PubMed · 7371087
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R Tománek. 1980. [Industrial audiometry].. https://pubmed.ncbi.nlm.nih.gov/7371087/
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A morphological analysis was performed on a human cochlea removed during skull base surgery. The patient experienced a noise-induced hearing loss following 30 years of mechanical exposure. The tissue was processed according to the block surface technique and the organ of Corti, osseous spiral lamina and spiral ganglion were analyzed at different levels. There was a circumscribed lesion approx. 10 mm from the round window extending to about 13 mm. At this site, the dominant pathological feature was the loss of outer hair cells that was comprehensive in the centermost area and partial in the peripheral region of the damage. The degradation of inner hair cells was less severe with signs of cell atrophy yet with limited loss. Outer pillar cells were often collapsed leading to deformation of the acoustic ridge. The Deiters cells were often present and physically interactive with remaining nerve fibers. In the reticular lamina, surgical manipulation and dissection resulted in tears which may be attributed to a reduction of intercellular strength between cells. In the damaged area, there was a 45% loss of myelinated nerve fibers measured at the osseous spiral lamina. Pathological changes could not be observed in the spiral ganglion with certainty although the type II cells innervating the outer hair cells were often difficult to discern.
We have developed a database and an analysis program (NoiseScan) for noise-induced hearing loss (NIHL). The exposure data are based on the evaluation of the noise immission level, which includes duration, frequency content, and the use of, and the attenuation performance of, hearing protectors. The input data can handle an unlimited number of exposure periods. If the noise exposure level is not known, the program lists noise levels of comparable work places, and thus provides an estimate of exposure. Confounding medical factors that may contribute to NIHL, such as elevated serum cholesterol level, hypertension, and extensive use of pain killers, are collected. Combined exposure to agents that clearly contribute to NIHL, such as hand-arm vibration, tobacco smoking, use of aminoglycosides and exposure to solvents are also assessed. An unlimited number of audiograms can be stored, and all the data can be completed and edited following collection. The program gives the predicted hearing loss according to the ISO 1999 model based on total exposure. At present, our NoiseScan program (under continuous development in an EU research program) is suitable for the data collection of various risk factors. It can be used to determine whether the hearing loss is occupational in origin and to estimate the efficiency of hearing conservation measures. NoiseScan also predicts the development of hearing loss in individuals in 5-year periods. The goal is to improve and validate the rules by which single and combined risk factors contribute to HIHL, thus leading to more precise prediction of individual hearing loss, and for the evaluation of success of the hearing conservation programs.
In clinical measurements of hearing sensitivity, a given earphone is assumed to produce essentially the same sound-pressure level in all ears. However, recent measurements [Voss et al., Ear and Hearing (in press)] show that with some middle-ear pathologies, ear-canal sound pressures can deviate by as much as 35 dB from the normal-ear value; the deviations depend on the earphone, the middle-ear pathology, and frequency. These pressure variations cause errors in the results of hearing tests. Models developed here identify acoustic mechanisms that cause pressure variations in certain pathological conditions. The models combine measurement-based Thévenin equivalents for insert and supra-aural earphones with lumped-element models for both the normal ear and ears with pathologies that alter the ear's impedance (mastoid bowl, tympanostomy tube, tympanic-membrane perforation, and a "high-impedance" ear). Comparison of the earphones' Thévenin impedances to the ear's input impedance with these middle-ear conditions shows that neither class of earphone acts as an ideal pressure source; with some middle-ear pathologies, the ear's input impedance deviates substantially from normal and thereby causes abnormal ear-canal pressure levels. In general, for the three conditions that make the ear's impedance magnitude lower than normal, the model predicts a reduced ear-canal pressure (as much as 35 dB), with a greater pressure reduction with an insert earphone than with a supra-aural earphone. In contrast, the model predicts that ear-canal pressure levels increase only a few dB when the ear has an increased impedance magnitude; the compliance of the air-space between the tympanic membrane and the earphone determines an upper limit on the effect of the middle-ear's impedance increase. Acoustic leaks at the earphone-to-ear connection can also cause uncontrolled pressure variations during hearing tests. From measurements at the supra-aural earphone-to-ear connection, we conclude that it is unusual for the connection between the earphone cushion and the pinna to seal effectively for frequencies below 250 Hz. The models developed here explain the measured pressure variations with several pathologic ears. Understanding these mechanisms should inform the design of more accurate audiometric systems which might include a microphone that monitors the ear-canal pressure and corrects deviations from normal.