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Noise and OAEs
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Report compiled by : Guiscardo
Lorito MA, Center of Bioacoustics, University of Ferrara,
Italy
Noise has always been a relevant
environmental problem for mankind. Since the second half of XX century,
an enormous number of cars regularly crosses our cities and the
countryside. Among heavy car traffic, day and night large trucks
equipped with diesel engines, very poorly silenced for both engine
and exhaust noises, travel on city roads and highways. Aircrafts
and trains add up to the environmental noise background. In industry,
machinery emits high noise levels, while leisure and amusement places,
such as pubs and disco dances, constantly broadcast high volume
music. Hearing protections must be provided at levels above 90dBA,
but no one can imagine people permanently living with a mechanical
hearing protection. However, hearing protection can be provided
in several forms. Presently we are trying to develop a pharmaceutical
way of hearing protection. Following a decade of research in the
field, our aim is to obtain a protection drug for the inner ear.
One of our investigating instrument is OAEs technique, it can reveal
problems in the inner ear, or it can be used to find threshold shifts
in the experimental animals.
It was found
by Hamerik and Qiu (2000) that
there are Correlations among evoked potential thresholds, distortion
product otoacoustic emissions and hair cell loss following various
noise exposures in the chinchilla. Changes in cubic distortion product
otoacoustic emissions (Delta-DPOAEs), evoked potential
threshold shifts (TSs) and outer hair cell (OHC)
losses were measured in a population of 95 noise-exposed chinchillas.
Each animal was exposed to one of 23 different noises in an asymptotic
threshold shift (ATS) producing paradigm or an
interrupted noise paradigm which typically produced a toughening
effect. Noises were narrow band (400 Hz) impacts with center frequencies
of 0.5, 1.0, 2.0, 4.0 or 8.0 kHz presented 1 impact/s at peak SPLs
of 109, 115, 121 or 127 dB. The duration of the exposures was 24
h/day for 5 days (ATS paradigm) or 6 h/day for 20 days (toughening
paradigm). Based on a linear regression analysis of individual subject
and group mean data, correlations among the following dependent
variables were made: DeltaDPOAEs, ATS, toughening or TS recovery
(TS(r)), permanent threshold shift (PTS) and OHC loss. Correlations
among these metrics were generally highest for DPOAE primary frequency
levels, L(1)=L(2)=70 dB. Correlation between DeltaDPOAE and TS(r)
was typically low, while a considerably higher correlation was found
between DeltaDPOAE and ATS. Correlations among the permanent measures
of noise-induced effects, i.e. for DeltaDPOAE/PTS and DeltaDPOAE/OHC
loss were typically poor when there was only a small or a moderate
noise-induced effect (PTS less than 25 dB and DeltaDPOAE less than 20 dB). However,
for PTS less than 25 dB the correlation between PTS and OHC loss was considerably
better than the correlation between DeltaDPOAE and OHC loss. For
more severe noise-induced changes there was generally a good correspondence
between OHC loss, PTS and DeltaDPOAE metrics.
Another recent
study made by Fraenkel et al. (2001)
investigated the effect of various durations of
noise exposure in animals on physiological responses from the cochlea.
The study used ABR, TEOAE and DPOAE measurements. Rats were exposed
to 113 dB SPL broad-band noise (12 h on/12 h off)
for durations of 3, 6, 9, 12, 15 and 21 days, and tested 24 h after
cessation of the noise and again after a period of 6 weeks. ABR
threshold to click stimuli and to a 2-kHz tone burst (TB), TEOAE
energy content and DPOAE amplitude in the exposed rats were compared
to those in a group of control rats not exposed to noise. ABR thresholds
(click and TB) were significantly elevated in all exposure duration
groups compared to control rats. DPOAE amplitudes and TEOAE energy
content were significantly reduced. The mean ABR thresholds following
21 days exposure were significantly greater (click = 100 dB pe SPL;
TB = 115 dB pe SPL) than those following 3 days exposure (click
= 86 dB pe SPL; TB = 91 dB pe SPL). Linear regression analysis between
recorded responses and duration of noise exposure (days) showed
a significant increase in ABR thresholds of approximately 0.8--
1.4 dB/day. TEOAE and DPOAE responses showed no such dependence
on noise duration and were already maximally reduced after only
3 days of exposure. This can be explained by the possibility that
short noise exposures may cause damage to the early, more active
stages of cochlear transduction (as shown by TEOAEs and DPOAEs).
As the noise exposure continues, further damage may be induced at
additional, later stages of the cochlear transduction cascade (as
shown by ABR). Thus, ABR seems more sensitive to noise duration
than OAE measures.
Another study by Attias et al. (2003)
discovered that increasing magnesium (Mg2+) intake in guinea-pigs
provides a significant biological cochlear protective effect. In
this study thirteen animals were fed with high Mg2+ intake (39 mmol
Mg2+/l in drinking water) and 12 without the Mg2+ additive. The
OAE amplitudes and frequency ranges as well as the DPOAE thresholds
were affected significantly less by noise exposure in the animals
fed Mg2+-enriched water. Following the exposure, the auditory recovery
was faster in the high than the low Mg2+ animals (controls). In
addition, a relationship was found between the Mg2+ level and the
emission loss. The post-exposure measures may result from the effect
of Mg2+ on cochlear metabolic processes and vascular microcirculation.
The results demonstrate that pre-existing low Mg2+ levels will exacerbate
noise induced hearing loss (NIHL), and increased Mg2+ intake provides
a significant biological cochlear protective effect.
The most recent
study by Davis et al (2004)
was focused on the use of distortion product otoacoustic emissions
in the estimation of hearing and sensory cell loss in noise-damaged
cochleas. Distortion product otoacoustic emissions (DPOAE),
permanent threshold shifts (PTS). and outer hair
cell (OHC) losses were analyzed in a population of 187 noise-exposed
chinchillas to determine the predictive accuracy (sensitivity and
specificity) of the DPOAE for PTS and OHC loss. Auditory evoked
potentials (AEP) recorded from the inferior colliculus of the brainstem
were used to estimate hearing thresholds and surface preparation
histology was used to determine sensory cell loss. The overlapping
cumulative distributions and high variability in emission responses
for both PTS and OHC loss made it difficult to predict AEP threshold
and OHC loss from DPOAE level measurements alone. Using a strict
criterion (i.e. emissions better than the 5th percentile of the
pre exposure DPOAE level, and PTS < or = 5 dB or OHC loss< or =
5%), it was found that the post exposure DPOAE level could be used
with reasonable confidence to determine if the status of peripheral
auditory system was either normal (i.e. PTS< or = 5 dB) or abnormal
(PTS>30 dB or OHC loss>40%). However, the high variability of individual
DPOAE responses resulted in a broad region of 'uncertainty' (i.e.
5 less than PTS less than or = 30 dB and 5% less than OHC loss less
than or = 40%) making it difficult in the chinchilla model to use
the post exposure DPOAE level with confidence to predict in individual
subjects the amount of PTS or OHC loss. Our results also indicate
that significant reductions in the amplitude of the DPOAE are related
primarily to a systematic loss of OHCs, and that a post exposure
DPOAE level< or = 10 dB SPL, obtained with a low frequency primary
level of 65 dB SPL, represents a criterion value which can serve
as an indication of significant OHC loss (> or = 50%) or PTS (>
or = 35 dB) in noise-exposed chinchillas. Based on an exponential
regression analysis of individual subjects, correlations were higher
for PTS/DPOAE than for OHC loss/DPOAE.
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Useful References (in chronological order)
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Hamernik RP, Qiu W., Correlations among evoked
potential thresholds, distortion product otoacoustic emissions and
hair cell loss following various noise exposures in the chinchilla.,
Hear Res. 2000 Dec; 150(1-2): 245-57.
Fraenkel R, Freeman S, Sohmer H., The effect of
various durations of noise exposure on auditory brainstem response,
distortion product otoacoustic emissions and transient evoked otoacoustic
emissions in rats., Audiol Neurootol. 2001, Jan-Feb; 6(1): 40-9.
Attias J, Bresloff I, Haupt H, Scheibe F, Ising H.,
Preventing noise induced otoacoustic emission loss by increasing
magnesium (Mg2+) intake in guinea-pigs., J Basic Clin Physiol Pharmacol.
2003; 14(2): 119-36.
Davis B, Qiu W, Hamernik RP., The use of distortion
product otoacoustic emissions in the estimation of hearing and sensory
cell loss in noise-damaged cochleas., Hear Res. 2004 Jan; 187(1-2):
12-24.
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