NOISE

TLV® exposures of 80 dBA or greater should be used in

the above calculations. With sound level meters, this
formula should be used for sounds with steady
These TlVs refer to sound pressure levels and
levels of at least 3 seconds. For sounds in which this
durations of exposure that represent conditions
condition is not met, a dosimeter or an integrating
under which it is believed that nearly all workers may
sound level meter must be used. The limit is
be repeatedly exposed without adverse effect on
exceeded when the dose is more than 100% as
their ability to hear and understand normal speech.
indicated on a dosimeter set with a 3 dB exchange
Prior to 1979, the medical profession had defined
rate and an 8-hour criteria level of 85 dBA.
hearing impairment as an average hearing threshold
The TLV is exceeded on an integrating sound
level in excess of 25 decibels (ANSI S3.6-1989i 1>at
level meter when the average sound level exceeds
500, 1000, and 2000 hertz (Hz). The recommended
the values given in Table 1.
values should provide protection against a hearing
loss at higher frequencies, such as 3000 Hz and
TABLE 1. Threshold Limit Values for NoiseA
4000 Hz. The values should be used as guides in
the control of noise exposure and, due to individual Duration Sound Level
susceptibility, should not be regarded as fine lines per Day dBA8
between safe and dangerous levels. Hours 24 80
It should be recognized that the application of 16 82
the TlVs for noise will not protect all workers from 8 85
the adverse effects of noise exposure. The TlVs 4 88
should protect the median of the population against 2 91
a noise-induced hearing loss exceeding 2 dB after 1 94
40 years of occupational exposure for the average of Minutes 30 97
0.5, 1, 2, and 3 kHz. A hearing conservation 15 100
program with all its elements including audiometric 7.50C 103
testing is necessary when workers are exposed to 3.75C 106
noise at or above the TLV levels. 1.88C 109
0.94C 112
Continuous or Intermittent Noise
SecondsC 28.12 115
The sound pressure level should be determined 14.06 118
by a sound level meter or dosimeter conforming, as 7.03 121
a minimum, to the requirements of the American 3.52 124
National Standards Institute (ANSI) Specification for 1.76 127
Sound Level Meters, S1 .4-1983, Type S2A,<2>or 0.88 130
ANSI S1.25-1991 Specification for Personal Noise 0.44 133
Dosimeters.<3> The measurement device should be 0.22 136
set to use the A-weighted network with slow meter 0.11 139
response. The duration of exposure should not
No exposure to continuous, intermittent, or impact noise in
exceed that shown in Table 1. These values apply to
excess of a peak C-weighted level of 140 dB.
total duration of exposure per working day 8 Sound levels in decibels are measured on a sound level meter,
regardless of whether this is one continuous conforming as a minimum to the requirements of the
exposure or a number of short-term exposures. American National Standards Institute Specification for Sound
When the daily noise exposure is composed of two Level Meters, Sl.4 (1983)<2>Type S2A, and set to use the A-
or more periods of noise exposure of different levels, weighted network with slow meter response.
their combined effect should be considered rather cLimited by the noise source - not by administrative control.
than the individual effect of each. If the sum of the It is also recommended that a dosimeter or integrating sound
following fractions: level meter be used for sounds above 120 dB.

C1 C2 Cn
+ + Impulsive or Impact Noise
T1 T2 Tn
By usinc% the instrumentation specified by the
(4)
exceeds unity, then the combined exposure should ANSI S1 .4, S1 .25,<3>or IEC 804, impulsive or
be considered to exceed the TLV. C 1 indicates the impact noise is automatically included in the noise
total duration of exposure at a specific noise level, measurement. The only requirement is a
and T 1 indicates the total duration of exposure measurement range between 80 and 140 dBA and
permitted at that level. All on-the-job noise the pulse range response must be at least 63 dB. No

ACGIH® © 2006 Noise-1

exposures of an unprotected ear in excess of a
C-weighted peak sound pressure level of 140 dB
should be permitted. If instrumentation is not avail-
able to measure a C-weighted peak, an unweighted
peak measurement below 140 dB may be used to
imply that the C-weighted peak is below 140 dB.
Notes
1. For impulses above a C-weighted peak of 140
dB, hearing protection should be worn. The
MIL-STD-1474c<5>provides guidance for those
situations in which single protection (plugs or
muffs) or double protection (both muffs and
plugs) should be worn.
2. Exposure to certain chemicals may also result in
hearing loss. In settings where there may be
exposures to noise and to carbon monoxide,
lead, manganese, styrene, toluene or xylene,
periodic audiograms are advised and should be
carefully reviewed. Other substances under
investigation for ototoxic effects include arsenic,
DOCUMENTATION
CONTINUOUS OR
INTERMITTENT NOISE
Airborne sound can be described as propagated
fluctuations in atmospheric pressure capable of
causing the sensation of hearing. In occupational
health, the term "noise" is used to denote unwanted
sound. Noise-induced hearing loss has been
recognized and reported for several hundred years.
However, prior to about 1950, reliable dose-effect
data were not available. Before World War II, due to
lack of uniformity in instrumentation and related units
and scales, studies from various parts of the world
often yielded a significant difference in result.
Present day American, European, and
International standards< 1-s> relating to the
instrumentation and methodology of both noise and
hearing acuity measurement are now in reasonable
accord. This accord resulted in an international
standard, ISO-R-1999.2 (1990), issued by the
International Organization for Standardization
(IS0).<5>This standard had been available for review
for over 12 years and was well accepted
internationally upon its promulgation.
This standard<5>is the basis for the changes to
the TLV with respect to the time intensity trading
relation and for combining continuous noise with
impulse noise. For example, the statement that the
TLV should protect the median of the population
against a noise-induced hearing loss exceeding 2
dB after 40 years of occupational exposure for the
average of 0.5, 1, 2, and 3 kHz was developed from
the ISO-R-1999, Table E-1, which provided median
2-Noise
carbon disulfide, mercury, and trichloroethylene.
3. There is evidence to suggest that noise exposure
in excess of a C-weighted, 8-hour TWA of 115
dBC or a peak exposure of 155 dBC to the
abdomen of pregnant workers, beyond the fifth
month of pregnancy, may cause hearing loss in
the fetus.
4. The sum of the fractions of any one day may
exceed unity, provided that the sum of the
fractions over a 7-day period is 5 or less and no
daily fraction is more than 3.
5. Table 1 is based on daily exposures in which
there will be time away from the workplace in
which to relax and sleep. This time away from the
workplace will allow any small change to the
worker's hearing to recover. When the worker, for
times greater than 24 hours, is restricted to a
space or series of spaces that serve as both a
workplace and a place to relax and sleep, then
the background level of the spaces used for
relaxation and sleep should be 70 dBA or below.
noise-induced permanent threshold shift (NIPTS)
values for a 40-year exposure to 85 dB. These
values are 0 dB, 0 dB, 1 dB, and 5 dB for the
audiometric frequencies of 0.5 kHz, 1 kHz, 2 kHz,
and 3 kHz, respectively.
Before 1950, overall sound pressure levels, in
decibels, were used to define the noise aspect of
damage risk criteria.<7> Following recognition that the
overall intensity of a noise, by itself, was not
sufficient to describe the potential for damage and
that the frequency characteristic must also be
considered, criteria incorporating spectral levels
(usually octave band levels) were developed. Many
of these are summarized in the U.S. National
Institute for Occupational Safety and Health (NIOSH)
Noise Criteria Document.<8>An octave band analysis
is a relatively lengthy procedure requiring expensive
instrumentation, and there was some concern that
the layman had difficulty in interpreting the results.
Recognizing the desirability of a single reading and
the fact that most industrial NIPTS data were
available for single weighted noise levels, the
lntersociety Committee in 1967 proposed the use of
A-weighted sound levels in the development of
criteria.<9>The A-weighted characteristic of a sound
level meter is designed to approximate the
frequency-selective response of the human ear at
moderate intensities. In one report, Botsford< 10>
demonstrated that A-weighted levels are as reliable
as octave band levels in the prediction of effects on
hearing in 80% of the occupational noises
considered and slightly more conservative in 16% of
the cases. Passchier-Vermeer< 11 >and Cohen et a1.< 12>
similarly demonstrated that A-weighted levels
ACGIH® © 2006
provide a reasonable estimate of the hazard to
hearing in most industrial environments. The
abbreviation dBA is used to denote decibels A-
weighted and can be described as a unit of
measurement of sound level corrected to the A-
weighted scale as defined in ANSI S1.41983.<2>
Today, A-weighted sound levels are in general use
in hearing risk criteria.
Permanent noise-induced hearing loss is related
to the intensity and frequency distribution of the
noise, the time pattern and duration of exposure,
and individual susceptibility. The ability to hear and
understand everyday speech under normal
conditions is regarded as the most important
function of the hearing mechanism. Thus, most
present-day studies focus on the resultant or
predicted hearing loss in the speech frequency
range. However, research has clearly shown that the
speech range does not stop at 2000 Hz and should
include frequencies from 2000 to 4000 Hz. For this
reason, the American Academy of Ophthalmology
and Otolaryngology (MOO) included 3000 Hz in
their hearing impairment formula in 1979_<13>This
inclusion also impacts the selection of the TLV.
Audiometric testing is carried out to determine
an individual's hearing threshold for pure tones. In
this testing, a series of tones is presented to the
subject through earphones. Each ear is tested in
turn. The test tones normally used are 500, 1000,
2000, 3000, 4000, 6000, and 8000 Hz. The intensity
of each tone is adjusted until the subject indicates
that he/she can just hear the signal. The threshold of
hearing for each test tone is then recorded in
decibels. The amount in decibels by which the
subject's threshold exceeds the zero setting on the
audiometer is then called the hearing threshold level,
or loss, at that particular frequency. The zero
settings on the audiometer are based on response
levels derived from testing large groups of young
people. There is general agreement that progression
in hearing loss at 500, 1000, 2000, and 3000 Hz
eventually will result in impaired hearing, i.e., ability
to hear and understand speech. The MOO
Subcommittee on Noise<1<iJ and the American
Medical Association< 15>defined estimated hearing
level for speech as the simple average of hearing
levels at the three frequencies 500, 1000, and 2000
Hz. The point at which impairment begins was then
set at the 25-decibel average hearing level. This was
referred to as the hearing loss index (0.5, 1,2) or HLI
(0.5, 1,2) = 25 dB. In an investigation by A.H.
Suter< 15f it was reported that, "Correlation tests
revealed that frequency combinations that included
frequencies above 2000 Hz were significantly better
predictors of speech discrimination scores than the
combination of 500, 1000, and 2000 Hz." By 1980,
there was also general agreement that the hearing
level at 3000 Hz is related to the hearing and
understanding of speech, particularly in the
presence of noise.
The inclusion (or exclusion) of 3000 Hz in an
ACGIH® © 2006
impairment definition is particularly important when
one considers that, in almost all cases, noise-
induced hearing loss first appears in the frequency
range from 3000 to 6000 Hz. With continued
exposure, the loss in hearing eventually spreads to
the lower frequencies of 500, 1000, and 2000 Hz.
Clearly, it is necessary to define the beginning of
impairment before one can propose a damage risk
criterion, either in terms of a zero-risk criterion such
that the prevalence of impairment in an exposed
group is no greater than the prevalence in a control
or a no-noise group, or in terms of a percentage-risk
criterion that would provide an estimate of the
increase in the number of impaired subjects in a
group exposed to noise levels in a stated excess of
the zero-risk criterion.
For these reasons, the TLV is based on a
formula that includes 3000 Hz. Using ISO-R-
1999.2,<5> the median amount of NIPTS after 40
years of exposure to 90 dB is 2 dB for the average
of 500, 1000, and 2000 Hz. The same 40-year
exposure at 85 dB for the average of 500, 1000,
2000, and 3000 Hz is 1. 75 dB. Thus, everything else
being equal, inclusion of 3000 Hz will drop the 8-
hour criterion level from 90 dB to 85 dB.
History
In 1954, the ANSI Z.24.X.2 Committee reported
the need to define hearing impairment and
protection goals. There was some indication that
exposure to octave band levels in excess of 80 dB
could cause some loss in hearing.<17>
After experimenting with and proposing the 3-dB
rule and after extensive study by the National
Research Council Committee on Hearin_fi Bio-
acoustics, and Biomechanics (CHABAi i of the
National Academy of Sciences, the U.S. Air Force
introduced the equal energy rule in its re~ulation on
Hazardous Noise Exposure in 1956.<19·20
In 1961, the ISO published a series of noise
rating curves and proposed that the noise rating
curve N85 be used as the limit for habitual workday
exposure to broadband noise. A permissible
temporary threshold shift (TTS) was considered, and
a series of curves based on the average level of the
300 to 600, 600 to 1200, and 1200 to 2400 Hz
octave bands was suggested to provide an estimate
of permissible exposure to intermittent noise.<21 >
In 1963, Kryter<22>proposed a family of 1/3
octave and octave band curves based on predicted
TTS in the speech frequencies. The slope of the
curves varied significantly from those of ISO. The
criteria provided limits for daily exposure times
ranging from 1.5 minutes or less (ceiling) up to 8
hours. Kryter's criteria were the same as those
contained in the draft of the Technical Report of the
Armed Forces< 19>and CHABA.< 15>
In 1964, the MOO Subcommittee on Noise
reported that, " ... If the sound energy of the noise is
distributed more or less evenly throughout the eight
Noise-3
octave bands and if a person is to be exposed to this
noise regularly for many hours a day, five days a
week for many years, then if the noise level in either
the 300 to 600 Hz or the 600 to 1200 Hz band is 85
dB, the initiation of noise exposure control and tests
of hearing is advisable. <23>
11
In 1967, the lntersociety Committee on
Guidelines for Noise Exposure Contro1<9>reviewed
published data and some private communications
and provided an estimate that at 85 dBA, in terms of
percentage risk, some 3% of a population exposed
throughout a working lifetime would suffer some
hearing impairment (HLI [0.5, 1.2] > 25 dB). In view
of the data scatter, however, the Committee
indicated that this was not significant. At 90 dBA, the
percentage risk was approximately 10% and this
was felt to be significant. Again, frequencies above 2
kHz were not used in making this determination.
In May 1967, the ACGIH Threshold Limit Values
for Physical Agents (TLv®-PA) Committee, which
had representation on the lntersociety Committee,
recommended a limit of 90 dBA for an 8-hour day,
40-hour week exposure, on the basis that this
should protect 90% of the long-term exposure group.
For exposures less than 8 hours per day, the TLv®-
PA Committee recommended that, for each halving
of the exposure time, the limit be increased by 5 dBA
(5 dBA slope). Even at that time, there was some
evidence that damage to the hearing mechanism
may be directly related to the acoustical energy
involved. If this is true, the limit should be increased
by only 3 dBA (3 dBA slope) for each halving of
exposure time.
While even at the time there was some
substantiation for the 3-dBA slope for uninterrupted
exposure to steady-state noise, the TLv®-PA
Committee felt that, based on the available TTS and
animal studies, the ear could tolerate more
acoustical energy briefly than it could for continuous
8-hour exposure. Furthermore, the Committee felt
that, in most plant situations, rest periods plus
equipment shutdowns contributed to interruptions in
exposure that significantly increased the ear's
tolerance. This first TLV (90 dBA) was subsequently
adopted in 1970.
In 1967, Baughn first [>resented data, later
published in a final report,<24>based on the
evaluation of audiograms of 6835 noise-exposed
workers. This was one of the largest groups studied
at that time. There was some stated lack of controls
in the study. Acknowledging this constraint, the
indication was that there was an 8% risk of hearing
impairment at 85 dBA and that the risk factor was
increased to 18% at 90 dBA.
A study by Burns and Robinson<25>in 1970
included such factors as the use of dBA, variability in
audiometric measurement, the relationship of
temporary threshold shift to permanent loss, and the
use of the equal-energy approach. Their analysis
supported the use of the equal energy approach and
A-weighting of sound pressure measurements.
4-Noise
NIOSH published its Criteria Document on
occupational exposure to noise in 1972_<5>This
included audiometric and noise exposure data
NIOSH obtained from 792 noise-exposed workers
from various industries and 380 workers from the
same industries without noise exposure, who served
as controls. An analysis of the data indicates
approximately 19% risk of impairment (HL[0.5, 1,2] >
25 dB) for workers exposed for more than 30 years
to 85 dBA. The NIOSH document contains a
comprehensive review of published data from many
studies. The NIOSH percent risk values for long-
term exposures to various noise levels were
compared with those derived from three other
studies: 1) the lntersociety Study, <9>2) the early ISO
Recommendation R-1999,<25>and 3) the Burns and
Robinson study.<25>The ISO risk values, which were
based on Baughn's data,<24>were similar to those of
NIOSH. When the Burns and Robinson<25>
audiometric data were adjusted to conform with the
audiometric baseline normally present in United
States studies, the risk values were comparable.
The lntersociety Study risk values were significantly
lower. This difference was attributed to several
factors including a) use of results from one ear only,
b) nonseparation of experience groups, c) use of
speech interference levels and subsequent
conversion into approximate dBA values, and d) use
of a dissimilar composite population in the
lntersociety Study. The importance of 3000 Hz in the
hearing and understanding of speech under
everyday conditions was reviewed. It was concluded
that HL1(1,2,3) > 25 dB should be accepted as the
beginning of impairment.
In 1974, the U.S. Environmental Protection
Agency (EPA) published the "Levels" document.<21>
In this document, an 8-hour level of 75 dBA was
established as the level that would protect "public
health and welfare with an adequate margin of
safety." Much of this result was based on the work of
Johnson,<25>who combined the works of Passchier-
Vermeer,<29> Baughn,<24>and Burns and Robinson.<25>
These were the same data available to the TLv®-PA
Committee. A major difference, however, was the
use of 4000 Hz as the most sensitive indicator of
hearing loss. Johnson<25>observed that the
difference between protecting 4000 Hz and the
average of 0.5, 1, and 2 kHz is about 15 dB.
In 1974, having reviewed the published data, the
TLv®-PA Committee believed that 85 dBA provided
an appropriate limit for an 8-hour day, 5-day week,
long-term exposure to occupational noise. On the
basis of HLl(0.5, 1,2) > 25 dB, the 85-dBA limit
should ensure the protection of approximately 90%
of exposed workers.
Concerning "uninterrupted" exposures to steady-
state noise of less than 8 hours per day, the TLv®-
PA Committee favored the retention of the 5-dB
slope. Concerning intermittent exposures throughout
a work day, the Committee proposed a simple
summation of such episodes over the work day.
ACGIH® © 2006
While the 5-dB doubling rate was thought to be
overly permissive in some plant situations for
continuous exposure, for the case of intermittency, it
would tend to make some allowance for the recovery
periods between exposures. The Committee
recognized the need for more field study in this area.
As will be shown later, additional studies have
shown that the 3-dB slope (equal-energy) is more
likely the better concept.
A "Notice of Intended Change," incorporating the
above limits, was made in 1974 and subsequently
adopted in 1976.
The Equal-Energy Rule
Three studies on two data sets are of inter-
est. <30--32> The Inter-Industry Noise Study, reported by
Yerg et a1.,<30>collected data on male and female
workers exposed to steady-state noise in the range
of 82 to 92 dBA. The protocol was designed to en-
sure rigorous control of both exposed and control
groups. The exposed workers were divided into
groups according to sex and to plant noise level,
e.g., low intensity group 82 to 85 dBA and high
intensity group 86 to 92 dBA. However, subsequent
to the start of the study, repeat checks on the plant
noise levels revealed that in some cases there was a
marked change in these levels. Thus, there was
some movement of subjects between the high and
low groups during, and presumably before, the study
period. The conclusions drawn from this study were
that a) the hearing levels in the high-intensity group
were not observably different from the hearing levels
in the low-intensity group, b) differences between
females in the exposed and control groups were not
statistically significant, and c) differences in hearing
levels between males exposed to 82 to 92 dBA and
their controls were small and were not statistically
significant at 500, 1000, and 2000 Hz. However, at
3000, 4000, and 6000 Hz, the levels of hearing loss
in the noise-exposed group significantly exceeded
those in the control group by approximately 6 to 9
dB.
Schori and Johnson<31 >independently analyzed
the same database. One conclusion of their study
was that the hearing changes found in the Inter-
Industry Noise Study were consistent with the ISO
R-1999.2 revised standard.<5>
The Berger et al. report<32>is notable for the
precise measurement and steady-state character-
istic of the plant noise. Following careful screening
during the study period, only 100 exposed subjects
(42 males and 58 females) were retained from an
original group of 459 employees. The conclusion
was that" ... Averaging the results for all 1OO
subjects, in order to make comparisons to other
available data, yielded results in close agreement to
predictions based upon the work of Burns and
Robinson, Baughn, NIOSH and Passchier-Vermeer,
indicating that 10 years of exposure to a daily Leq of
89 dBA causes measurable hearing loss at 4
ACGIH® © 2006
kHz."<32 >
While not all researchers have supported the 3-
dB rule,<33 •34>a general consensus favors its use.
In a special meeting in 1982, many of the world's
leading investigators of noise-induced hearing loss
reviewed the available literature with respect to the
use of equal-energy.<35>The group endorsed the use
of equal-energy as the most practical and reason-
able method of measuring both intermittent and
impacUimpulse noise between 80 dBA and 140 dBA.
This meeting produced the international consensus
that was the basis of ISO-R-1999.2.<5>
Suter<35l reviewed the history of the various
trading relations as well as the research that would
best support these relations. She concluded that
" ... While the 3-dB rule may be somewhat
conservative in truly intermittent conditions, the 5-dB
rule will be under-protective in most others." Suter<35>
also concluded that the 3-dB exchange rate was the
method most firmly supported by the scientific
evidence now available. Some of the key arguments
she summarized are as follows:
• TTS measured 2 minutes after exposure (TTS2)
"is not a consistent measure of the effects of a
single day's exposure to noise, and the NIPTS
after many years may be quite different from the
TTS 2 produced at the end of an 8-hour day.
Research has failed to show a significant
correlation between TTS and PTS; 11<25,37 l the
relationships between PTS, TTS, and cochlear
damage are equally unpredictable.<38-42J
• Data from animal experiments presented by
Ward and associates<39•40 •43 l "... support the use
of the 3-dB exchange rate for single exposures of
various levels within an 8-hour day." However,
evidence gathered by Ward and Turner,<39>Ward
et a1.,<40>Bohne and Pearse,<44>Bohne et a1.,<45,45>
and Clark et a1.<47>indicates" ... that
intermittency can be beneficial, especially in the
laboratory." Nevertheless," ...these benefits are
likely to be smaller or even nonexistent in the
industrial environment, where sound levels during
intermittent periods are considerably higher and
where interruptions are not evenly spaced."
• Data from a number of field studies correspond
well to the e~ual-energy rule, as Passchier-
Vermeer<45•49 and Shaw<50l have demonstrated.
• The assumption by CHABA of the equal
temporary effect theory is also questionable in
that some of the CHABA-permitted intermittent
exposures can produce delayed recovery
patterns even though the magnitude of the TTS
was within 'acceptable' limits, and chronic,
incomplete recovery will hasten the advent of
PTS. The CHABA criteria also assume regularly
spaced noise bursts, interspersed with periods
that are sufficiently quiet to permit the necessary
amount of recovery.
In addition to Suter•s<35l conclusions, there are
several other reasons to change to the equal-
Noise - 5
energy rule. These reasons should benefit industry
as well as increase assessment accuracy. One of
the foremost reasons is the elimination of the
awkward all-or-nothing limit of 115 dBA. A short
burst of noise such as an aircraft flyover or a siren
might exceed this limit. Yet, a burst of broadband
noise as long as 10 msec at 130 dB has been
shown to cause almost no TTs.<51 -s3 J On the other
hand, research has shown that broad-band noise of
115 dB for 15 minutes is likely to cause excessive
TTs.<52> Use of equal energy eliminates this arbitrary
115 dB limit.
Second, use of equal energy better predicts the
hazard of noises for exposure durations greater than
8 hours. For an 8-hour criterion level of 85 dB, the 5-
dB rule would dictate a 16-hour exposure at 80 dBA
and a 24-hour exposure as 77 dBA. The equal-
energy rule will allow 82 dBA for 16 hours and 80
dBA for 24 hours. The threshold of any TTS to
broadband noise for periods as long as 24 hours has
been shown to be between 78 and 80 dBA.<54 -55> On
the other hand, 85 dBA for 8 hours will cause some
TTS. It is certainly more reasonable to anchor the
24-hour point to 80 dBA. The only time that a limit
lower than 80 dBA would be appropriate is the very
unusual circumstance when the exposure consists of
a steady pure tone.
A third reason is the inclusion of hearing levels
at 3000 Hz. What is often forgotten is that the benefit
of intermittency, as shown in the CHABA WG46
curves,<1 8' did vary with the audiometric frequency
considered. Higher audiometric frequencies required
smaller trading relations than the lower audiometric
frequencies to produce equal TTS. Therefore, even
if the equal TTS 2 model was correct, inclusion of
3000 Hz would dictate reducing the 5-dB trading
relation to a lower number. In some cases, this
number might even be slightly lower than 3 dB.
In summary, the equal-energy rule (3-dB rule)
appears to be a better predictor of noise hazard for
most practical conditions and is strongly recom-
mended by ACGIH
Reference is made to the following formula for
determining hearing impairment. The main point at
issue is the inclusion of the hearing threshold level at
3000 Hz in such a formula. In 1979 the American
Academy of Otolaryngology developed a new
formula for determining hearing impairment.<13> The
formula includes the 3000 Hz frequency and is as
follows:
1. The average of the hearing threshold levels at
500, 1000, 2000, and 3000 Hz should be
calculated for each ear.
2. The percentage of impairment for each ear
should be calculated by multiplying by 1.5% the
amount by which the average hearing threshold
level exceeds 25 dB. The impairment should be
calculated up to 100% reached at 92 dB.
3. The impairment then should be calculated by
multiplying the percentage of the better ear by 5,
adding this figure to the percentage from the
6-Noise
poorer ear, and then dividing the total by 6.
IMPULSE NOISE
The previous approach for assessing impulse/
impact noise was to allow 100 impulses or impacts
per day at 140 dB, 1000 per day at 130 dB, or
10,000 per day at 120 dB. Impacts or impulses refer
to discrete noise of short duration, less than 500
milliseconds (ms), in which the sound pressure level
rises and decays very rapidly. One of the problems
with this approach is that it is difficult, if not impos-
sible, to properly measure. A manufactured instru-
ment is available that can sum the number of
measured impulses at each 1 dB increment and
divide by the number of allowable impulses. From
this sum, a dose can be calculated. However, the
calculation of this dose requires several assumptions
that were not explicit in the previous TLV. While
these assumptions could be clarified here, there
exists a more accurate approach for addressing
impulse/impact noise.
Besides the complexity of using the previous
TLV, there were several fundamental problems with
this TLV. The first problem is that the duration of the
impulse or impact was not considered. A short 1-ms
pulse was considered as harmful as a long 200-ms
pulse. This is not consistent with the CHABA
guidelines on impulse noise<55l or any known
research. Second, impulse or impact noise was
treated separately from nonimpact noise. This
separate treatment is inconsistent with research
which has shown that at exposures causing
moderate or high levels of TTS, combined impact
and continuous noise can cause a synergistic effect;
i.e., the resulting effect is greater than just the
addition of the results from the impact exposures
and the results from the continuous noise
exposures.<57> Fortunately, these same researchers
have shown that at exposure levels which will cause
only a small amount of TIS, as much as the
proposed 8-hour 85 dBA threshold, this synergistic
effect disappears. <55>
The proposed method of assessing impulse or
impact noise resolves both these problems. By
combining all sound energy between 80 dB and 140
dBA, impacUimpulse noise is combined with
continuous and intermittent noise. Longer impulses
are considered more dangerous than short impulses.
Finally, the measurement of noise becomes greatly
simplified. An integrating sound level meter that
meets the requirement of IEC-804<4 > or a dosimeter
that meets the requirements of S1 .25<3> is all that is
required with one exception. The IEC-804<4 > for Type
II instruments and the ANSI S1 .25<3> specify only a
minimum pulse range of 53 dB. The instruments
used for this TLV must have a pulse range of at
least 63 dB if all sounds from 80 dB to 140 dB are to
be combined. The dosimeters used for this TLV also
must have a pulse range of 63 dB set on the 3-dB
exchange range. Obtaining instrumentation that
ACGIH® © 2006
meets this re~uirement should not be a problem.
The IEC-804< l already requires a 63-dB pulse range
for Type I instruments. In addition, the major
manufacturers of dosimeters in the United States all
have instruments with more than a 63-dB pulse
range.
It should be noted that the previous impulse
noise TLV was already based on equal energy;
therefore, the major change is the combining of all
noise into one measure.
Support of this procedure comes from numerous
documents and standards. The revised ISO
standard<5l uses this approach. The published draft
standard, ANSI S3.28 1986,<59l also has adopted this
measurement approach.
Several European field studies also support the
combining of impact noise with continuous noise. At
the Southampton meeting on this subject,<35l
Passchier-Vermeer<29l presented data that indicated
the possibility that equal energy may slightly
underestimate the combined effect, especially for 8-
hour criteria levels above 90 dB. The majority of the
researchers did not see the need for adjusting for
the combined effect; however, the revised ISO-R-
1999.2<5l states in note three: "The prediction
method presented is based primarily on data
collected with essentially broad-band steady non-
tonal noise. The application of the data base to tonal
or impulsive/impact noise represents the best
available extrapolation. Some users may, however,
wish to consider tonal noise and/or impulsive/impact
noise about as harmful as a steady non-tonal noise
that is approximately 5 dB higher in level."
Because the TLV is an 8-hour criterion level of
85 dB, such a correction was not used nor is such a
correction recommended.
The selection of 140 dB as a ceiling limit for
unprotected ears remains a reasonable level. This
level was reviewed by the working group that
prepared ANSI S3-28. After this review, the working
group recommended the continuation of this limit.
The key research for that limit was that of Wardcsoi
and Price.<51 l A report<52l by the Committee on
Hearing and Bio-Acoustics (CHABA) of the National
Research Council also suggests this level as the
breakpoint above which the CHABA criteria of 1969
should be used.
The use of a C-weighted peak resolves a long-
standing problem with measurement of the peak.
The term "unweighted peak" is undefined. Without
specifying the low end cutoff frequency of the
measurement devices, different measurement
devices could vary greatly. For example, an
innocuous car door slam might cause a 140-dB
unweighted peak on some instruments but not on
others. Use of C-weighting defines the frequency
response of the instrument and eliminates very low
frequency impulses and sounds. The C-weighting
discounts such sounds. Thus, the low frequency
pulse that comes from closing a car door or other
such innocuous very low frequency pulses can be
ACGIH® © 2006
more properly assessed. lnfrasound exposures
(exposures below 20 Hz) will also be better
assessed. Such exposures are rare and, even if they
could occur at levels found in industry directly, they
are not likely to be dangerous to a person's hearing
or health.<62-=-a5J
The TLV does not address the case in which the
impulse exposure exceeds a C-weighted peak of
140 dB. In such cases, MIL-STD-1474c<5 should be
used. The MIL-STD recommends that hearing
protection be worn whenever exposures exceed 140
dB. In addition, guidance is provided for those
situations in which double hearing protection {both
muffs and plugs) should be worn.
FETAL NOISE EXPOSURE
The significance of this note to the Noise TLV is
to alert workers and heath officials to the possibility
of noise-induced hearing loss to the fetus. Especially
of concern are those situations in which the hearing
of the pregnant female is shielded by hearing
protection that is better than the natural protection
afforded the fetus. Thus, the fetus is assumed to be
more at risk of hearing loss than the expectant
mother. This natural protection or sound isolation is
similar to a good hearing protector and consists of
the sound attenuation of the abdomen and the lack
of middle ear function. However, this may not
provide as much protection for impulse noise.
Therefore, the Documentation is separated into two
general discussions, one for the time-weighted
average (TWA) recommenda-tion of 115 dBC and
one for the peak recommen-dation of 155 dBC.
The 8-Hour TWA C-Weighted Level
of 115 Decibels
Background
There has been concern for some time that the
fetus may be overexposed to damaging noise. In
1982, CHABA published a report<55l that reviewed
the data known at that time. One of the conclusions
was that" ... There is no conclusive evidence of
detrimental effects of high-intensity external sound in
higher mammals." The report also showed that the
natural protection is probably adequate for most
industrial noise. However, the report went on to
recommend
"... Until better information is available,
however, it would appear prudent for pregnant
women to avoid exposures of long duration (several
hours per day) to sounds of 90 dB and above ... "
This latter statement is not well supported and
undoubtedly errs on the side of excessive caution.
The problem with such caution is that pregnant
women might be unnecessarily deprived of their
livelihood. Since 1982, there have been additional
investigations on this subject, none of which has
proven entirely conclusive. Pierson<57l provides a
summary of these investigations. Three retro-
Noise - 7
spective studies have looked at the hearing level of
children whose mothers were noise-exposed during
pregnancy.<5a-7oJ None of these had a sufficient
sample size or made use of proper research
methodology, but they did show hearing levels
indicative of some effect.<57•71 l
Several key animal studies have experimented
with pregnant sheep. Dunn et a1.<72l used 18
pregnant ewes. Nine of these ewes were exposed to
pink noise 4 hours/day, 5 days/week at an overall
level of 130 dB for approximately the last half of their
pregnancy. Nine ewes were used as controls and
followed the same regimen, including sitting in the
reverberant noise exposure room without the noise
source for 4 hours/day. Hearing of the lambs born of
both the noise-exposed and control animals was
evaluated by recording auditory brainstem
responses (ABR) from scalp electrodes when the
lambs were between 30 and 40 days of age. The
ABRs for both groups were found to be in the range
of normal thresholds. The lambs were then
sacrificed, and examination of the cochleae showed
that approximately half of the 18 exposed ears had
morphological anomalies, while approximately one
quarter of the control ears had the same anomalies.
Dunn et al. concluded that " ... Even though the
exposed ears exhibited almost twice the number or
morphological anomalies found in the control group,
we are reluctant to interpret these findings as being
directly related to noise exposure since they
occurred in both groups. We are inclined to interpret
them as being postmortem fixation artifacts. On the
other hand, the higher incidence of cellular
anomalies in the cochleae of the noise-exposed
lambs than of the controls could not be
explained."<72l
The other animal studies include a series on the
exposure of pregnant ewes by Griffiths et a1.<73l and
Pierson et a1.< 74l In contrast to Dunn et a1.,< 72l these
studies evaluated the effect of a single 120 dB
broadband noise for 16 hours on the ABR thresholds
of in utero fetal sheep. Griffiths et a1.< 73l showed
temporary changes in the ABR thresholds when the
gestation age was from 126 to 134 days at the time
of exposure (average gestation period is 145 days).
In a follow-up experiment, Pierson et a1.,<57,74l
showed some small permanent changes in the ABR
thresholds when the exposure to the same 120 dB
for 16 hours noise occurred on day 113 of gestation.
The high exposure levels of these studies gave
support to the belief that one does not need to be
overly concerned with fetal noise exposure.
However, these studies also suggested that some
upper limit of noise exposure should be set.
The TWA recommendation of 115 dBC as an
upper exposure limit is based on the assumption that
the ears of the fetus should be protected at least as
well as an adult. Thus, the sound levels at the
cochlea should not exceed the threshold of injury
levels used in ISO-R-1999.2<5l or ANSI S3.44-
1995<75l recommendations. These levels are 93 dB
8-Noise
for 500 Hz, 89 dB for 1000 Hz, 80 dB for 2000 Hz,
77 dB for 3000 Hz, 75 dB for 4000 Hz, and 77 dB for
6000 Hz.
Using the sound isolation values of Gerhardt et
a1.,<75l the abdomen provides at least 25 dB of
attenuation at 500 Hz, 35 dB at 1000 Hz, and well
over 40 dB at 2000 Hz and above. The sound
isolation data from Gerhardt et al. <75l show the
reduction of sound from air to the fetal inner ear.
Subtracting these values from 115 dB results in
levels below the threshold of injury levels, even if the
occupational noise was a tone rather than
broadband noise. The 115 dB limit is also lower than
the TWAs of the animal exposures described earlier.
Specifically, 120 dB for 16 hours<73,74l is like an 8-
hour TWA at 123 dB, and the 4-hour exposure at
130 dB<72l is like an 8-hour TWA at 27 dB.
C-weighting the noise measurements is recom-
mended rather than A-weighting because, just like
the attenuation of most hearing protectors, the atten-
uation of the abdomen declines as the frequency
decreases. In fact, as with hearing protection, this
de-cline is approximated by the inverse of the A-
weighted curve for frequencies below 1000 Hz.
Thus, to estimate a safe A-weighted level at the ear
of the fetus, the C-weighted TWA should be used.
This same concept is used in calculating the NRR
for hearing protectors_<77l
The Peak Exposure of 155 dBC
Background
The 155 dBC recommendation is supported by
the study of Gerhardt et al. <75l Eleven pregnant
sheep at gestational day 127 were exposed to 20
impulses using a shock tube 4 feet from the sheep.
With the sheep removed, average peak noise levels
of 169.7 dBC were measured at the position of the
fetus. Using a hydrophone within the uterus, the
differences in attenuation between the air and the
uterus varied between 2 dB and 20 dB. Slight
elevations of evoked potential threshold were noted
for low-frequency stimuli. Scanning electron
microscopy revealed damage to hair cells in the
middle and apical turns of the cochlea.
The 155 dBC TLV-Ceiling was derived using
two approaches. The first apwoach assumed, during
the study by Gerhardt et al.,< 5l that the average
attenuation between the air measurements and the
fetal head was 11 dB ([2 + 20]/2). This would imply
that 158. 7 dBC (169. 7 - 11) at the head of the fetus
could result in damage. However, the worst-case
situation of the fetal head next to the surface of the
abdomen could result in such hair-cell injury
occurring 9 dB lower or at a peak of 161 dBC
because of reduced attenuation. Thus, injury to the
hearing of the fetus could occur at a peak of 160.7
dBC (158.7 + 2) as measured outside the abdomen.
Because there is only one experimental point, the
threshold of injury is difficult to predict. However,
reducing the peak pressure by at least a factor of 2
ACGIH® © 2006
(or 6 dB) appears reasonable. This results in an
estimated peak exposure limit of about 155 dBC.
The second approach is to adjust the current
peak (TLV-C) of 140 dBC for impulse noise by a
reasonable estimate of the amount of protection
afforded by the abdomen and the lack of middle ear
function. As shown in the previous approach, the
womb may provide as little as 2 dB of attenuation;
thus, the peak limit of 140 dBC can be raised to 142
dBC to account for the attenuation of the womb. The
lack of middle ear function in the fetus results in
attenuation values that range from 10 to 40 dB at
frequencies of 125 Hz to 2000 Hz.<75> This would
indicate that a limiting level of noise impulses in air
could be anywhere from 152 (142 + 10) dBC to 182
(142 + 40) dBC. The 152 dBC is a worse-case
estimate for both frequency and fetal position. Thus,
a slightly higher value seems reasonable. The 155
dBC TLV-C, measured at the abdomen, is close to
the lower end of this range and is considered to be a
reasonable estimate of what the limited available
data suggests is necessary to protect the hearing of
the developing fetus.
EXTENDED EXPOSURES
Allowing the daily dose to exceed unity if the
weekly exposure is less than 5 is allowed under the
current international standard that relates noise
exposure to noise induced hearing loss (ISO R-
1999). In fact, the international standard allows a
daily fraction to be 10 times (10 dB) the yearly
average. The proposed note allows much less daily
variability and is more protective. Based on an 8-
hour level of 85 dBA, the factor of 3 could equate to
a level of 90 dBA for 1 day, 82 dBA for 4 days, and
less than 80 dBA for 2 days.
The noise exposure guidelines depicted in Table
1 assume that after a work shift, the worker would be
able to relax and sleep at home for a time such that
if any temporary shifts in hearing did occur during
the time at work, these changes would recover
during the time the worker was away from work. This
assumption is most likely violated when the worker is
confined to a set of spaces such as a ship, space
station, jail cell, or similar situation. Studies of long
duration broadband noise exposures have shown
that temporary changes in hearing or Temporary
Threshold Shifts (TTS) can occur at levels of 80
dB.<79> At 75 dB this does not occur. Long duration
studies have also shown that after 8 to 16 hours of
exposure, TTS stops increasing. This behavior is
interpreted to mean that if TTS has not occurred by
the time a persons been exposed for 24 hours to
some level of steady noise, then TTS will not occur
regardless of the duration of the noise exposure. For
this reason, the level of 75 dBA is considered the
safe level for causing hearing loss for long duration
broadband noise. If the noise is tonal in nature, this
level needs to be reduced by as much as 5 decibels.
ACGIH® © 2006
Thus, 70 dBA is the safer level when nothing is
known about the spectrum of the noise.
When there is a steady background noise, there
can be other noise exposure, such as the sound
from communication headsets, that can also cause
TTS. The background level can affect the recovery
of this TTS. Research has shown that TTS recovery
can be hampered by background octave band levels
from 65 to 80 dB.caor Ward called this level required
to prevent the delay TTS recovery as "Effective
Quiet". If an A- weighted level is used, the
suggested level to allow recovery is an A-weighted
level of 75 dB. However, for noise with strong tonal
components, "Effective Quiet" may need to be at
least as low as 70 dB. "Effective Quiet for an octave
band of noise at 4000 Hz starts at 65 dB, however,
the situation in which all the sound energy is only in
this octave band is expected to be rare. The
committee believes that the 70 dBA is the proper
level.
For the above reasons the committee has
recommended an A-weighted level of 70 dB or
below as the background noise exposure for
sleeping and relaxation for situations in which the
work time extends beyond 24 hours.
OTOTOXICITY
Exposure to certain chemicals, either alone or in
concert with noise, may result in hearing loss.
Certain chemical substances have shown some
ototoxic effects but may not be ototoxic in typical
occupational settings. Since the exposure threshold
where such ototoxic effects is not known, the only
reliable way to know if the substance is affecting the
hearing of exposed workers is to take audiograms.
While audiometric data is useful for any worker
exposed to any measurable level of a chemical
substance, yearly audiograms are highly
recommended for workers whose exposures are at
20% or more of the TLV for the substance in
question. This 20%, while somewhat arbitrary, will
ensure data from sub-TLV exposures. If a worker is
currently participating in a hearing conservation
program due to excessive noise, the reviewers of the
audiometric data should be alert to possible
synergistic effects between exposure to noise and
the chemical substance and, if necessary, suggest
reducing the exposure to one or both.
A summary of the evidence for ototoxicity of the
substances listed in Note 2 follows.
Trichloroethylene
A study<51 > conducted in 1976 demonstrated
bilateral, high frequency sensori-neural hearing loss
in 26 out of 40 workers exposed to excessive
concentrations (above international recommended
values at that time) of trichloroethylene (TCE).
Cases with previous or current noise exposure were
Noise-9
excluded from the study. Another study,!52l on the
health status of populations exposed to trichloro-
ethylene {TCE) through contaminated water {n =
4281) indicated a significant increase in reported
hearing losses for the 0 through 9 years of age
group. No human study has investigated occupa-
tional TCE exposures for ototoxicity at the current
TLV, either alone or in concert with noise.
Carbon Disulfide
Three studies were conducted with workers from
viscose rayon plants, where exposure to carbon
disulfide constitutes its main hazard_(53-85 l The
Sulkowski study!53l of workers exposed to both noise
and carbon disulfide showed that a larger percent-
age of the workers had been poisoned with carbon
disulfide, than merely exposed to carbon disulfide,
and incurred sensori-neural hearing losses. A large
percentage of these had retrocochlear losses.
Morata!MJ studied workers exposed simultaneously
to carbon disulfide at 29 ppm and noise between 86
and 89 dBA. Levels for both agents were excessive.
Carbon disulfide-exposed workers had worse
hearing than those ex~osed to noise alone. The
study by Hirata et al? l was conducted with workers
currently exposed {exposure duration,> 240 months
[n=34]), current exposed {exposure duration, 24-84
months), and former workers {exposure duration, >
120 months). Exposure to carbon disulfide ranged
from 3.3 to 8.2 ppm, averaging 4.76 ppm. The
Industry exhaust ventilation apparatus had under-
gone major improvement 14 years before the
investigation was conducted. Thus, workers with
exposure duration longer than 14 years were ex-
posed to undetermined higher levels than the ones
reported. Auditory brainstem responses were signifi-
cantly altered only for the group with the longest
exposure {> 20 years) and a history of excessive
exposure. The results suggested that chronic
exposure to carbon disulfide in humans affects the
ascending auditory tract in the brainstem_!55l
Carbon disulfide may not be ototoxic at the
current TLVof 10 ppm; however, since Hirata did not
report the values workers were exposed at before
the ventilation system was improved, and no other
human study investigated this level alone or in
concert with noise, these data indicate that carbon
disulfide is potentially ototoxic.
Styrene
Workers exposed to low levels of styrene did not
appear to have increased age-dependent hearing
loss at high frequencies_!55l However, a comparison
within the group of exposed workers between the
least exposed and the most exposed {limit-
normalized exposures ranging from 14 to 106 ppm),
in hearing thresholds at high frequencies. Routine
hearing tests of workers exposed to styrene {levels
not reported) in a plastic boat plant did not indicate
10-Noise
hearing losses resulting from causes other than
exposure to noise_!57l Nevertheless, 7 of 18 workers
displayed abnormal results in central auditory
system testing. Styrene and noise exposures were
meticulously assessed for 299 workers in the fiber-
reinforced industry. !55l Noise levels were found to be
in the range between 85 and 90 dBA, while styrene
levels were generally below the recommended level
of 50 ppm. The association between noise
exposure, based on the developed lifetime noise-
dose estimate, and hearing loss was significant.
That was not the case for styrene exposure. Styrene
exposure approached significance for hearing loss
only at some specific frequencies.
Styrene may not be ototoxic at the current TLV
of 50 ppm, but since no human study investigated
this level alone or in combination with noise, styrene
should be considered potentially ototoxic.
Toluene
A review paper!59l on the ototoxicity of toluene
discusses the abuse of toluene {from glue sniffing)
and cites four references showing dramatic hearing
loss originating from the central auditory pathways.
In another study,!90l an accidental acute exposure to
toluene produced hearing loss in half of the exposed
{N=6).
A study of 190 workers!91 l was carried out with
rotogravure printing workers. The hearing and
balance functions of a group of printers exposed
simultaneously to noise (88-98 dBA) and toluene
(100-365 ppm) were compared with a group of
printers exposed to noise alone (88-97 dBA), a
group exposed to a solvent mixture in which toluene
was the major component, and a group neither
exposed to noise nor toluene. The adjusted relative
risk estimates for hearing loss were 4 times greater
for the noise group, 11 times greater for the noise
and toluene group, and 5 times greater for the
solvents group. Acoustic reflex measurements
suggested that the hearing losses found in the group
exposed to both agents might be due to lesions in
the central auditory system.
The effects of toluene on the auditory system
was studied in a group of rotogravure printers
through the use of auditory brainstem responses
(ABR).!92l Forty workers with normal hearing ability
{assessed by pure tone audiometry), who had been
exposed at an average of 97 ppm styrene for 12 to
14 years, were selected to participate. Their results
were compared with those from a group of workers
of the same age but not occupationally exposed to
solvents. The study indicated that exposure to tol-
uene was able to induce a statistically significant
alteration in the evoked responses, visible for all
waves and all the intervals studied. The auditory
brainstem responses demonstrated auditory nervous
system modifications before the occurrence of neu-
rological clinical signs due to chronic exposure to
toluene.
ACGIH® © 2006
 Another study on rotogravure printers!93l noted
an association between hearing loss and the bio-
logical marker (of hippuric acid in urine, normalized
to the creatinine levels) for exposure to toluene. The
odds-ratio estimates for hearing loss were 1. 76
times greater for each gram of hippuric acid per
gram of creatinine. Urinary hippuric acid of 2.5 gig
creatinine was first recommended by ACGIH in 1984
as one of the Biological Exposure Indices (BEls) for
occupational exposure to toluene at a TLV-TWA of
100 ppm_!94 ,95l ACGIH revised the BEi to 1.6 grama
of hippuric acid per gram creatinine when TLV-TWA
was lowered to 50 ppm_!94l Field studies conducted
during the 1970s and 1980s indicated that hippuric
acid levels correlated well with occupational expo-
sure to toluene at air concentrations of 100 ppm_!95l
Due to its high background levels in many countries
(1 to 1.5 g), hippuric acid is no longer considered as
a good biological marker for occupational exposure
to toluene below 50 ppm. It is still, however, recom-
mended as an easy-to-analyze biological marker for
exposure to toluene when nonoccupational back-
ground levels of toluene are low?6l In the printers
study, low hippuric acid levels were observed for the
majority of the group studied, which had no or little
occupational exposure to toluene (52% with ≤ 0.5 g
hippuric acid/g creatinine; 75% with 1 g/g or less).
The authors stated that it provided valuable informa-
tion on occupational exposure.
At the previously recommended BEi of 2.5 g
hippuric acid/g of creatinine (corresponding to a
TLV-TWA of 100 ppm), the odds ratio for hearing
loss estimated in the present study is 4.4 (odds of
1. 76 per gram x 2.5 grams of hippuric acid /gram of
creatinine = 4.4; 95% confidence interval [Cl] =
2.50-7.45).
The current ACGIH TLV–TWA of 50 ppm is one
of the lowest recommended international limits for
toluene, !97l and even in this concentration, the
estimated odds ratio is greater than 2. The U.S.
Occupational Safety and Health Administration
(OSHA) set a permissible exposure limit 4 times the
TLV recommended by ACGIH (i.e, 200 ppm TWA).
The U.S. National Institute for Occupational Safety
and Health (NIOSH) recommends a recommended
exposure limit of twice that of ACGIH (i.e., 100 ppm
TWA)_!97l Each of these exposure limits may be
adequate for preventing a series of health outcomes,
but none of them seem to be adequate for preven-
ting hearing loss. On the other hand, there is a pos-
sibility that peak, nontrivial exposures to solvents
may be contributing considerably in causing the
losses. Thus, a lowering of limit-normalized levels
might not eliminate the risk. More research is
needed on solvent-induced hearing loss, both to
address the adequacy exposure limits and the
ototoxicity of toluene at these levels.
Lead
Children considered to be at risk for lead
ACGIH® © 2006
intoxication from peeling lead paint or dust brought
home from parents had their auditory systems
examined through ABR.!95l The results of children
with elevated blood lead levels showed that the
latencies of waves Ill and IV increased linearly with
blood lead level (range, 6-59 g/dl), indicating a
slowing of auditory nerve conduction velocity due to
lead exposure. A 5-year follow-up of the children
with low to moderate lead exposures (range, 6-30
g/dl) showed persistence of the prolonged latencies
at repeat testing_!95l Audiometric data were obtained
by the Second National Health and Nutrition
Examination Survey on 5717 children, most of whom
had blood levels measured?9l The probability of
elevated hearing thresholds increased significantly
with increasing blood lead levels ~range, 0-50 g/dl).
Auditory brainstem responses! 100• 01 l and auditory
event-related potentials! 102l were recorded in
workers occupationally exposed to lead who had
their blood lead levels monitored. Discalzi et a1.! 101 J
divided workers into two groups by lead
concentration: above or below 50 g/dl. In the Araki et
al. study,! 102l blood lead concentration ranged from
12 to 59 g/dl (median 30 g/dl). Blood lead levels
were significantly correlated with abnormalities in the
recorded evoked potentials.! 100-102i
Mercury
Although less pronounced than the alterations
caused by lead exposure, significant alterations in
the ABR were also observed in the case of
occupational exposure to mercury.! 101 l Mercury
intoxication has been associated with hearing
loss.!103l Gerstner and Hutr104l found in mercury-
poisoned clinical patients that hearing loss develops
early in mercury poisoning, extends over nearly the
entire frequency range, and results in difficulty in
understanding speech when other voices are
present. Autopsies of these patients showed no
evidence of cochlear damage, an indication of more
central lesions.
Up to 80% of patients treated for the fatal
Minimata disease (due to ingestion of mercury
contaminated food and water) suffered hearing loss.
Long-term follow-up studies have been
reported.! 105•106l Twenty-eight percent of the patients
retested showed deterioration of hearing, while 7%
showed an improvement. Bekesy audiometry and
the Short Increment Sensitivity Index indicated that
the early and middle stages of mercury intoxication
may have resulted from cochlear lesions, whereas
hearing impairments in late stages may have
resulted from retrocochlear lesions.!105J Brain
autopsy studies of the mercury intoxicated patients
showed demyelination in the temporal lobes and
heavy deposition of heavy metals in the transverse
temporal gyri.!106l
Although mercury is ototoxic, it appears that this
happens mainly in cases of acute poisoning, and it is
accompanied by other neurological symptoms.
Noise-11
Manganese
Altered hearing and balance functions have
been reported in a study that examined workers
exposed to manganese alone or in concert with
noise.< 107> Pure-tone audiograms of manganese
exposed workers were affected in both low and high
frequencies. Manganese ototoxicity appeared to be
accelerated and exacerbated by noise exposure.
Arsenic
An epidemiologic study was conducted on a
population of children living by a plant responsible
for an emission of arsenic in the air.< 108•109 Analysis
of the children's hair, blood, and urine revealed
elevated arsenic content. Arsenic concentrations
ranged from 0.01 to 10.33 g/g in hair and from 0.001
to 0.1050 mg/g in urine. Significant hearing losses
were observed in the low frequencies of the audio-
gram when they were compared with unexposed
children. Current ACGIH BEi for Arsenic is 35 g
arsenic/g urine.
Although data indicate that arsenic is potentially
ototoxic, no studies have been conducted on the
effects of occupational exposure to arsenic and
ototoxicity.
Carbon Monoxide
Cases of accidental carbon monoxide poisoning
which caused severe neurologic, psychiatric
symptoms and hearing impairments that partially
improved with time were reported.< 110 -111 > A 78%
prevalence of sensori-neural hearing loss among
700 cases of carbon monoxide intoxication was
observed.< 112> Auditory brainstem responses were
studied in 32 patients with acute carbon monoxide
poisoning.< 113> The abnormalities observed were
divided into two patterns: a peripheral pattern of
prolongation of wave I latency without the
prolongation of interpeak latency (6 cases), and a
central pattern of prolongation of latencies for all
waves and interpeak latencies (2 cases). The
prevalence of ABR abnormalirx increased with the
duration of unconsciousness.< 13>
TLV Chronology: Noise
Table 2 provides a summary of the development
of the Noise TLVs (see page 13).
References
1. American National Standards Institute: Specification
for Audiometers. ANSI S3.6-1989. ANSI, New York
(1989).
2. American National Standards Institute: Specification
for Sound Level Meters. ANSI S1.4-1983. ANSI, New
York (1983).
3. American National Standards Institute: Specification
for Personal Noise Dosimeters. ANSI S1 .25-1991.
ANSI, New York (1991 ).
12-Noise
4. International Electrotechnical Commission:
Integrating-Averaging Sound Level Meters. IEC 804.
IEC, New York (1985).
5. U.S. Department of Defense: Noise Limits for Military
Materiel (Metric). MIL-STD-1474C. U.S. DOD,
Washington, DC (1991).
6. International Organization for Standardization:
Acoustic Determination of Noise Exposure and
Estimation of Noise Induced Hearing Impairment.
ISO-R-1999.2. ISO, Geneva (1990).
7. Jones H: Industrial Noise and Hearing Conservation,
Chap. II. Olishijski J; Harford E (Eds.). National
Safety Council, Chicago (1975).
8. U.S. National Institute for Occupational Safety and
Health: Criteria for a Recommended Standard:
Occupational Exposure to Noise. DHEW (HSM) Pub.
No. 73-11001. In: NIOSH Criteria Documents Plus
CD-ROM. DHHS (NIOSH) Pub. No. 97-106; NTIS
Pub. No. PB-502-082. National Technical Information
Service, Springfield, VA (1997).
9. Ad Hoc lntersociety Guidelines for Noise Exposure
Control: Am Ind Hyg Assoc J 28(5):418-424 (1967).
10. Botsford JH: Simple method for identifying
acceptable noise exposures. J Acoust Soc Am
46:418 (1967).
11. Passchier-Vermeer W: Hearing loss due to exposure
to steady-state broadband noise. Report No. 35.
Research Institute for Public Health Engineering,
Delft, Netherlands (1968).
12. Cohen A; Amticaglia JR; Carpenter P: Temporary
threshold shift in hearing from exposure to different
noise spectra at equal dBA level. J Acoust Soc Am
51 :503 (1972).
13. American Academy of Ophthalmology and
Otolaryngology: Guides for evaluation of hearing
handicap. Otolaryngol Head Neck Surg 87:539-551
(July-August 1979).
14. American Academy of Ophthalmology and
Otolaryngology: Guides for the evaluation of hearing
impairment. Trans Am Acad Ophthalm Otolaryngol
63:236-238 (1959).
15. American Academy of Ophthalmology and
Otolaryngology: Guides for the evaluation of hearing
impairment: ear, noise, throat and related structures.
JAMA 177(7):489--501 (1961 ).
16. Suter AH: Speech recognition in noise by individuals
with mild hearing impairment. J Acoust Soc Am
78:887-900 (1985).
17. American Standards Association: The relations of
hearing loss to noise exposure. Z24-X-2 Committee
Report. ASA, New York (1978).
18. Committee on Hearing and Bio-Acoustics: Some
damage risk criteria for exposure to sound. Draft of
Technical Report. CHABA Working Group, St. Louis,
MO (1956).
19. Eldred KM; Gannon WJ; van Gierke HE: Criteria for
short time exposure of personnel to high intensity jet
aircraft noise. WADC Technical Note 55-355. Wright-
Patterson AFB, OH (1955).
20. Air Force Medical Services: Hazardous noise
exposure. FR 160-3. U.S. Dept. of the Air Force,
Washington, DC (1956).
21. International Organization for Standardization: Noise
rating numbers with respect to conservation of
hearing, speech communication and annoyance.
ISO/TC 43. ISO, Helsinki (1961 ).
22. Kryter KD: Exposure to steady-state noise and
ACGIH® © 2006
TABLE 2. History of the Noise TLVs
1968: Proposed CONTINUOUS
ƒ 85 dB average for 500, 1000, and 2000 Hz octave bands; narrow band correction; 92 dBA, 8-
hour TWA
IMPULSE
ƒ140 dB ceiling
1969: Adopted CONTINUOUS
ƒ 90 dBA, 8-hour TWA
ƒ 115 dB ceiling
ƒ 5 dB doubling rate
IMPULSE
_________________________ƒ140 dB ceiling --------------------------------------------------------------------------------------
1970: Adopted CONTINUOUS
_________________________ƒ
Continuous, 90 dBA, measurement threshold ------------------------------------------------------
1973: Proposed CONTINUOUS
_________________________ƒ85 dBA, 8-hour TWA; 5 dB doubling rate; measurement threshold 80 dBN16 hours ____________ _
1975: Adopted CONTINUOUS
ƒ85 dBA, 8-hour TWA
ƒ115 dB ceiling
ƒ5 dB doubling rate
ƒ80 dBA measurement threshold
Proposed IMPULSE
ƒ140 dB, ceiling; 3 dB doubling rate; 120 dB measurement threshold; 10,000 impulses at 120
___________________________ dB, 1000 at 130 dB, and 100 at 140 dB ----------------------------------------------------------
1976: Adopted IMPULSE
ƒ140 dB, ceiling
ƒ
3 dB doubling rate
ƒ120 dB measurement threshold
______ƒ10,000 impulses at 120 dB, 1000 at 130 dB, and 100 at 140 dB------------------------------------
1993: Proposed CONTINUOUS and IMPULSE
__________________________
ƒ85 dBA, 8-hour TWA; 140 dBC ceiling; 3 dB doubling rate; 80 dBA measurement threshold ___ _
1994: Adopted CONTINUOUS and IMPULSE
ƒ85 dBA, 8-hour TWA
ƒ140 dBC ceiling
3 dB doubling rate
ƒ
ƒ80 dBA measurement threshold
-------------------------------------------------------------------------------------------------------------------------------
1999: Proposed CONTINUOUS and IMPULSE
Note on fetal hazard*, 115 dBC 8-hour TWA, 155 dBC ceiling, 3 dB doubling rate, 80 dBC
measurement threshold
-------------------------------------------------------------------------------------------------------------------------------
2000: Adopted CONTINUOUS and IMPULSE
Note on fetal hazard
-------------------------------------------------------------------------------------------------------------------------------
2000: Proposed CONTINUOUS and IMPULSE
Note on extended exposures to
ƒ Allow TWA averaging over 7 days if any daily TWA < 90 dB
_________________________ƒ
Recommended rest and sleep time at< dBA. ______________________________________________________ _
2001: Adopted CONTINUOUS and IMPULSE
______________________ Note on continuous exposure -------------------------------------------------------------------------
2002: Proposed CONTINUOUS and IMPULSE
Revision to Note 2.
-------------------------------------------------------------------------------------------------------------
2006 Adopted CONTINUOUS and IMPULSE
Revision to Note 2.
* Measured at the pregnant worker's abdomen.

impairment of Hearing: J. Acoust. Soc. Am and hearing loss. AMRL-TR-73-53. Aerospace

35(10):1515-1525 (1963).
23. American Academy of Ophthalmology and
Otolaryngology: Guide for conservation of hearing on
noise (Revised). MOO, Rochester, MN (1964).
24. Baughn WL: Relation between daily noise exposure
Medical Research Lab., Wright-Patterson AFB, OH
(June 1973).
25. Burns W; Robinson DW: Hearing and Noise in
Industry. Health and Safety Executive. Her Majesty's
Stationery Office, London (1970).

ACGIH® © 2006 Noise-13

26. International Organization for Standardization:
Acoustics-Assessment of Occupational Noise
Exposure for Hearing Conservation Purposes. ISO-
R-1999. ISO, Geneva (1971).
27. U.S. Environmental Protection Agency: Information
on levels of environmental noise requisite to protect
public health and welfare with an adequate margin of
safety. EPA 550-9-74-004. U.S. EPA, Washington,
DC (1974).
28. Johnson DL: Prediction of NIPTS due to continuous
noise exposure. EPA-550/9-73-001-8; AMRL-TR-73-
91 (AD-676205). U.S. Environmental Protection
Agency, Washington, DC; Wright-Patterson Air Force
Base, OH (1973).
29. Passchier-Vermeer W: Hearing loss due to exposure
to steady-state broadband noise. Report No. 36.
Research Institute for Public Health Engineering,
Delft, Netherlands (1968).
30. Yerg RA; Sataloff J; Glorig A; Menduke H: Inter-
Industry noise study. J Occup Med 20(5):351-358
(1978).
31. Schori TR; Johnson,DL: Inter-industry noise study:
another look. J Sound Vibrat, pp. 16-21 (January
1979).
32. Berger EH; Royster DH; Thomas WG: Presumed
noise-induced permanent threshold shift resulting
from an exposure to an A-weighted Leq. of 89 dB. J
Acoust Soc Am 64(1):192-197 (1978).
33. Clark WW; Popelka GR: Hearing levels of railroad
trainman. Laryngoscope 99(11):1151-1157 (1989).
34. Bies DA; Hanson CH: An alternative mathematical
description of the relationship between noise and
hearing loss. J Acoust Soc Am 88(6):2743-2754
(1990).
35. von Gierke HE; Robinson D; Karmy SJ: Results of
the workshop on impulse noise and auditory hazard.
Institute of Sound and Vibration Research,
Southampton, UK, ISVR Memorandum 618; October
1981. J Sound Vibrat 83:579--584 (1982).
36. Suter AH: The relationship of the exchange rate to
noise-induced hearing loss. Contractor report to
NIOSH. NTIS Pub. No. PB-93-118-610. National
Technical Information Service, Springfield, VA
(September 1992).
37. Ward WD: Noise-induced hearing loss: research
since 1973. In: Proceedings of the Third International
Congress on Noise as a Public Health Problem.
Tobias JV:; Jansen G; Ward WD (Eds.). ASHA
Reports 10. American Speech-Language Hearing
Association, Rockville, MD (1980).
38. Ward WD: Temporary threshold shift and damage
risk criteria for intermittent noise exposures. J Acoust
Soc Am 48:561-574 (1970).
39. Ward WD; Turner CW: The total energy concept as a
unifying approach to the prediction of noise trauma
and its application to exposure criteria. In: New
Perspectives on Noise-Induced Hearing Loss.
Hamernik RP; Henderson D; Salvi R (Eds.). Raven
Press, New York (1982).
40. Ward WD; Turner CW; Fabry DA: lntermittence and
the total energy hypothesis. Presented at the 104th
Meeting of the Acoustical Society of America (1982).
41. Clark WW; Bohne BA: Animal model for the 14 kHz
tonal dip. Ann Otol Rhinol Laryngol 87(Suppl 51 ):1-
16 (1978).
42. Clark WW; Bohne BA: Cochlear damage: audiometric
correlates? In: Sensorineural Hearing Loss:
14-Noise
Mechanisms, Diagnosis and Treatment. Collins MJ;
Glattke T; Harker LA (Eds.). University Iowa Press,
Iowa City (1986).
43. Ward WD; Nelson DA: On the equal energy
hypothesis relative to damage-risk criteria in the
chinchilla. In: Occupational Hearing Loss. Robinson
DW (Ed.). Academic Press, London; New York
(1971 ).
44. Bohne BA; Pearse MS: Cochlear damage from daily
exposure to low-frequency noise. Unpublished
manuscript. Washington University Medical School,
Dept. Otolaryngology, St. Louis, MO (1982).
45. Bohne BA; Zaht SJ; Bozzay DG: Damage to the
cochlea following interrupted exposure to low
frequency noise. Ann Otol Rhinol Laryngol 94:122-
128 (1985).
46. Bohne BA; Yohman L; Gruner MM: Cochlear damage
following interrupted exposure to high-frequency
noise. Hear Res 29:251-264 (1985).
47. Clark WW; Bohne BA; Boettcher FA: Effect of
periodic rest on hearing loss and cochlear damage
following exposure to noise. J Acoust Soc Am
82:1253-1264 (1987).
48. Passchier-Vermeer W: Steady-state and fluctuating
noise: its effect on the hearing of people. In:
Occupational Hearing Loss. Robinson DW (Ed.).
Academic Press. London; New York (1971 ).
49. Passchier-Vermeer W: Noise-induced hearing loss
from exposure to intermittent and varying noise. In:
Proceedings of the International Congress on Noise
as a Public Health Problem. EPA Report 550/9-73-
008. U.S. Environmental Protection Agency,
Washington, DC (1973).
50. Shaw EAG: Occupational noise exposure and noise-
induced hearing loss: scientific issues, technical
arguments and practical recommendations. APS 707.
Report prepared for the Special Advisory Committee
on the Ontario Noise Regulation. NRCC/CNRC No.
25051. National Research Council, Ottawa, Canada
(1985).
51. Kryter KD; Daniels R; Fair P; et al.: Hazardous
exposure to intermittent and steady-state noise.
Report of Working Group 46. National Academy of
Science National Research Council Committee on
Hearing, Bioacoustics, and Biomechanics (CHABA).
ONR Contract NONR 2300(05). NAS, Washington,
DC (1965).
52. Schori TR: Evaluation of exposure guidelines for
moderate and high intensity continuous noise.
Technical Report AMRL-TR-76-97. Aerospace
Medical Research Laboratory, Wright-Patterson AFB,
OH (1976).
53. Johnson DL; Schori TR: How safe is 115 dBA for 15
minutes? In: Proc. 93rd Meeting of the Acoustical
Society of America. J Acoust Soc Am 61 (Suppl 1)
(Spring 1977).
54. Melnick W: Human temporary threshold shift (TTS)
and damage risk. J Acoust Soc Am 90:147-154
(1991).
55. Stephenson MR; Nixon CW; Johnson DL:
Identification of minimum level of noise capable of
producing an asymptotic temporary threshold shift.
Aviat. Space Environ. Med. 51(4):391-396 (1980).
56. National Research Council, Committee on Hearing
Bioacoustics and Biomechanics: Proposed damage-
risk criterion for impulse noise (gunfire). Report of
Working Group 57, W. Dixon Ward, Chairman. U.S.
ACGIH® © 2006
 Dept. of the Navy, Office of Naval Research,
Washington, DC (1968).
57. Hamernik RP; Henderson D; Crossley JJ; Salvi R:
Interaction of continuous and impulse noise:
audiometric and histological effects. J Acoust Soc
Am55:117-121 (1974).
58. Hamernik RP; Henderson D; Salvi R: Potential for
interaction of low-level impulse and continuous noise.
Technical Report AFAMRL TR-80-68. Aerospace
Medical Research Laboratory, Wright-Patterson AFB,
OH (1980).
59. American National Standards Institute: Draft ANSI
S3.28-1986 (ASA 66). ANSI, New York (1986).
60. Ward WD; Selters W; Glorig A: Exploratory studies
on temporary threshold shift from impulses. J Acoust
Soc Am 33:781-793 (1961).
61. Price GR: Implications of a critical level in the ear for
assessment of noise hazard at high intensities. J
Acoust Soc Am 69:171-177 (1981 ).
62. National Research Council, Committee on Hearing
and Bio-Acoustics: Hazardous Exposure to Impulse
Noise. National Academy Press, Washington, DC
(1992).
63. von Gierke HE; Parker DE: lnfrasound. In: Handbook
of Sensory Physiology, Vol. V: Auditory System.
Springer-Verlag, New York (1976).
64. Johnson DL: Auditory and Physiological Effects of
lnfrasound. Technical Report AMRL-TR-75-33.
Aerospace Medical Research Laboratory, Wright-
Patterson AFB, OH (1975).
65. Johnson DL: Hearing hazards associated with
infrasound. In: New Perspectives on Noise Induced
Hearing Loss, pp. 407-421. Hamernik RP;
Henderson D; Salvi R (Eds.). Raven Press, New
York (1982).
66. National Research Council, Committee on Hearing,
Bioacoustics, and Biomechanics: Prenatal Effects of
Exposure to High-level Noise. Report of Working
Group 85. National Academy Press, Washington,
DC, 1982; also as a □TIC TR Document NAS3-82.
67. Pierson LL: Hazards of noise exposure on fetal
hearing. Semin Perinatol 20(1):21-29 (1996).
68. Lalande NM; Hetu R; Lambert J: Is occupational
noise exposure during pregnancy a high risk factor of
damage to the auditory system of the fetus? Am J
Ind Med 10:427-435 (1986).
69. Laciak J; Majcherska-Matuchniak B: Hearing in
children whose mothers are working in noise. In:
Pamietnik XXVII Zjasdu Otolaryngologow Polskick w
Katowicach, pp. 155--158. Meleck J; Baradin T
(Eds.). Warsaw, Poland (1968).
70. Daniel T; Laciak J: Observations Cliniques et
experiences concernant l'etat de l'appareil
cochleovestibulaire des sujets exposes au bruit
durant la vie fretale [Clinical observations and
experiments concerning the condition of the
cochleovestibular apparatus of subjects exposed to
noise in fetal life]. Rev Laryngol Otol Rhinol (Bord)
103(4):313-318 (in French) (1982).
71. Niemtzow RC: Loud noise and pregnancy. Mil Med
158:10-12 (1993).
72. Dunn DE; Lim DJ; Ferraro JA; et al.: Effects on the
auditory system from in utero noise exposure in
lambs. Abstracts of the Fourth Midwinter Research
Meeting of the Association for Research in
Otolaryngology. ARO, Mt. Royal, NJ (1981).
73. Griffiths SK; Pierson LL; Gerhardt KJ; et al.: Noise-
ACGIH® © 2006
induced hearing loss in fetal sheep. Hear Res
74:221-230 (1994).
74. Pierson LL; Gerhardt KJ; Griffiths SK; et al.: Effects
of exposure to intense sound on fetal sheep in utero.
Abstracts of the 18th Midwinter Research Meeting of
the Association for Research in Otolaryngology.
ARO, Mt. Royal, NJ (1995).
75. American National Standards Institute: Determination
of occupational noise exposure and estimation of
noise-induced hearing impairment. ANSI
S3.44(1996). ANSI, New York (1996).
76. Gerhardt KJ; Otto R; Abrams RM; et al.: Cochlear
microphonics recorded from fetal and newborn
sheep. Am J Otolaryngol 13(4):226-233 (1992).
77. Johnson DL; Nixon CW: Simplified methods for
estimating hearing protector performance. Sound
Vibrat 8(6):20-27 (1974).
78. Gerhardt BK; Huang X; Griffiths SK; Abrams RM:
Effects of impulse noise on the hearing of fetal sheep
in utero. In: Proceedings of the 16th International
Congress on Acoustics and the 135th meeting of the
Acoustical Society of America, Seattle, WA, 20-26
June 1998, pp. 2641-2642. ASA, New York (1998).
79. Stephenson MR; Nixon CW; Johnson DL:
Identification of the minimum noise level capable of
producing an asymptotic temporary threshold shift.
Aviat Space Environ Med 51(4):391-6 (1980).
80. Ward WD: Transient Changes in Hearing. In:
Proceed. Congresso lntemasionale: Man and
Hearing. Torino, Italy, June 7-10, 1975, pp. 391-
396. Rossi G; Vigone M (Eds.).
81. Szulc-Kuberska J; Tronczynska J; Latkowski B:
Otoneurological investigations of chronic
trichloroethylene ppoisonmg. Minerva Otorinolaryngol
108-112 (1976).
82. U.S. Agency for Toxic Substances and Disease
Registry: Trichloroethylene (TCE) Subregistry-
Baseline Technical Report. ATSDR, Atlanta, GA
(1993).
83. Sulkowski WJ: Badania nad prxydatnoscia kliniczna
audiometrii I elektronystagmografii w diagnostyce
przewleklych zatruc dwusiarczkiem wegla. Med
Pracy 135--145 (1979).
84. Morata TC: Study of the effects of simultaneous
exposure to noise and carbon disulfide on worker's
hearing. Scand Audiol 19:53--58 (1989).
85. Hirata M; Ogawa Y; Okayama A; et al.: A Cross-
sectional study on the brainstem auditory evoked
potential among workers exposed to carbon disulfide.
Int Arch Occup Environ Health 64(5):321-324 (1992).
86. Muijser H; Hoogendijk EMG; Hooiisma J: The Effects
of Occupational Exposure to Styrene on High
Frequency Thresholds. Toxicology 49:331-340
(1988).
87. Moller C; Odkvist LM; Larsby B; et al.:
Otoneurological findings in workers exposed to
styrene. Scand J Work Environ Health 16:189--194
(1990).
88. Sass-Kortsak AM; Corey PN; Robertson JMcD: An
investigation of the association between exposure to
styrene and hearing loss. Ann Epidemiol 5(1):15--24
(1995).
89. Morata TC; Nylen P; Johnson AC; Dunn DF: Auditory
and vestibular functions after single or combined
exposure to toluene: a review. Arch Toxicol. 69:431-
443 (1995).
90. Biscaldi GP: Mingardi M; Pollini G: et al.: Acute
Noise-15
 toluene poisoning. Electroneurophysiological and
vestibular investigations. Toxicol Eur Res 1981
3(6):271-273 (1981).
91. Morata,TC; Dunn DE; Kretschmer LK; et al.:
Occupational exposure to organic solvents and
noise: effects on hearing. Scand J Work Environ
Health 19:245--254 (1993).
92. Abbate C; Giorgianni C; Munao F; et al.:
Neurotoxicity induced by exposure to toluene. an
electrophysiologic study. Int Arch Occup Environ
Health 64:389-392 (1993).
93. Morata TC; Fiorini AC; Fischer FM; Colacioppo S;
Wallingford KM; Krieg EF; Dunn DE; Gozzoli L;
Padrao MA; Cesar CL: Toluene-induced hearing loss
among rotogravure printing workers. Scand J Work
Environ Health 23(4 ):289--298 (1997).
94. American Conference of Governmental Industrial
Hygienists: Threshold Limit Values and Biological
Exposure Indices for 1995-1996. ACGIH, Cincinnati,
OH (1995).
95. Lauwerys RR; Hoet P: Industrial Chemical Exposure.
Guidelines for Biological Monitoring, 2nd ed. Lewis
Publishers, Boca Raton, FL (1993).
96. Chang MJW; Hsu KH; Chen YC; et al.: Biological
monitoring of urinary hippuric acid in a taiwanese
semiconductor company. In: International
Symposium on Biological Monitoring in Occupational
and Environmental Health. Espoo, Finland, Sept 11-
3, 1996, pp. 94-95 (1996).
97. U.S. National Institute for Occupational Safety and
Health: NIOSH Manual of Analytical Methods, 4th ed.
P.M. Eller, Ed. DHHS (NIOSH) Pub. No. 94-113.
NIOSH, Cincinnati, OH (1994).
98. Otto D; Robinson G; Bauman S; et al.: Five-year
follow-up study of children with low-to-moderate lead
absorption: electrophysiological evaluation. Environ
Res 38:168--186 (1985).
99. Schwartz J; Otto D: Blood lead, hearing thresholds,
and neurobehavioral development in children and
youth. Arch Environ Health 42:153-160 (1987).
100. Discalzi GL; Capellaro L; Bottalo D; et al.: Auditory
brainstem evoked potentials (baeps) in lead-exposed
workers. Neurotoxicol. 13:207-21 O (1992).
101. Discalzi GL; Fabbro D; Meliga F; et al.: Effects of
occupational exposure to mercury and lead on
16-Noise
brainstem auditory evoked potentials. Int J
Psychophysiol 14:21-25 (1993).
102. Araki A; Murata K; Yokohama K; et al.: Auditory
event-related potential (p300) in relation to peripheral
nerve conduction in workers exposed to lead, zinc,
and copper: effects of lead on cognitive function and
central nervous system. Am J Ind Med 21 :539--547
(1992).
103. Kurland LT; Faro SN; Siedler H: Minimata disease:
the outbreak of a neurologic disorder in Minimata,
Japan, and its relationship to the ingestion of seafood
contaminated by mercury compounds. World Neural
1:370-395 (1960).
104. Gerstner HB; Huff JE: Clinical toxicology of mercury.
J Toxicol Environ Health 2:491-526 (1977).
105. Mizukoshi K; Nagaba M; Ohno Y: Neurotological
studies upon intoxication by inorganic mercury
compounds. ORL J Otorhinolaryngol Relat Spec
37:74-87 (1975).
106. Mizukoshi K; Watanabe Y; Kobayashi H; et al.:
neurotological follow-up studies upon minimata
disease. Acta Otolaryngol (Stock.) Suppl 468:353-
357 (1989).
107. Nikolov Z: Hearing reduction caused by manganese
and noise. JFR OtoRhino Laryngol Audiophonol Chir.
Maxillofac 23:231-234 (1974).
108. Beneke V; Symon K; Chladek V; Pihrt J: Health
aspects of nurning coal with a high arsenic content.
II. hearing changes in exposed children. Environ Res
13:386-395 (1977).
109. Beneke V; Symon K: Test of environmental exposure
to arsenic and hearing changes in exposed children.
Environ Health Perspect 19:95--101 (1977).
110. Garland H; Pearce J: Neurological complications of
carbon monoxide poisoning. Q J Med 36:445-455
(1967).
111. Morris TMO: Deafness following carbon monoxide
poisoning. J Laryngol Otol 83:1219-1225 (1969).
112. Lumio JS: Clinical findings following chronic carbon
monoxide exposure. Acta Otolaryngol Suppl 71 :1-
112 (1948).
113. Choi IS: Brainstem auditory evoked potentials in
acute carbon monoxide poisoning. Yonsei Med J
26:29--34 (1985).
ACGIH® © 2006