EFFECTS OF NOISE
I
INTRODUCTION:
Noise
is derived from the Latin word “nausea” implying ‘unwanted sound’ or ‘sound
that is loud, unpleasant or unexpected’. The noise originates from human
activities, especially the urbanization and the d evelopment of transport and
industry. Though, the urban population is much more affected by such pollution,
however, small town/villages along side roads or industries are also victim of
this problem. Noise is becoming an increasingly omnipresent, yet unnoticed form
of pollution even in developed countries.
According
to Birgitta and Lindvall (1995), road traffic, jet planes, garbage trucks,
construction equipment, manufacturing processes, and lawn mowers are some of
the major sources of this unwanted sounds that are routinely broadcasted into
the air.
EPIDEMIOLOGY OF NIHL
Srivastava (1987)
had carried out a study on 430 patients at Bokaro Steel
Plant and found a 37% incidence of mild to severe sensorineural
hearing loss. With rapid industrialization and urbanization, the
occupational and environmental health research has assumed increasing
importance in recent years. One component is the pioneering work of The
National Institute of Occupational Health, Ahmadabad, in the area of industrial
noise, i.e. exposure and risk assessment, and interventional studies.
EFFECTS
OF OCCUPATIONAL NOISE EXPOSURE
Exposure
to damaging levels of noise has a tremendous impact on the well-being of the
individual because noise related damage affects not only the auditory system,
but also the other bodily systems. These effects of noise may be
classified as:
a) Auditory effects
b) Non- Auditory effects
AUDITORY
EFFECTS
The cause and effect
relationship between noise exposure and hearing loss has been appreciated for
many years. “Boilermaker’s deafness” was a term coined in the 1700s
and 1800s to refer to a high frequency hearing loss seen in labourers that
could be diagnosed with tuning forks. The increased mechanization
seen during the Industrial Revolution was associated with a rise in the
incidence of this disorder. Noise is a common occupational hazard that leads to
one of the most common complaints in the adult population seen by the
otolaryngologist—noise induced hearing loss (NIHL). It is
the most common preventable cause of permanent sensori-neural hearing
loss.
Exposure to intense noise can produce
hearing loss. If the exposure is prolonged over many months and
years, and the hearing loss develops gradually, the condition is called chronic
noise-induced hearing loss (NIHL). The majority of chronic NIHL is due to
occupational exposure such as in the military and industry (occupational
hearing loss). However, in today’s noisy society even people
with quiet jobs may suffer from NIHL. Such non-occupational NIHL is
also called socioacusis. Sources of non-occupational
noise include recreational such as gunfire, loud music—via concerts or
headphones, open vehicles such as motorcycles; household appliances such as
power tools; traffic noise etc. to name just a few. This hearing
loss also demonstrates the characteristics of occupational or industrial
hearing loss.
In contrast, if the noise exposure is very
intense and brief, such as the effect on the ear of a single pistol shot,
explosion or, firecracker, the sudden hearing loss produced is called acoustic
trauma.
In general, the effects of noise on hearing
may be temporary or permanent. The principle index of the existence
of these effects has been the measured changes in the hearing sensitivity or
the threshold of hearing levels. These changes in the hearing
sensitivity are represented by the difference in the hearing threshold levels
measured before and after a specified exposure to noise. The
difference in hearing threshold is known as threshold shift or,
more precisely noise-induced threshold shift. If the
change in hearing sensitivity is reversible and it recovers to pre-exposure
levels within some time interval following the noise exposure, it is called
as noise-induced temporary threshold shift (NITTS) or
simply temporary threshold shift (TTS). However, if the
loss of hearing sensitivity persists throughout the lifetime of the affected
person, then it is called noise-induced permanent threshold shift
(NIPTS) or simply permanent threshold shift (PTS). When
the threshold shift is permanent, there is no possibility for further recovery
of hearing. Permanent threshold shifts may result from acoustic
trauma or may be the result of an accumulation of noxious effects of noise
exposures repeated over a period of many years.
1.
ACOUSTIC TRAUMA
Acoustic
trauma refers to a sudden permanent hearing loss caused by a single exposure to
an intense sound. This is most often caused by an impulse noise,
typically in association with an explosion. Here the sound levels
reaching the structure produce complete breakdown and disruption of organ of
Corti. They may also have ruptured eardrum or damaged
ossicles. Hearing loss from acoustic trauma is to a large degree
permanent. The sound pressure levels capable of causing acoustic trauma
vary between individuals but average around 130-140dB sustained for less than
0.2 seconds. The degree of hearing impairment seen after acoustic
trauma is also variable and may range from a mild to profound SNHL. The
mechanism of injury in acoustic trauma is thought to be direct mechanical
injury to the sensory cells of the cochlea.
Patients
suffering from acoustic trauma tend to present within a short time period
following the event. They report a sudden, sometimes painful hearing
loss that is often followed by a new onset tinnitus. Shortly after the
exposure, the individual has a compound threshold shift (CTS) which suggests
that hearing loss has both temporary and permanent components. Threshold
partially recovers over 1-2 weeks post exposure. This recovery represents the
disappearance of the TTS. The individual so exposed is often left
with a 60dB PTS at one or more frequencies.
Audiogram
may show the typical 3-6 kHz sensory neural notch that is seen with chronic NIHL
but down-sloping or flat audiograms that affect a broad range of frequencies
are more common. Conductive losses will be seen in cases of tympanic
membrane perforation or ossicular discontinuity. Management of acute
acoustic trauma injuries most often involves observation with strict noise
avoidance. Some improvement can generally be expected in the days
immediately following the injury and serial audiograms are performed until
hearing levels stabilize.
Pathophysiology
of Acoustic Trauma
Acoustic
trauma has its pathophysiologic basis in mechanical tearing of membranes and
physical disruption of scala walls with mixing of endolymph and perilymph.
Damage from impulse noise appears to be direct mechanical disruption of inner
ear because their elastic limit was exceeded. At high energy level, acoustic
trauma can result in disruption of the tympanic membrane and ossicular injury.
2.
Chronic NIHL, in contrast to acoustic trauma, is a
disease process that occurs gradually over many years of exposure to less
intense noise levels. This type of hearing loss is generally caused
by chronic exposure to high intensity continuous noise with superimposed
episodic impact or impulse noise. The amount of sound that is capable
of producing cochlear damage and subsequent hearing loss is related by
so-called “damage risk criteria” which is based upon the equal energy concept.
equal
energy concept
(Burns
and
Robinson (1970):
That
is to say that it is the total sound energy delivered to the cochlea that is
relevant in predicting injury and hearing loss. Both an intense
sound presented to the ear for a short period of time and a less intense sound
that is presented for a longer time period will produce equal damage to the
inner ear. An increase in sound intensity of 3dB is associated with
a doubling of sound pressure. Therefore, for each 3dB increase in
sound exposure, the time exposed must be cut in half in order to deliver equal
sound energy to the ear. Because noise levels are likely to
fluctuate throughout the time of exposure, the standard accepted by OSHA is
known as the 5dB rule; for every 5dB increase in noise intensity, exposure time
must be cut in half. A 90dBA exposure is allowed for 8 hours, a
95dBA exposure is allowed for 4 hours, and so on to a maximum allowable intensity
of 115dBA for 15 minutes.
Like
in acoustic trauma, the hearing loss associated with chronic NIHL is variable
between individuals—a subject that will be discussed in more detail
later. However, the principal characteristics of chronic,
occupational NIHL as specified by the American College of Occupational Medicine
Noise and Hearing Conservation Committee include the following:
1. It
is always sensory neural.
2. It
is nearly always bilateral and symmetric.
3. It
will only rarely produce a profound loss.
4. It
will not progress once noise exposure is stopped.
5. The
rate of hearing loss decreases as the threshold increases.
6. The
4 KHz frequency is the most severely affected and the higher frequencies (3-6
KHz) are more affected than the lower frequencies (500Hz-2 KHz).
7. Maximum
losses typically occur after 10-15 years of chronic exposure.
8. Continuous
noise is more damaging than intermittent noise
The
majority of chronic NIHL is due to occupational or industrial
exposure. It is important to remember, however, that in today’s
noisy society even people with quiet jobs may suffer from NIHL. Such
non-occupational NIHL is also called socioacusis. Sources
of non-occupational noise include gunfire, loud music—via concerts or
headphones, open vehicles such as motorcycles, snowmobiles or tractors, and
power tools to name just a few. This hearing loss also demonstrates
the characteristics listed above. One caveat to these features would
be the individual who had significant noise exposure secondary to rifle
shooting. In this case, an asymmetrical loss, with the ear nearest
the gun barrel (the left ear in a right handed shooter) demonstrating slightly
worse hearing, would be expected.
DEVELOPMENT
OF NIHL:
The
development of chronic NIHL progresses through two phases. The
phases are
1. Temporary
threshold shift (TTS)
2. Permanent
threshold shift (PTS)
(1)
Temporary Threshold Shift (TTS)
TTS
is a short term effect that may follow an exposure to noise. There is an
elevation in the threshold of hearing which recovers gradually. There is a
transient shift in the threshold and is called NITTS (Noise Induced Temporary
threshold shift). After termination of noise, hearing sensitivity returns to
the pre-exposure levels in few minutes to several weeks.
Ward
(1973) reported that low frequency noises are not as effective as high
frequency noise to produce TTS. Noises with energy concentrated in
the high frequency range of 2 KHz – 6 KHz produce more TTS than noises with
energy elsewhere in the frequency range. Mills (1984) reported that if the
noise level exceeds 75dBA and if person is exposed to 8-16 hours then there
will be TTS. Above this TTS will increase with increase in intensity and
duration of exposure.
Mills
et al (1970), Moscow et al (1970), Melnick (1974), Maves (1974), reported that
if the exposure duration exceeds 8-16 hrs then there will not be any further
increase in the magnitude of threshold shift. The threshold shift
becomes asymptotic.
· Asymptotic
threshold shift
The experiments of prolonged noise
exposure with human subjects have indicated, without exception, that threshold
shift will plateau if the noise exposure is of sufficient duration. Mills et al
(1970) study indicates that when exposed to an octave band of noise centered at
500Hz for 48 hrs at 81.5dBSPL, and for 29.5 hours at 92.5dBSPL leads to an
asymptotic level of threshold shift (ATS). This ATS was achieved sometime
between 8 and 16 hrs of exposure.
Melnick
(1974) in his study exposed adult male subjects continuously for 16 hrs to an
octave band of noise 300-600 Hz at octave band levels 80-95dB, and concluded
that the 16 hr duration was not long enough to establish firmly that an
asymptote in threshold shift had been reached. A subsequent
experiment which extended the duration of exposure to 24 hrs indicated that the
asymptotic levels are reached by 12 hrs of exposure.
Asymptotic
threshold levels were definitely observed in human subjects if noise exposures
were of sufficient duration. Although there are individual
variations, it is probable that the threshold shift for the average human
subject will plateau between 8 and 12 hrs of exposure.
Factors
§Characteristics of
stimulus.
§Freq. at which TTS measured.
§Time interval b/w end of exposure
and starting of the measurements.
Stimulus characteristics
- Exposure sound freq.
- Sound intensity.
- Exposure time.
- Exposure pattern
TTS
Recovery:
An
interrupted exposure to noise (e.g.; 6 hours a day for 36 days) initially
produces the same magnitude of TTS as continuous exposure. However, as the
interrupted exposure paradigm is continued, threshold improves and may
eventually return to within 10-15dB of pre-exposure baseline
Because TTS does recovers, the amount of
shift observable depend on the time interval between the end of fatiguing sound
and the threshold measurement. In the early stages of recovery,
within the first few minutes (up to 3 minutes) of post exposure, the recovery
pattern is complex and is influenced by short term processes such as adaptation
and sensitization that accompany auditory stimulation.
A
polyphasic pattern called “bounce effect” was reported by Hirsh and Ward (1952).
Immediately following exposure, there is rapid recovery with threshold level
reaching a minimum between 1 and 1 ½ minutes following exposure. The
threshold shift then increases to another maximum at about 2 minutes post
exposure.
After
2 minutes, recovery continues in a monotonic pattern. To avoid the
complicated interaction of several rapidly changing auditory processes and the
problems of the complex early recovery pattern, measurement of TTS is usually
made when these are negligible at about 2 minutes post exposure (TTS2).Measurement
of TTS is usually delayed for a period of a 2 minutes or more following the end
of noise exposure. The TTS2 post exposure commonly
has been used to detect the amount of TTS produced by a particular noise
exposure.
(2) Permanent
Threshold Shift (PTS)
PTS are those hearing changes that persist throughout the
life of the affected person. It shows no possibility of further
recovery with the passage of time. Most frequently PTS is a result
of an accumulation of exposures repeatedly on a daily basis over a period of
years. This type of threshold shift is called NIPTS (Noise Induced
Permanent Threshold Shift). Based on the field studies on hearing
loss in the industrial environment as well as lab investigations of PTS, there
are four major factors that contribute to the potential hazard of noise to
hearing.
(1) overall
sound level in db
(2) spectral
distribution
(3) duration
and distribution of noise (sound exposure in typical workday)
(4) Cumulative
noise exposure in days, weeks, years.
Susceptibility to NIPTS:
As has been mentioned,
individual susceptibility to NIHL is highly variable. Both animal research and
retrospective studies of humans exposed to industrial noise have demonstrated
this remarkable variation in susceptibility. Several large studies have been
done which have shown that, on average, 5% of individuals with long-term
exposure to noise levels of 80dBA will have significant hearing
loss. This risk increases to 5-15% with 85dBA noise and 15-25% with
90dBA noise. These averages are useful in terms of counseling patients on the
risks of noise exposure, but we do not have a good understanding why, within a
population exposed to the same noise intensity for the same time period, some
individuals will have a significant reduction in hearing thresholds and others
will not. i.e. the biological bases for these differences are
unknown.
Gender:
Men had worse hearing
thresholds compared to women, when matched for age [Berger, Royster and Thomas
(1978); Cooper (1994)]. Johnson(1991) attributed much of this difference to the
level of non-occupational noise exposure that men are subject to relative to
that of women rather than to their inherent susceptibility to its effects.
Genetic pre-disposition:
Some recent investigations
have shown genetic predisposition to NIHL in experimental mice. In a study of
two in bred strains of mice Li (1992) demonstrated that genetic predisposition
can affect susceptibility to auditory degeneration and noise impairment in a
systematic manner
Di Palma et al. (2001) have shown the wild
type Ahl gene codes for a hair cell specific cadherin known as
the otocadherin. Cadherins are calcium-dependent proteins that holds
cells together to form tissues and organs. The otocadherin was found
localized to the stereocilia of OHCs. The authors proposed that
these cadherins may form the lateral links in the stereocilia. Therefore
reduction in the otocadherin may weaken the stereocilia and allow them to be
more easily damaged by loud sounds. However, NIHL genes have not
been identified in humans.
Pigmentation:
Hanselman et al. (1995),
who compared the hearing loss amongst soldiers representing
different race groups, found that, on an average, a significant difference
existed in the hearing threshold levels among the race groups, with black
soldiers having the most sensitive hearing and white soldiers having the
poorest. Barrenas et al., 1991 - melanin estimation with skin and eye colour
show that black or dark-skinned people have reduced threshold shifts in
comparison with white people with blue eyes.
The colour of the skin and
fur reflects the tyrosinase activity. The lower the activity, the fairer the
complexion, the smaller absolute melanin amounts and the larger relative
pheomelanin concentrations than eumelanins. Fujita et al., 1990 - eumelanins
and pheomelanins show a relationship to skin and to inner ear pigmentation, red
animals having more pheomelanins and black animals having more eumelanins.
Eumelanin has been regarded as being more photo protective and pheomelanin as
more phototoxic (Thody et al., 1991). So, it could be assumed that individuals
with a fair complexion run a greater risk of developing NIHL, than individuals
with pronounced pigmentation, and it should be considered a risk factor in view
of NIHL.
Magnesium:
Animal and human studies have shown that
magnesium deficiency increase the risk of NIHL in a given noise exposure.
Joachims et al. (1983) - rats fed with a high Mg diet suffered smaller NIHLs as
measured by ABR responses when subjected to impulsive
noise. Correlations were also found between the Mg plasma and
perilymph levels and the severity of NIHL. Joachims et al. (1987)-Mg may play a
role in the NIHL susceptibility in humans was reported by In a retrospective
study it was found that subjective thresholds across 3, 4 and 8 kHz were
negatively correlated to serum magnesium levels. Magnesium plays an essential
role in intracellular metabolism. It regulates extracellular membrane
permeability and neuromuscular energy production and consumption. The hearing
process is an active process that requires energy and exposure to an excessive
stimulus will exaggerate these requirements. Mg plays a crucial role in the
energy-cycle of the cell. A controlled influx of Ca following the stimulation
of the stereocilia is a critical process in the depolarization of hair calls
(Hudspeth, 1985). Decrease in the extracellular Mg affect the
intracellular ion content of the hair cells, especially the Ca levels
In normal humans exposed to hazardous
noise, reduced Mg levels either by increased consumption or dietary deficiency
lead to a low Mg level at the hair cell membrane. This causes an increase in
the membrane permeability, which causes greater transport activity with respect
to Ca and Na. A lasting decrease in Mg levels can increase the Ca content of
the hair cells and increase the risk of a hearing loss. Attias et al., 1994 -
oral prophylactic intake of magnesium supplement has been shown to reduce the
level of threshold shift to a given noise exposure in individuals exposed to
military noise
Reduced micro-circulation and oxygenation of
the cochlea:
One of the possible mechanisms in the
development of NIHL is the vascular pathology in the micro-circulation of the
cochlea as demonstrated by histological evidence of reduced cochlear blood flow
following noise exposure. Latoni et al., 1996- localized ischemia during noise
exposure. Treating with pentoxifylline a xanthine derivative was shown to
maintain cochlear blood flow as assessed by continuous red blood cell movement
and reduce noise-induced temporary threshold shift. Sokas et al. (1995) - clear
correlation between blood pressure and NIHL. Altura et al. (1992) have shown
that noise induces a significant elevation in the systolic and diastolic
arterial pressure and further, reduced levels of plasma magnesium increase the
micro-vascular constriction raising arterial blood pressure further after
trauma. This effect is found to be enhanced by exercise, which reduces
magnesium levels and oxygenation and raises body temperature. (Vittitow et al.,
1994). Vavrina et al., 1995 - hyperbaric oxygen therapy has been shown to
improve hearing recovery in acute acoustic trauma. Hatch et al. 1991 - guinea
pigs given 100% oxygen during noise exposure has a markedly reduced threshold
shift.
Although the etiology of NIHL is poorly
understood, individuals with poor circulation may be susceptible
Smoking and susceptibility to NIHL:
Pouryaghoub,
Mehrdad and Mohammadi (2007) reported significantly higher incidence
of NIPTS in smokers as compared to non-smokers. The percentage of workers with hearing
threshold differences of greater than or equal to 30 dB between 4000 Hz and
1000 Hz in both ears were 49.5% and 11.2% in smoker and non smoker groups,
respectively. The percentage of workers with a hearing threshold of greater
than 25 dB at 4000 Hz in the better ear were 63.6% and 18.4% in smoker and non
smoker groups, respectively. Smoking and NIPTS- This difference was
statistically significant after adjustment for age and exposure duration.
Smoking can accelerate noise induced hearing loss, but more research is needed
to understand the underlying mechanisms
Transmission of sound to the inner ear:
Conductive hearing loss of
a substantial degree (>30 dB ABG between 500 Hz and 4 kHz should decrease
the susceptibility to NIHL (National institutes of health consensus conference
report on noise and hearing loss, 1990). Sound input to the cochlea will be
reduced at least as effectively as with very well fitted EPDs. One of the other factors that is theoretically associated
with differences in susceptibility is an unusually efficient acoustic transfer
through the external and middle ear, as a determinant of the amount of energy
coupled to the inner ear structures. An unusually efficient system
should increase the risk. However there is no empirical data to
reach a conclusion on this as of now
Effect of an initial noise induced hearing
loss on subsequent noise induced hearing loss:
Perez, Freeman, Sohmer (2004) studied
the effect of previous noise induced hearing loss (NIHL) on subsequent NIHL in
rats. Three
groups of animals were initially exposed to different durations of 113 dB SPL
broad band noise (21 days, 3 days or 0 days – unexposed). Their permanent threshold shifts (PTS) from
this exposure (PTS1) were evaluated using auditory nerve-brainstem evoked
responses (ABR). All
the animals were then noise-exposed for an additional 12 days, and the
incremental PTS following this exposure (PTS2) was also assessed. The 21 day group showed the greater PTS1
[mean ± SD: 27.03 ± 6.78 dB, compared with
11.67 ± 10.47 dB (3 day group)] and the lowest PTS2
[9.84 ± 8.19 dB, compared with 13.33 ± 14.60 dB (3 day
group) and 24.04 ± 12.4 dB (0 day group)]. This group also showed the highest total PTS
following the two noise exposures [36.88 ± 6.29 dB, compared with
25.00 ± 12.68 dB (3 day group) and 26.35 ± 11.93 dB (0 day
group)]. The
results could be because of the lower effective intensity of the second noise
exposure for the animals with a large PTS1 compared to those with little or no
NIHL from the first noise exposure
Changes within Individuals:
Among the causes of
differences of susceptibility to noise exposure within individuals
are ototoxic drugs and other chemicals, age, vibrations etc
Ototoxic drugs:
Simultaneous exposure to
noise and ototoxic medications may have an amplifying affect on hearing loss,
producing more threshold elevation than with either factor alone. This effect
has been definitively demonstrated in noise- exposed animals given
aminoglycoside antibiotics. The chemotherapy drug cisplatin was not found to
cause hearing loss alone, but in animals given the drug and exposed to noise
the hearing was worse than in animals exposed to noise alone. Although the
diuretic furosemide is potentially ototoxic when given intravenously to
patients with altered renal function, oral administration in people with normal
kidneys has not been associated with hearing loss. It has also not
been shown to worsen NIHL. The literature on the combined effect of salicylates
and noise is contradictory. Some studies have demonstrated a
potentiating effect, while others have not. Two separate studies done in the
mid 1980’s found that in noise exposed individuals, if higher doses of aspirin
(1.9 gr/day) were taken, their TTS was of greater magnitude and slower to
recover. Therefore, it seems reasonable to counsel patients with significant
noise exposure to avoid high dose aspirin therapy. Clinical evidence of
corresponding effects in human patients has not been established, but
precautions should be taken with regard to noise exposures of individual
patients treated with these medications.
Chemicals:
Simultaneous exposure to
hazardous noise and certain chemical pollutants may have an additive effect on
hearing loss. Toluene, carbon monoxide and carbon disulphide in combination
with noise are known to cause a more severe high frequency hearing loss than
noise alone. Other agents such as lead, mercury, xylene and trimethyltin are
suspected to either worsen NIHL or alter susceptibility to NIHL
Age:
In certain animal models
there is evidence of heightened susceptibility to noise exposure shortly after
birth--a "critical period". However, it is not clear
that data from such animal models can be generalized to full-term normal human
infants. Premature infants in noisy environments (e.g. neonatal intensive care
units), however, may be at risk. Pujol (1992) proposed that the sensitive
period extends from 5 months in utero to a few months after
birth. The increased susceptibility may stem from the immaturity of
the efferent system and cochlea active mechanisms.
Vibrations:
Although vibration alone is
known not to cause hearing loss, it is not known if vibration has any influence
on NIHL. Animal studies have found more severe hearing loss and hair cell loss in
animals exposed to both vibration and noise compared to those exposed to noise
alone. In humans, vibration causes a larger TTS after a noise exposure,
however, it is not clear if this can be translated to larger PTS also
Comments
Post a Comment