of the ears and 63 in both sides. No clear correlation was observed between C5-dip and age, but C5-dip tended to increase with the period of working. It appears that C5-dip is formed in the relatively early period after the start of work. There was a slight proportional relation between the noise level and C5-dip. Simular aging phenomenon as that in normal subjects was observed in the C5-dip cases in high frequency area. In the high frequency area of over 10kHz, no difference was observed between normal group and C5-dip group in the same age group.
Exposure to a loud noise in many years in some industries may cause hearing impairment. Average noise level in the Nishizin textile workshops was 94dB(A) at weaver's ear level and peak range of its frequency was 2, 000-3, 000Hz. 105 patients with some otologic complaints who were working in the Nishizin textile workshops were statistically analyzed in the last 5 years. The patients were ranged 20-70 years old with 2-40 working years and male and female ratio was 2:3. Chief complaints were tinnitus (60%), hard of hearing (30%) and dizziness (8%), and the higher incidence was found between 40 years and 10 years of experience. Audiogram showed C5 dip type or high tone abrupt type in the most cases. The average hearing impairment over 40dB were 25%. The average hearing impairment in the workers below 20 years experience tended to become worse in proportion to the number of working years, however the proportion of hearing impairment to the working years was hardly found in the workers over 21 years experience.
In 1975, 530 conductors on working for the Shinkansen railroad were studied by questionares referring to deafness, tinnitus and fullness in the ears. The hearing of 37 persons with one or other complaints were measured by an audiometer, but the hearing of 15 persons among them were normal. It was found that the results of study on hearing impairment by questionare contained about 50% false positive. The audiogram of the hearing impaired did not showed hearing loss at frequencies under 2, 000 Hz. The hearing loss over 25dB at 4, 000Hz were recognized in 14 persons. The audiogram of 5 persons among them showed C5 dip. The rate of hearing impairment over 21dB=C4+2C5+C6/4 tested by us was 0.19% which was less than the results (3.5%) obtained by Kubo in 1963 concerning to hearing impairment in the railroad conductors. The hearing impairment showed by us might be caused by noise in passenger coach in Shinkansen railroad, it might also be accelerated by working in Shinkansen railroad after they exposed to noise in working, as former railroad conductros in a certain period of time.
While working under noise ranging from the safety noise level up to the harmful, workers are liable to suffer from chronic occupational deafness or sudden hearing loss due to industrial noise. The latter case has been made a subject of the Workmen's Compensation Insurance in Japan since April, 1959. Mention was also made of Aptitude Test in the field (by Kawamura) as a counter measure against hearing losses and Temporary Threshold Shift as criteria of treatment of occupational deafness. On the other hand, a wide range revision of grades of the hearing losses was effected in September, 1975, and the lowest compensation criteria was raised from 60dB to 30dB. Since this kind of revision is related not only to compensation for, but also prevention of hearing losses and arresting their further progress, it is considered that it will pose a serious problem.
In order to establish the application of action potentials (AP) of the cochlear nerve and brain stem auditory evoked response (BSR) in clinical audiology, the frequency specificity of them was studied using the special masking techniques. The change of AP and BSR latencies and amplitudes of white noise evoked responses were observed using the high and low pass filtered masking noise. Secondaly the band stop (reject) noise was produced during the tone pip stimuli by the frequency selective masking. According to the first examination, AP responses depended on the frequency range of cochlear partitions higher than 2kHz, while those responsive for BSR extended to a octave lower range. It is considered that the latencies of responses are dependent to the most basal part of the cochlear partition, which is stimulated when the stimulus conditions are held constant. The amplitudes of AP are decided by the length of the stimulated cochlear partition, when the stimlus conditions areheld constant and the lower frequency bands of masking are changed. The following results were obtained from the second examination. The thresholds of responses were 5dB above subjective ones to the 4kHz and 81kHz tone pip stimuli. On the other hand AP and BSR thresholds to the 2kHz tone pips were 20dB and 15dB above subjective threshold respectively. The AP responses were not obtained and BSR were unstable to the the tone pips at 1kHz. The intensity-latency curves of AP and BSR were shifted in parallel with the frequency from high to low. It is concluded that the effective frequency of the tone pips were 4kHz or higher for AP, and 2kHz or higher for BSR in clinical application. The frequency selective masking of the band stop noise is necessary for us to obtain the responses from more restricted part of the cochlear partition.