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Temporary and Permanent Noise-induced Threshold Shifts: A Review of Basic and Clinical Observations

Ryan, Allen F.; Kujawa, Sharon G.; Hammill, Tanisha; Le Prell, Colleen; Kil, Jonathan

doi: 10.1097/MAO.0000000000001071

Objective: To review basic and clinical findings relevant to defining temporary (TTS) and permanent (PTS) threshold shifts and their sequelae.

Data Sources: Relevant scientific literature and government definitions were broadly reviewed.

Data Synthesis: The definitions and characteristics of TTS and PTS were assessed and recent advances that expand our knowledge of the extent, nature, and consequences of noise-induced hearing loss were reviewed.

Conclusion: Exposure to intense sound can produce TTS, acute changes in hearing sensitivity that recover over time, or PTS, a loss that does not recover to preexposure levels. In general, a threshold shift ≥10 dB at 2, 3, and 4 kHz is required for reporting purposes in human studies. The high-frequency regions of the cochlea are most sensitive to noise damage. Resonance of the ear canal also results in a frequency region of high-noise sensitivity at 4 to 6 kHz. A primary noise target is the cochlear hair cell. Although the mechanisms that underlie such hair cell damage remain unclear, there is evidence to support a role for reactive oxygen species, stress pathway signaling, and apoptosis. Another target is the synapse between the hair cell and the primary afferent neurons. Large numbers of these synapses and their neurons can be lost after noise, even though hearing thresholds may return to normal. This affects auditory processing and detection of signals in noise. The consequences of TTS and PTS include significant deficits in communication that can impact performance of military duties or obtaining/retaining civilian employment. Tinnitus and exacerbation of posttraumatic stress disorder are also potential sequelae.

*Department of Surgery/Otolaryngology, University of California, San Diego, La Jolla

Veterans Administration, San Diego, California

Department of Otology and Laryngology, Harvard Medical School, Boston, Massachusetts

§Defense Hearing Center of Excellence, 59MDW/SG02O, JBSA Lackland

||Hearing Science Program, Callier Center for Communication Disorders, Dallas, Texas

Sound Pharmaceuticals, Seattle, Washington

Address correspondence and reprint requests to Allen F. Ryan, Ph.D., University of California, San Diego, La Jolla, CA 92093, U.S.A.; E-mail:

A.F.R. discloses the following conflicts of interest: consultancy, Otonomy, Inc., L-3 Communications; employment, UCSD, Veterans Administration; grants/grants pending, NIH, Veterans Administration; stock/stock options, Otonomy, Inc. S.G.K. discloses the following conflicts of interest: employment, Massachusetts Eye and Ear Infirmary; grants/grants pending, NIDCD, ONR, DoD; patents/patents pending. T.H. discloses the following conflicts of interest: employment and travel/accommodations/meeting expenses paid, DoD Hearing Center of Excellence. C.L.P. discloses the following conflicts of interest: consultancy, Gateway Therapeutics, Hearing Health Science; employment, University of Florida and University of Texas at Dallas; grants/grants pending, Edison Pharmaceuticals, Inc., Sound Pharmaceuticals, Inc., American Suppressor Association, MaxSound, Inc., DoD, NIH; patents/patents pending; royalties, Springer. J.K. discloses the following conflicts of interest: employment, Sound Pharmaceuticals.

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Hearing loss because of noise has been recognized in humans for centuries (1). However, it was only in the 20th century that the phenomenon of noise-induced hearing loss (NIHL) was rigorously investigated in animals, allowing a more accurate determination and definition of the disease. Such studies have demonstrated that exposure to excessive sound produces hearing loss (threshold sensitivity loss), with the magnitude of the initial shift and the degree of recovery depending on characteristics of the exposure in the level, time, and frequency domains, and on characteristics of the individual, as noted later. Threshold shifts that recover to baseline levels in the hours, days, or weeks after exposure are termed temporary threshold shifts (TTS). More injurious exposures can produce threshold sensitivity losses containing both temporary and permanent components, in which the majority of the TTS resolves but a measurable permanent threshold shift (PTS) has evolved (e.g. [2,3]). Threshold shifts of up to ∼50 dB immediately after a single-noise exposure may recover completely, whereas more extensive immediate hearing losses are likely to result in permanent losses of hearing sensitivity (e.g. [3,4]). Continuous or repeated exposures to noise that only induce a TTS may evolve to a PTS if repeated (5), as occurs in occupational noise exposure. Therefore, PTS can be defined as noise-induced threshold shift that persists after a period of recovery subsequent to the exposure. In animal models, recovery has been reported for periods extending up to 3 weeks; therefore, it may be premature to define a threshold shift as temporary until at least 3 weeks postexposure, when a permanent threshold shift arises.

Although the smallest level of TTS or PTS that can be reliably measured in an individual has not been well defined given test-to-test variability in individuals, several standards have been set for what is considered a significant hearing loss or “standard threshold shift” (STS). The Occupational Safety and Health Administration states that an STS is a 10 decibel (dB) increase in hearing threshold averaged across 2000, 3000, and 4000 Hz in the same ear from an individual's baseline or recent annual audiogram (29 CFR 1910.95). An STS is a reportable work-related injury once it has been reconfirmed with a retest within 30 days of the initial test and results in a hearing threshold of at least 25 dB in the affected ear. Therefore, most occupational hearing loss or PTS is under reported since Occupational Safety and Health Administration only requires an STS to be reported.

The Department of Defense (DoD) policy for the military's Hearing Conservation Program and the American Speech-Language-Hearing Association (ASHA) similarly define STS by a 10 dB shift average using the same frequencies, “in either ear without age corrections” (DoD I 6055.12, 2010 [currently under revision]; ASHA,, 2015). In contrast, the National Institute of Occupational Safety and Health recommended definition of an STS is “an increase of 15 dB in hearing threshold level at 500, 1000, 2000, 3000, 4000, or 6000 Hz in either ear, as determined by two consecutive audiometric tests,” with the second test required to reduce false-positive findings (6). A significant negative STS (improved hearing) is further defined by the DoD as a decrease of 10 dB or greater change (improvement in hearing) for the average of 2, 3, and 4 kHz in either ear. An early warning shift STS (decrease in hearing) is defined as a 10 dB or greater change at 1, 2, 3, or 4 kHz in either ear. Therefore, a consistent measure between TTS and PTS involves a 10 dB shift from baseline hearing involving one or more frequencies in the same ear.

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PTS is sensorineural and varies across frequencies, depending on characteristics of the exposure, the transmission characteristics of the external and middle ears, and the innate sensitivity of different regions of the cochlea to damage.

Noise damage is typically most extensive at frequencies above those of the exposure (7), a phenomenon well explained by nonlinearities in the cochlear mechanical response to sound (8). This is most apparent for TTS and for low levels of PTS. However, noises to which human ears are exposed often are broadband in frequency composition. These signals are shaped (some frequencies amplified, others reduced by filtering) by passage through the external and middle ears (9). Resonance in the ear canal produces amplification of acoustic frequencies whose wavelengths are approximately four times the length of the canal, which for humans results in enhancement of frequencies around 4 kHz. This contributes to an enhanced “notch” of PTS at 4 to 6 kHz for exposure to broad-band stimuli. Finally, as with many other forms of damage, the basal cochlea seems to be most vulnerable to noise. Although the reason for this is not entirely clear, it may be related to higher levels of antioxidants in apical hair cells as well as higher rates of metabolic activity in basal hair cells (10). This basal sensitivity results in a tendency for TTS and PTS to be more extensive at high frequencies.

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TTS is a change in hearing threshold that recovers to preexposure levels (baseline) over time. The amount of time to recover to baseline may be relatively fast (minutes to hours) or slow (days to weeks). The severity of the initial insult, as well as the time course of the recovery, is dependent on a number of factors including: the type of insult or trauma, the intensity and duration of the insult (single versus repeated, short versus long exposures), and the stimulus type (impulse/impact sound or continuous noise including wide or narrow-band noise). Individual susceptibility is dependent on the use of hearing protective devices, the quiet time or rest between exposures, and the level of hearing loss before exposure. Individual susceptibility to TTS may also be influenced by age, sex, previous history of noise exposure, diabetes, genotype, and other personal or environmental factors such as smoking and diet. Although these factors are at play for PTS as well, unlike PTS, TTS is a change in hearing sensitivity that recovers to baseline or within test/retest criteria in minutes, hours, days, or weeks with the upper limit being 30 days postexposure. TTS and PTS outcomes will vary as a function of the insult and individual factors.

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Historically, TTS was largely thought to be a mechanical process that involved structures within the outer and middle ears including the ear drum, ossicular chain, and middle ear muscles through the acoustic reflex. Extremely intense noise exposure is also known to mechanically damage the cochlea, disrupting the connections between the tectorial membrane and outer hair cell stereocilia, damaging the stereocilia themselves, breaching the integrity of the reticular lamina, or even disrupting the basilar membrane.

However, recent work in several preclinical studies has demonstrated a significant involvement of several sensorineural inner ear structures including hair cells and their stereocilia, supporting cells within the organ of Corti, endothelial cells and fibrocytes within the stria vascularis and spiral ligament, and dendritic processes of the auditory nerve (11,12). Molecular and biochemical changes have been identified which include proinflammatory and proapoptotic processes (13). These changes have been shown to alter the normal function of several critical processes within the cochlea including the endolymphatic potential that drives hair cell depolarization (14), cellular membranes, and mitochondria responsible for hair cell and supporting cell activity, and neural innervation of the inner hair cell that conduct impulses to the auditory brainstem. In addition, changes in the activity or metabolism of neurons in the cochlear nucleus, superior-olivary complex, and inferior colliculus have been observed (15). In support of this noise-induced change in inner ear biology and pharmacology and its relevance in establishing the TTS, several preclinical studies have demonstrated a significant reduction in TTS when the animals were administered otoprotective compounds or drugs immediately before noise exposure (16–20).

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Although intense sounds such as blast can damage the conductive apparatus of the outer and middle ears, producing permanent hearing loss through tympanic membrane rupture or ossicular dislocation, PTS is generally considered to be a sensorineural phenomenon restricted to the cells of the cochlea. The most recognized cause of PTS is damage to and loss of cochlear hair cells. The mechanisms by which this damage can occur are not known with certainty. However, there is extensive evidence implicating the generation of reactive oxygen species within hair cells during and after overexposure (12). This leads to the activation of stress signaling pathways such as the JNK MAP kinase cascade (21), which can in turn lead to cell damage, apoptosis, and/or necrosis (22). The biochemical pathways leading to hair cell damage/death are undoubtedly complex, and also seem to include competing survival pathways that attempt to rescue hair cells and restore their function. It is the balance of these competing pathways that determine the fate of the cell. The outer hair cells, responsible for the exquisite sensitivity and frequency and selectivity of the cochlea, are the most sensitive to damage (2,3).

Noise also can target hair cell synapses and neurons directly, even when the hair cells themselves remain and recover normal function. The insult is observed acutely as a glutamate-like “excitotoxicity” that includes swelling and retraction of afferent terminals from beneath inner hair cells (23). Recent work in animal models shows that noise-induced loss of synapses and afferent terminals is rapid and permanent (24,25). Loss of spiral ganglion neurons is comparatively slow, and can be “primary,” that is, occurring without noise-induced hair cell loss (24,25) or “secondary” to the loss of their inner hair-cell targets (26,27). Such synaptic and neural loss can exacerbate the functional consequences of noise exposure by reducing the ability of the VIIIth nerve to encode auditory signals with fidelity, with or without loss of threshold sensitivity (28). Thus, lack of PTS does not imply that auditory function is normal.

It should be noted that our understanding of the mechanisms of NIHL remains incomplete. For example, many of the processes that have been proposed to mediate hearing loss would take considerable time to develop. However, impulse exposures, even those that do not result in PTS, produce hearing loss essentially instantaneously, without immediate loss of cells. Presumably, this represents a disruption of cochlear cells at the microstructural and protein levels. In another example, it has recently been suggested that the initial 10 to 15 dB of TTS may serve as a mechanism to extend the dynamic range of hearing, rather than representing a damage mechanism (29). Finally, noise exposure that accumulates over a lifetime of occupational exposure may well involve different processes than more acute damage (30). Further studies of NIHL mechanisms are clearly warranted.

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ASHA uses the following threshold-based definitions of hearing loss: none (normal hearing) (−10–15 dB), slight (16–24 dB), mild (25–40 dB), moderate (41–55 dB), moderately severe (56–70 dB), severe (71–90 dB), or profound (>91 dB). Thus, 10 dB of PTS would have different consequences depending upon the initial level of hearing, for example leaving one individual with normal hearing (by definition) while increasing hearing loss from mild to moderate in another. One reasonable strategy may be to calculate the resulting hearing handicap as per the American Academy of Otolaryngology (AAO) 1979 criteria, or using the ASHA criteria, both of which incorporate a low fence of 25-dB HL. Key differences include the frequencies included in the calculation (AAO-1979: 0.5, 1, 2, and 3 kHz; ASHA: 1, 2, 3, and 4 kHz) and the growth rate for impairment for PTA thresholds above the low fence value (AAO-1979: 1.5% per dB; ASHA: 2% per dB) (31,32). However, if PTA thresholds were below 25 dB HL after the exposure, the PTS would be “missed” using this scheme, as there is deemed to be no handicap below the low fence value. Moreover, functional losses that have no threshold change correlate would not be recognized using these strategies.

The consequences of threshold sensitivity loss have been well documented in animal studies of auditory physiology and psychophysical studies of human auditory function. Loss of 40 dB of hearing sensitivity is associated with a loss of outer hair cells, which as noted above are responsible for the lower ranges of hearing sensitivity, and for the sharply tuned responses of the cochlea to individual frequencies. The loss of these cells leads to a degraded ability to discriminate sounds, especially in noisy environments. More severe hearing loss is associated with the loss of inner hair cells, which transmit sensory information from the cochlea to the central auditory system. In addition, a rearrangement or loss of the adjacent supporting cells including Hensen's cells, Dieter's cells, and inner and outer pillar cells may contribute to further impairment or loss of passive amplification. Loss of all inner hair cells from a cochlear region eliminates auditory response and loss from the entire cochlea results in total deafness.

Of course, the consequences of PTS are dependent upon the degree and frequency range of the loss and total loss of hearing from noise exposure is rare. However, with PTS leading to moderate and especially severe hearing loss, many facets of life become extremely challenging (33). Communication is significantly impacted. This can lead to difficulty in performing military duties or in obtaining/retaining civilian employment. Social interactions are also heavily impacted, with the result that individuals with hearing loss can become withdrawn and isolated. This can in turn lead to depression and possibly cognitive decline (33). In the case of blast injury, hearing loss can exacerbate the effects of traumatic brain injury, even when traumatic brain injury is mild (34). Another consequence of noise exposure is an increase in sensitivity to other forms of hearing loss, including ototoxicity (35) and aging (36).

There is also a strong, positive correlation between the presence of noise-induced permanent hearing loss and tinnitus (37). Although tinnitus can be a benign condition, a large fraction of individuals with tinnitus experience distress that can be extreme (e.g. [38]). A lesser correlation is observed for hyperacusis (e.g. [39]), another negative sequela of PTS.

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The authors acknowledge the DOD Hearing Center of Excellence for the support of Pharmaceutical Interventions for Hearing Loss (PIHL) working group and publication of this article.

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1. Thurston FE. The worker's ear: A history of noise-induced hearing loss. Am J Ind Med 2013; 56:367–377.
2. Eldredge DH, Mills JH, Bohne BA. Anatomical, behavioral, and electrophysiological observations on chinchillas after long exposures to noise. Adv Otorhinolaryngol 1973; 20:64–81.
3. Ryan A, Bone RC. Noise-induced threshold shift and cochlear pathology in the Mongolian gerbil. J Acoust Soc Am 1978; 63:1145–1151.
4. Clark WW, Bohne BA. Effects of noise on hearing. JAMA 1999; 281:1658–1659.
5. Lonsbury-Martin BL, Martin GK, Bohne BA. Repeated TTS exposures in monkeys: Alterations in hearing, cochlear structure, and single-unit thresholds. J Acoust Soc Am 1987; 81:1507–1518.
6. NIOSH, National Institute of Occupational Safety and Health, publication 98–126: Available at: Accessed January 12, 2016.
7. Cody AR, Johnstone BM. Acoustic trauma: Single neuron basis for the “half-octave shift”. J Acoust Soc Am 1981; 70:707–711.
8. Robles L, Ruggero MA. Mechanics of the mammalian cochlea. Physiol Rev 2001; 81:1305–1352.
9. Rosowski JJ. The effects of external- and middle-ear filtering on auditory threshold and noise-induced hearing loss. J Acoust Soc Am 1991; 90:124–135.
10. Sha S-H, Taylor R, Forge A, Schacht J. Differential vulnerability of basal and apical hair cells is based on intrinsic susceptibility to free radicals. Hear Res 2001; 155:1–8.
11. Mulroy MJ, Fromm RF, Curtis S. Changes in the synaptic region of auditory hair cells during noise-induced temporary threshold shift. Hear Res 1990; 49:79–87.
12. Kujawa SG, Liberman MC. Adding insult to injury: Cochlear nerve degeneration after “temporary” noise-induced hearing loss. J Neurosci 2009; 29:14077–14085.
13. Henderson D, Bielefeld EC, Harris KC, Hu BH. The role of oxidative stress in noise-induced hearing loss. Ear Hear 2006; 27:1–19.
14. Yan D, Zhu Y, Walsh T, et al. Mutation of the ATP-gated P2X2 receptor leads to progressive hearing loss and increased susceptibility to noise. Proc Natl Acad Sci U S A 2013; 110:2228–2233.
15. Ryan AF, Axelsson GA, Woolf NK. Central auditory metabolic activity induced by intense noise exposure. Hear Res 1992; 61:24–30.
16. Seidman MD, Shivapuja BG, Quirk WS. The protective effects of allopurinol and superoxide dismutase on noise-induced cochlear damage. Otolaryngol Head Neck Surg 1993; 109:1052–1056.
17. Attias J, Sapir S, Bresloff I, Reshef-Haran I, Ising H. Reduction in noise-induced temporary threshold shift in humans following oral magnesium intake. Clin Otolaryngol 2004; 29:635–641.
18. Yamasoba T, Pourbakht A, Sakamoto T, Suzuki M. Ebselen prevents noise-induced excitotoxicity and temporary threshold shift. Neurosci Lett 2005; 380:234–238.
19. Lynch ED, Kil J. Compounds for the prevention and treatment of noise-induced hearing loss. Drug Discovery Today 2005; 10:1291–1298.
20. Kil J, Pierce C, Tran H, Gu R, Lynch ED. Ebselen treatment reduces noise induced hearing loss via the mimicry and induction of glutathione peroxidase. Hear Res 2007; 226:44–51.
21. Pirvola U, Xing-Qun L, Virkkala J, et al. Rescue of hearing, auditory hair cells, and neurons by CEP-1347/KT7515, an inhibitor of c-Jun N-terminal kinase activation. J Neurosci 2000; 20:43–50.
22. Bohne BA, Harding GW, Lee SC. Death pathways in noise-damaged outer hair cells. Hear Res 2007; 223:61–70.
23. Robertson D. Functional significance of dendritic swelling after loud sounds in the guinea pig cochlea. Hear Res 1983; 9:263–278.
24. Lin HW, Furman AC, Kujawa SG, Liberman MC. Primary neural degeneration in the Guinea pig cochlea after reversible noise-induced threshold shift. J Assoc Res Otolaryngol 2011; 12:605–616.
25. Kujawa SG, Liberman MC. Acceleration of age-related hearing loss by early noise exposure: Evidence of a misspent youth. J Neurosci 2006; 26:2115–2123.
26. Bohne BA. Time course of nerve-fiber regeneration in the noise-damaged mammalian cochlea. Int J Dev Neurosci 1997; 15:601–617.
27. Puel JL, Ruel J, Gervais d’Aldin C, Pujol R. Excitotoxicity and repair of cochlear synapses after noise-trauma induced hearing loss. Neuroreport 1998; 9:2109–2114.
28. Bharadwaj HM, Verhulst S, Shaheen L, Liberman MC, Shinn-Cunningham BG. Cochlear neuropathy and the coding of supra-threshold sound. Front Syst Neurosci 2014; 8:26.
29. Housley GD, Morton-Jones R, Vlajkovic SM, et al. ATP-gated ion channels mediate adaptation to elevated sound levels. Proc Natl Acad Sci U S A 2013; 110:7494–7499.
30. Kirchner DB, Evenson E, Dobie RA, et al. Occupational noise-induced hearing loss. JOEM 2012; 54:106–108.
31. AAO Committee on Medical Aspects of Noise and American Council of Otolaryngology. Guide for the evaluation of hearing handicap. JAMA 1979; 241:2055–2059.
32. ASHA. American Speech-Language Hearing Association: Degree of Hearing Loss. Available at: Accessed January 12, 2016.
33. Arlinger S. Negative consequences of uncorrected hearing loss—a review. Int J Audiol 2003; 42 (Suppl 2): 2S17–20.
34. Lew HL, Garvert DW, Pogoda TK, et al. Auditory and visual impairments in patients with blast-related traumatic brain injury: Effect of dual sensory impairment on Functional Independence Measure. J Rehabil Res Dev 2009; 46:819–826.
35. Bone RC, Ryan AF. Audiometric and histologic correlates of the interaction between kanamycin and subtraumatic levels of noise in the chinchilla. Otolaryngology 1978; 86: ORL400-4.
36. Campo P, Venet T, Rumeau C, et al. Impact of noise or styrene exposure on the kinetics of presbycusis. Hear Res 2011; 280:122–132.
37. Mazurek B, Olze H, Haupt H, Szczepek AJ. The more the worse: The grade of noise-induced hearing loss associates with the severity of tinnitus. Int J Environ Res Public Health 2010; 7:3071–3079.
38. Gomaa MA, Elmagd MH, Elbadry MM, Kader RM. Depression, anxiety and stress scale in patients with tinnitus and hearing loss. Eur Arch Otorhinolaryngol 2014; 271:2177–2184.
39. Jansen EJ, Helleman HW, Dreschler WA, de Laat JA. Noise induced hearing loss and other hearing complaints among musicians of symphony orchestras. Int Arch Occup Environ Health 2009; 82:153–164.

Auditory; Measurement; Significant threshold shift; STS; Temporary threshold shift; TTS

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