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Acoustic trauma from continuous noise: Minimum exposures, issues in

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Acoustic trauma from continuous noise: Minimum exposures,
issues in clinical trial design, and comments on magnetic
resonance imaging exposures
Elliott H. Bergera)
Berger Acoustical Consulting, 221 Olde Mill Cove, Indianapolis, Indiana 46260, USA
Robert A. Dobieb)
University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, Texas 78229,
USA

(Received 11 April 2019; revised 3 August 2019; accepted 8 August 2019; published online 27
November 2019)
Acoustic trauma (AT) is permanent hearing loss after a single noise exposure. A few human cases
resulting from continuous, i.e., nonimpulsive noise, have been reported as reviewed by Ward
[(1991). “Hearing loss from noise and music,” presented at Audio Engineering Society, New York,
October 4–8]. This paper updates that review by examining 11 cases in nine reports, from 1950 to
2006, with the intention of determining minimum exposures that may cause AT, including the
potential risk of exposure to noise from magnetic resonance imaging machines. Diffuse-field
related levels above 120 dBA for 10 s or more, or above 130 dBA for 2–3 s (values well above
OSHA’s unprotected exposure limits), can lead to AT. These cases appear to represent a susceptible
fraction of the population, because much more intense exposures (e.g., 130 dBA for 32 min) have
been tolerated by groups of volunteers who suffered only temporary threshold shifts. AT from con-
tinuous noise is unlikely to occur in OSHA-compliant hearing conservation programs, and probably
rare enough in the general civilian population that clinical trials of drugs aimed at treating it are
unlikely to be practical. AT from impulse noise, such as gunfire, which is specifically not the topic
of the current work, is more amenable to clinical trials, especially in military settings.
C 2019 Acoustical Society of America. https://doi.org/10.1121/1.5132712
V

[CGL] Pages: 3873–3878

I. INTRODUCTION (Govindaraju, 2011; McJury and Shellock, 2000; Price et al.,

Human noise-induced hearing loss (NIHL) usually devel-
ops over years of repeated exposure, several hours per day, to
average noise levels greater than 85 dBA. In contrast, single
brief exposures at much higher levels can also cause permanent
hearing loss; this is called acoustic trauma (AT). In the middle
of the last century the term “acoustic trauma” was often applied
to any hearing loss caused by noise, whether temporary or per-
manent, acute or chronic, but since about 1970 professional
consensus has defined AT as “a sudden [permanent] change in
hearing as a result of a single exposure to … sound” (Robinson
1971; Kirchner et al., 2012). Unfortunately, some contempo-
rary authors continue to treat the terms NIHL and AT as syno-
nyms (Sakat et al., 2016). This tendency may in part arise from
the fact that most “NIHL” research in animals actually deals
with AT, defined as permanent loss from a single exposure.
Our current interest in AT arose from conversations
between E.H.B. and R.A.D. regarding the potential hearing
hazard resulting from patient exposures to single magnetic
resonance imaging (MRI) procedures. Various authors have
measured MRI noise levels and found them to exceed
110 dB sound pressure level with exposure times lasting
from tens of minutes up to approximately an hour
a)
Electronic mail: eberger@compuserve.com
b)
Deceased.
2001; Ravicz et al., 2000). In one recent study, exposure lev-
els, duration, and thresholds were measured for 26 healthy
young adults wearing earplugs during testing. A small statis-
tically significant shift of 5 dB (measured via automated
ABR testing) was observed immediately after exposures but
disappeared when tested 25 days thereafter (Jin et al., 2018).
In an editorial in the same issue as the Jin et al. (2018),
study, Salvi and Sheppard (2018) observed that “the absence
of permanent hearing from the intense 1-h examination
should ease concerns in the radiological community about
the risk of MR-induced hearing loss, provided patients are
provided with adequate hearing protection during the exam-
ination.” Since data of this type are scarce, we decided to
further explore the literature and determine what could be
learned more broadly about AT from single exposures.
AT may occur after either impulse noise such as gunfire
(Segal et al., 1988) or brief continuous noise (Kung and
Sataloff, 2006). Ward (1991) described five previously pub-
lished cases of AT after exposure to continuous noise, (dura-
tion >1 s). As expected, shorter durations were required at
higher levels, and longer durations at lower levels. The graph
from Ward’s original paper, including a humorous note to
the second author, is reproduced as Fig. 1.1 For example,
one case from a series of experiments designed to cause only
a temporary threshold shift (TTS; Davis et al., 1950) showed
AT after an exposure of 120 dB for 8 min, while an exposure

J. Acoust. Soc. Am. 146 (5), November 2019 0001-4966/2019/146(5)/3873/6/$30.00 C 2019 Acoustical Society of America
V 3873

FIG. 1. Reproduction of Fig. 1 from Ward (1991), showing his four safe
exposures (encircled points) and his five unsafe exposures, together with a
dashed line representing all exposures equal in energy to 1 min of 135 dB,
and a dotted line connecting “the four weakest individual exposures that
produced permanent loss in a small but otherwise unknown fraction of those
exposed. Presumably any exposure above and to the right of this line can be
considered hazardous to the most susceptible ears.” Note that Ward’s time
axis extends beyond the range covered in Figs. 2–4, specifically starting at
less than 1 s to include the SN data point (simulated automotive airbag expo-
sure) which was excluded from the current analysis since its duration was
only 0.4 s.
at 137 dB from a cordless telephone required only 2 s of expo-
sure to cause AT (Orchik et al., 1987). The goal of this paper
is to review cases of human AT from continuous noise, updat-
ing Ward’s (1991) report by adding in more recent case
reports, to estimate the levels and durations that can cause AT
in susceptible people. Implications of these data for clinical
trials of interventions aimed at treating AT are discussed.
II. METHODS
The literature search began with papers cited by Ward
(1991) and over 10 000 papers in the authors’ files (over
6000 for E.H.B., over 10 000 for R.A.D., undoubtedly
including duplicates). The reference lists of relevant papers
that we identified as “interesting” were also searched. A
PubMed search in January 2019 used the following terms:
“acoustic trauma” OR (hearing loss AND (noise OR
music) AND (sudden OR acute)).
This search yielded 577 hits, only 11 of which seemed likely
to be relevant based on title and abstract. The Defense
Technical Information Center database was also searched,
and email queries were sent to 47 colleagues who were
known to be interested in NIHL and hearing conservation
(most are published authors in these fields).
Potentially relevant papers were reviewed by both
authors; nine papers were considered informative because
they provided data on exposures (level and duration) and
audiometric outcomes (pure-tone threshold shifts of at least
10 dB, at least 1 week post-exposure, compared with pre-
exposure audiograms, or in cases of unilateral exposure com-
parisons to the thresholds of the contralateral ear). Three of
the nine papers were cited by Ward (1991), four were in the
authors’ files, and the PubMed search yielded two more.
3874 J. Acoust. Soc. Am. 146 (5), November 2019
Prior to the 1980s, human TTS studies often used expo-
sures that were much more intense than exposures leading to
AT in case reports. In these studies groups of subjects sus-
tained only TTS, highlighting the variation in susceptibility to
AT. Selected TTS studies from both the reference list of
Ward (1991) and our own files were reviewed to illustrate
this phenomenon; no formal search was done for TTS studies.
In recent years, a new term, “acoustic shock,” has entered
the medical literature. A PubMed search in April 2019 yielded
only ten relevant references, generally defining this term as a
syndrome of persistent otalgia, hyperacusis, tinnitus, and/or
vestibular problems. This syndrome was reported primarily in
clusters of call center workers in Australia, New Zealand, the
United Kingdom, and Denmark who had experienced unex-
pected loud sounds. The syndrome is considered by many
authors to be primarily psychogenic (Hooper, 2014). We did
not address this condition, limiting our review to cases report-
ing measurable hearing loss after single noise exposures.
Because the case reports expressed sound levels in dif-
ferent ways [diffuse-field levels, dB hearing level (HL), cou-
pler levels, and manikin levels], all noise exposures were
converted to diffuse-field related levels (dBA) to make them
comparable to levels measured in occupational hearing con-
servation programs (HCPs) that represent the classical stud-
ies upon which accepted damage-risk criteria are based.
These conversions relied on ISO 11904-2 (2004) and on
tables provided by Bentler and Pavlovic (1989, 1992);
detailed computations are available on request. For AT cases
arising from acoustic reflex testing, it was sometimes unclear
which of the test tones (500, 1000, 2000, or 4000 Hz) had
caused the hearing loss; the assumption was made that the
tone with the highest A-weighted sound level had been
responsible.
III. RESULTS
Several TTS studies (i.e., no resultant AT) with very
intense exposures and the 11 informative cases of AT (three
of the data points are from a single study) are summarized in
Table I and Fig. 2. Three columns in Table I show sound lev-
els in different ways: L refers to levels as recorded in the
underlying papers, LDF refers to levels that have been cor-
rected to estimate diffuse-field levels, and LDF,A refers to
levels that have been corrected to estimate A-weighted dif-
fuse-field levels. In addition, 8-h equivalent exposures are
shown for diffuse-field levels, both LDF,eq8h and LDF,Aeq8h.
TTS-only studies included between 10 and 40 subjects
(89 in total), with the exception of Raleigh et al. (1963),
which was a report of two workers trapped without hearing
protection for 2 hours in a workplace where a steam line had
ruptured. In that report, a diffuse-field level of 136 dBA
caused no AT.
AT cases were documented after exposures such as a
diffuse-field related level of 121 dBA for 8 min (Davis et al.,
1950), and 123 dBA for 10 s (Arriaga and Luxford, 1993),
which were less intense than those tolerated by subject
groups in TTS studies. An apparent outlier was the report of
Elonka (1986) with a diffuse-field related level of 111 dBA
for 10 s; this was a Letter to the Editor showing only
Elliott H. Berger and Robert A. Dobie
TABLE I. TTS and AT cases and associated exposures. The L (dB) values are as reported in the papers cited; the diffuse-field values (LDF and LA,DF) are cor-
rected as discussed in text. The exposure durations (dur) are specified in seconds (s). In the frequency column “various” indicates that in different experiments
there were different tones or noise bands that were utilized, and “range” indicates the sound was a relatively broadband of noise. The first three rows of TTS
data and the first five rows of AT data were included in Ward (1991). All of the reflex text cases were on subjects that had prior significant sensorineural hear-
ing loss.

Freq L LDF LA,DF dur LDF,eq8h LDF,Aeq8h

Author Year Event Source Sound Type (Hz) (dB) (dB) (dBA) (s) (dBL) (dBA)

TTS Cases
Davis et al., point HD 1950 experiment speaker tones & noise various 130 130 130 1920 118 118
Eldred et al., point E 1955 experiment speaker jet noise range 135 135 135 60 108 108
Raleigh et al. 1963 accident steam line steam line rupt. range 138 138 136 7200 132 130
Schori 1976 experiment TDH-39 pink noise range 130 124 123 10 89 88
Brownsey 1973 experiment speaker pink noise range 129 127 127 30 97 97

AT Cases
Davis et al., subj WM 1950 experiment speaker tone 2000 130 130 131 60 103 104
Davis et al., subj S 1950 experiment speaker tone 4000 120 120 121 480 102 103
Davis et al., subj HD 1950 experiment speaker tone 500 140 140 137 1800 128 125
Lenarz and Gulzow 1983 reflex test audiometer tone 500 125 HL 135 132 10 100 97
Orchik et al. 1987 accident phone ring tone 750 137 135 134 2 93 92
Arriaga and Luxford 1993 reflex test audiometer tone 2000 120 HL 122 123 10 87 89
Elonka 1986 reflex test audiometer tone unstated 105 HL 111 111 10 76 76
Hunter et al. 1999 reflex test audiometer tone 1000 120 HL 126 126 20 94 94
Kung and Sataloff 2006 accident siren wail 1000 140 140 140 2 98 98
McMillan and Kileny 1994 accident bike horn bike horn 1500 143 143 144 5 105 106
Singleton et al. 1984 accident phone ring tone 750–1000 137 135 134 2.5 94 93

borderline threshold shifts 1 week after exposure (5–15 dB,
depending on which pre-exposure test was compared to the
post-exposure test) and lacking details such as the frequencies
of the test tones that were used to elicit acoustic reflexes.
Figure 2 also includes the U.S. Occupational Safety and
Health Administration (OSHA) and U. S. National Institute
for Occupational Safety and Health (NIOSH) limits.
OSHA’s unprotected permissible exposure limit is for daily
career-long immersion in noise, and specifies no exposure
exceeding 1 s for levels above 115 dBA, with a 5-dB
exchange rate for exposures between 90 and 115 dBA.
NIOSH’s recommended exposure limit is a 3-dB exchange
rate between 85 and 140 dBA. Although the OSHA and
NIOSH curves are quite different, all exposures resulting in
AT exceeded these criteria, with the exception of the outlier
previously mentioned (Elonka, 1986).
Figure 3 presents the same data as Fig. 2, with the labels
for the data points removed for simplification, but with the
addition of a curve that can be drawn from the data we
assembled, to indicate tentative levels and durations capable
of causing AT in the most susceptible persons as the result

FIG. 2. Single noise exposures leading to TTS in groups of normal subjects

(open circles) or leading to permanent threshold shift in individual cases
(AT; black diamonds) characterized by A-weighted diffuse-field related
sound level and duration. Gray dashed circular shapes group together similar
exposure types. See Table I for additional details. Exposures below the
short-dashed line are permissible without hearing protection according to
regulations of the U.S. OSHA. Exposures below the dashed line would be
permissible according to the recommendations of the U.S. NIOSH.
FIG. 3. Same individual data points and OSHA/NIOSH curves as in Fig. 2,
with the additional of a gray line labeled with double question marks that
provides tentative levels and durations capable of causing AT in the most
susceptible persons. The data point labeled with the single question mark is
the apparent outlier referred to in the text (Elonka, 1986).

J. Acoust. Soc. Am. 146 (5), November 2019 Elliott H. Berger and Robert A. Dobie 3875
of a single exposure. We emphasize the tentative nature of
this curve. It suggests that diffuse-field related levels above
120 dBA for periods of 10 s or more, or above 130 dBA for
periods of 2–3 s (values that are well above OSHA’s unpro-
tected exposure limits), can lead to AT. These cases appear
to represent a susceptible fraction of the population, because
much more intense exposures (e.g., 130 dBA for 32 min)
have been tolerated by groups of volunteers who suffered
only temporary threshold shifts.
One may note that our tentative curve is more restrictive
than Ward’s “safe” curve in Fig. 1. As an example, his curve
allows 135 dBA for 10 s whereas we suggest the limit for
10 s is only about 122 dBA. The differences in part are
because we corrected the original reported data points to
diffuse-field levels as noted in Sec. II, and also due to the
addition of new data showing risk at lower levels.
IV. DISCUSSION
Case reports are, by nature, anecdotal and represent the
lowest level of medical evidence, below stronger designs
such as clinical trials, cohort studies, and cross-sectional
studies. One case report (Kung and Sataloff, 2006) appeared
in a non-refereed publication and another (Elonka, 1986)
was a brief Letter to the Editor. However, it would be unethi-
cal to perform controlled experiments designed to cause AT
in humans; thus, case reports provide the only available evi-
dence for human AT from continuous noise that we were
able to uncover. Moreover, even in the absence of the ethical
issues, controlled clinical trials of the nature that might
reveal AT following short-duration exposures would of
necessity be limited to impulse noise from weapons (not
covered in this review) since those are the only types of
short-duration sounds that occur with some predictability or
regularity. Such trials would likely need to occur in military
populations, and a recent multi-center trial of tinnitus
retraining therapy (TRT), discusses the challenges of clinical
trials even for something as benign as TRT (Scherer et al.,
2018). Therefore, our review captured only cases of AT in
which clinicians chose to submit case reports; unreported
AT cases almost certainly outnumber those we reviewed.
In examining the nine papers that met our criteria, one
of them dating from 1950 and two-thirds having been con-
ducted over 25 yr ago, the authors noted a lack of precision
in many of these papers with respect to specification of the
actual transducers used, the acoustics of the test space (for
sound-field testing), the spectrum of the noise in the case of
non-pure tone sources, and even the actual tone in question
when more than one tone was used in the study. Thus, not
only did we need to adjust earphone values to diffuse-field
related sound levels, but also had to make judgment calls
about other factors such as those mentioned above.
Depending on the precision of the underlying reported
data, the accuracy of our estimated DF values varies.
Computed adjustments when all the transducers, the test sig-
nals, and the reported levels were sufficiently specified
would be expected to fall within the uncertainty of the stand-
ards we followed. In the case of computations following ISO
11904-2 (2004) the expanded uncertainty (95th percentile) is
3876 J. Acoust. Soc. Am. 146 (5), November 2019
2.2 dB. However, for those cases in which we had to use our
best judgment to understand the author’s intent, we suspect
that our uncertainties are at least twice that large, closer to
approximately 5 dB.
Because 89 healthy young human volunteers sustained
only TTS after exposures that were both more intense and
longer in duration than exposures reported to cause AT (indi-
vidual TTS studies had between 10 and 40 subjects), it is
reasonable to assume that AT cases represent more suscepti-
ble individuals. Patients suffering AT after acoustic reflex
testing had substantial pre-existing hearing loss (which is
why such high levels were required to elicit acoustic
reflexes); prior hearing loss due to factors besides noise
exposure could thus be a risk factor for AT.
Many subjects in the studies intended to elicit only TTS
sustained exceedingly large threshold shifts: up to 60 dB,
requiring more than 24 h to recover (Davis et al., 1950).
TTSs like these, even with no permanent threshold shift,
have been shown in animals to be associated with loss of
auditory nerve function (Kujawa and Liberman, 2009) and
cannot be confidently considered safe for humans.
All AT cases, with the exception of an outlier previously
mentioned, had exposures in excess of those permitted with-
out hearing protection by OSHA or recommended by
NIOSH. All cases involved either pure tones or narrowband
sounds, which are generally considered more hazardous on
an equal-energy basis than the broadband sounds that char-
acterize most occupational noise exposures [ISO 1999-2013
(2013)]. For these reasons clinical trials of NIHL in HCPs
would be unlikely to yield useful numbers of cases. Some
steady-state military exposures where even double hearing
protection can be inadequate (e.g., flight deck of aircraft car-
rier) might be exceptions to this rule.
As discussed in this review there are few published
reports of AT from non-occupational exposures to continu-
ous noise. Some studies document exposures that are now
far less prevalent: TTS research no longer permits large
threshold shifts that could cause permanent damage; contem-
porary cordless phones do not ring through the earpieces;
audiologists now may decline to test acoustic reflexes at
very high levels. While actual cases are probably more
numerous than well-documented case reports, they are
spread throughout the population at large. Clinical trials of
therapy for rare disorders like this typically require multiple
sites and long accrual periods, with accordant increase in
cost and threats to data quality. It is questionable, in the
opinion of E.H.B. and R.A.D., whether clinical trials for AT
from continuous noise could be practical.
Recent research (Campbell, 2019; Oishi and Schacht,
2011) has sought without notable success to find nutritional
or drug treatments for human NIHL and AT. An important
pitfall in NIHL clinical trials is that hearing protection devi-
ces (HPDs), such as earplugs and earmuffs, are readily avail-
able, ethically mandatory in clinical trials, and can markedly
reduce NIHL, thus necessitating large sample sizes to have a
chance to detect small changes in hearing. Another is that
NIHL develops slowly, requiring trials lasting years.
AT might seem a more attractive target for drug research,
because AT often results from unexpected exposures, with no
Elliott H. Berger and Robert A. Dobie
HPDs in place, and does not require long follow-up. But clini-
cal trials for AT have other inherent difficulties:
(1) Many people suffering AT will lack pre-exposure audio-
grams, making estimation of threshold shift difficult;
(2) unexpected exposures are often difficult to replicate and
measure;
(3) it would be unethical to subject human subjects to expo-
sures that are likely to cause AT. Thus, clinical trials are
typically limited to drug treatment given after AT (ani-
mal studies have shown that many interventions prior to
AT can reduce hearing loss, but few are effective after
AT, even when promptly delivered).
Impulse noise (e.g., gunfire from recreational or military
exposure) may be a more important cause of AT than contin-
uous noise, but was not considered in this review. Several
clinical trials been reported for AT from impulse noise, usu-
ally military in origin (e.g., Pilgramm and Schumann, 1985;
Kopke et al., 2015). AT trials in military settings have
accrued impressive numbers of subjects and appear feasible
for future research. It is often difficult in such trials to be
sure that the last exposure, after which the soldier reported
auditory symptoms, was really the cause of the threshold
shift; instead, the threshold shift may have developed over
days to weeks of training. Thus, results of such trials might
not be generalizable to cases of AT without prior exposure,
or to cases involving continuous noise.
In Fig. 4 we direct our attention toward the question that
was the genesis of this project, namely the hazardousness of
MRI exposures. The shaded box in the figure represents the
approximate levels and durations of MRI exposures reported
in the literature. It falls at or about the OSHA permissible
exposure limit, above the NIOSH recommended exposure
level, but less than our estimate of levels above which AT
has been shown to occur. However, the noises in the AT
cases we reviewed probably did not possess the high kurtosis
present in the type of noise characteristic of MRI machines
that appears to consist of a train of closely spaced pulses
(Ravicz et al., 2000); the literature suggests that highly
FIG. 4. The shaded box presents the approximate range of the LAeq values
reported in the MRI studies cited in this paper, as compared to the OSHA/
NIOSH curves from Fig. 2 and the tentative levels curve from Fig. 3.
J. Acoust. Soc. Am. 146 (5), November 2019
kurtotic noises are more hazardous than ones that are not
(Davis et al., 2012). Furthermore, the health of the subjects
in many of the studies we reviewed was not compromised in
ways that might be anticipated for those requiring an MRI.
The studies cited in Sec. I have reported TTSs following
MRIs. Although no permanent shifts were reported, most of
the authors recommended use of hearing protection. We too
recommend use of hearing protection and given the nature
of our findings summarized in Fig. 4, suggest that during
MRI scanning on patients wearing presumably well-fitted
hearing protection AT is unlikely to occur, but cannot be
ruled out.
ACKNOWLEDGMENTS
Portions of this work were presented at the annual
meeting of the National Hearing Conservation Association,
February 8, 2019, Grapevine, TX. Dr. Christian Giguère
consulted regarding methods of estimating diffuse-field
levels from HLs, coupler levels, and mannequin levels. Dr.
William Clark consulted regarding historical literature in the
fields of TTS and AT.
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3878 J. Acoust. Soc. Am. 146 (5), November 2019
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