Causes of Acquired Hearing Loss

6.2.1

Professional Musicians’ Exposure in Symphony Orchestras

Symphony orchestral music is generally louder than allowed by occupational noise legislation. Classical musicians individually are often exposed to sound levels greater than 85 dB(A) for long periods of time, both during practice and performance. In one of the first studies, measured the pure-tone hearing thresholds in 34 orchestral musicians. The audiometric results showed changes consistent with NIHL in 23 out of 68 ears (34%). The only other early large-scale study by measured the hearing thresholds from 139 classical musicians. Following their criteria for hearing loss, defined as 20 dB or worse in one ear and at one frequency between 3 and 6 kHz, 80 (58%) musicians were identified as having hearing loss. After considering the age factor, they still found hearing loss in 51 of these cases (37%) being partially or wholly due to music exposure. described that classical musicians of the Chicago Symphony Orchestra over a standard working day (8 h) were exposed at 85.5 dB(A), which is only 0.5 dB above the recommended safe threshold in North American industrial settings. However, the maximal sound peaks reached much higher levels. measured sound pressure levels at five rehearsals and two concerts by the City of Birmingham Symphony Orchestra and found over 85 dB(A) during half of the rehearsal time. The maximal sound peaks were measured at over 110 dB(A) in front of the trumpet, piccolo, and bassoon positions. tested 241 professional musicians of symphony orchestras, aged 23–64 years. Most musicians could be categorized as normal hearing, but their audiograms showed notches at 6 kHz ( Fig. 6.1 ). Musicians had more NIHL than could be expected on the basis of age and gender, but only at 6 kHz. However, these musicians scored very well on the speech-in-noise test, compensating for the loss of hearing sensitivity. This is a known phenomenon in active musicians (chapter 9 in ).

studied 63 musicians from four classical orchestras in Helsinki, Finland, and found that hearing loss in musicians was generally similar to that of the general population. However, highly exposed musicians had greater hearing loss at frequencies more than 3 kHz than less exposed ones. In a study on the hearing status of 182 classical symphony orchestra musicians, found that ears with the highest exposure (29 of 363 tested) had an additional threshold shift of 6.3 dB compared with the 238 ears with lowest exposure. However, the observed hearing loss of this group of musicians was less than the noise-induced permanent threshold shift expected from ISO1999. ISO1999 provides the basis for calculating hearing disability according to commonly measured audiometric frequencies, or combinations of such frequencies, which exceed a certain value. The measure of exposure to noise for a population at risk is the noise exposure level normalized to a nominal 8 h working day, Leq 8 h, for a given number of years of exposure. ISO1999 applies to noise at frequencies less than approximately 10 kHz which is steady, intermittent, fluctuating, or irregular ( http://www.iso.org/iso/catalogue_detail.htm?csnumber=45103 , accessed January 29, 2016). Whereas most of the musicians in the study had better hearing at 3, 4, and 6 kHz for age than expected, 29 ears with the highest exposure above 90.4 dB(A) with a mean exposure time of 41.7 years had significantly elevated hearing thresholds. Trumpet players and the left ear of first violinists showed significantly increased thresholds compared with the ears of other musicians ( ).

Active musicians also practice outside their concert performances. estimated sound exposure during solitary practice of 35 professional orchestral musicians, representing players of most orchestral instruments. Sound levels were recorded between 60 and 107 dB(A) with (C-weighted) peak levels between 101 and 130 dB(C). For comparison between A- and C-weighting see Fig. 4.2 . Note that the C-weighting is in fact an unweighted average. For average reported practice durations (2.1 h/day, 5 days a week) 53% would exceed accepted permissible daily noise exposure in solitary practice, in addition to sound exposure during orchestral rehearsals and performances. noted significant interaural differences in violin, viola, flute/piccolo, horn, trombone, and tuba. Only 40% used hearing protection while practicing. These findings indicate orchestral musicians that are already at risk of NIHL in ensemble performances are further at risk during solitary practice.

All in all, more than 30 years of evidence about the risk of hearing loss in professional classical musicians have not resulted in sufficient change in practice and prevention.

6.2.2

Active Musicians’ Exposure at Pop/Rock Concerts

reported that the prevalence of hearing loss among rock/pop musicians was 46% (38/83)—defining hearing loss the same as in their study in classical musicians ( Section 6.2.1 ). In a follow-up study of the same pop/rock musicians 16 years later, found a significant deterioration in hearing thresholds at 4 and 8 kHz in the left ear, and at 4 kHz in the right among those who had shown hearing loss at these frequencies in the original study. In addition, 22% of participants showed a deterioration of their hearing greater than 15 dB HL at one or more frequencies in one or both ears. reported a similar prevalence of hearing loss in 139 rock/jazz musicians. According to their definition of hearing loss, which was the hearing threshold more than 25 dB at two frequencies or thresholds more than 30 dB at one frequency in one or both ears, 68/139 (49%) showed a hearing loss compared with the ISO7029 standard for matching age and gender. Twenty-three percentage of male musicians had hearing thresholds beyond the 90th percentile, whereas hearing thresholds obtained from female musicians were distributed at or just below the ISO7029 median according to their age. ISO7029 describes the normal changes in pure-tone thresholds with age ( ).

assessed pure-tone audiometry in the conventional and extended high-frequency range in 42 nonprofessional pop/rock musicians, and in a control group of 20 normal hearing young adults with no history of long-term noise exposure. Relative to ISO7029, the mean hearing threshold in the frequency range of 3–8 kHz was 6 dB in the musicians and significantly higher than the 1.5 dB in the control group. Musicians, using regular hearing protection, had less hearing loss (average 3–8 kHz thresholds=2.4 dB) compared to musicians who never used hearing protection (average 3–8 kHz thresholds=8.2 dB). , in a prospective study, compared the effects of music exposure between professional pop/rock musicians ( N =16) and nonmusicians ( N =16). The musicians showed worse hearing thresholds in both conventional and high-frequency audiometry when compared to the nonmusicians. In addition, transient-evoked otoacoustic emissions (TEOAEs) were found to be smaller in the musicians group ( ).

examined the relationship between the years of professional experience of pop/rock/jazz musicians and their hearing loss. Forty-four pop/rock/jazz musicians were interviewed about symptoms of tinnitus and hyperacusis. Audiograms were measured for 1–8 kHz. All participants had a minimum of 4 years of experience playing their instrument with an average of 22.7±10.4 years. The average weekly exposure of participants to pop/rock/jazz was 23.6±17.7 h. Greater musical experience was positively and significantly linked to hearing loss in the frequency range of 3–6 kHz and to the presence of tinnitus. The number of hours/week playing had a greater effect on hearing loss in comparison to the number of years playing. The pure-tone average (1–8 kHz, age and gender corrected) was not significantly different for the right ear (2.8±8.8 dB) and for the left ear (5.4±10.4 dB).

6.2.3

Passive Exposure at Concerts and Discos

examined the effects of recreational noise exposure in adolescents during 4 years until 2001 when they turned 17. In the first year, there were 102 boys and 71 girls, and in the last year, 63 boys and 43 girls. They noted a tendency of the mean hearing threshold level to increase in both genders, especially at very high frequencies around 14–16 kHz. Boys had a higher mean hearing threshold level than girls and were more exposed to high sound levels than girls. subsequently reported on the exposure levels of the 14- to 15-year-old adolescents ( N =172) from this group. They found that the sound levels measured in their favorite discos were 107.8–112.2 dB(A) and for their PLDs 82.9–104.6 dB(A). The same group ( ) compared the hearing of these adolescents at ages 14–15 (test, N =172) and 17–18 (retest, N =59) and found a significant increase in hearing thresholds (increasing from 2.7 dB at 250 Hz, to 7.0 dB at 8 kHz, and then decreasing to 4.5 dB at 12 kHz, and again increasing to 7.0 dB at 16 kHz). This was accompanied by a significant decrease in the amplitude of TEOAEs in the moderate and high exposure groups. The decrease was 5.0 dB at 1 kHz and decreasing with frequency to 3.4 dB at 4 kHz. This clearly illustrates the onset and progression of significant NIHL in these adolescents.

Hearing loss in disc jockeys may also be related to their exposure to music and length of time in the profession. surveyed a group with average age of approximately 26 years (SD=6 years) who were on average 6.6 years in that profession and were on average exposed for approximately 22 (SD=13) hours weekly. Their audiograms showed the expected hearing loss at 6 kHz, but also low frequency losses at 125–500 Hz ( Fig. 6.2 ).

6.2.4

Personal Listening Devices

As has been clearly summarized by : “Concern is mounting as the use of personal listening devices (PLDs) has become de rigueur for today’s teenagers. There is still debate and uncertainty as to the exact extent and contribution of PLD usage to hearing loss. However, there is an increasing body of recent literature supporting the connection between extended and/or elevated usage of PLDs and documented hearing loss, with a clear correlation between such usage patterns and hearing loss in the extended high frequency range of hearing (8–16 kHz).”

In 33 volunteers, measured effects of PLDs use on hearing. Subjects selected either rock or pop music, which was then presented at 93–95 ( N =10), 98–100 ( N =11), or 100–102 ( N =12) dB(A) in-ear exposure level for a period of 4 h. Audiograms and distortion product otoacoustic emissions (DPOAEs) were measured before and after music exposure. Post-music tests were done 15 min, 1 h 15 min, 2 h 15 min, and 3 h 15 min after the exposure ended. Additional tests were conducted the following day and 1 week later. They found that TTS was reliably detected after higher levels of sound exposure. This was reflected in audiometric thresholds with a “notch” configuration, with the largest changes at 4 kHz (mean ~6±4 dB; range=0–14 dB). found that threshold recovery was largely complete within the first 4 h postexposure, and all subjects showed complete recovery of both thresholds and DPOAE measures when tested 1 week postexposure. The study by reviewed in Chapter 4 , Hearing Problems which showed that repeated TTS exposures can result in permanent hearing loss should be kept in mind here.

evaluated early hearing effects related to PLD usage in 35 young adult PLD users (listening for >1 h/day, at >50% of the maximum volume setting of their devices) and their age- and sex-matched controls using a combination of conventional and extended high-frequency audiometry as well as TEOAE and DPOAE measurements. The mean listening duration of the PLD users was 2.7±1.0 h/day while their estimated average listening volume was 81.3±9.0 dB(A) (free-field corrected). did not detect typical signs of NIHL in the audiogram of PLD users and their audiometric thresholds at 0.25–8 kHz were comparable with those obtained from controls. As expected, mean hearing thresholds of PLD users at many of the extended high frequencies (9–16 kHz) were significantly higher than in controls. In addition, TEOAE and DPOAE amplitudes in users were significantly smaller than in controls. These results indicate the presence of an early stage of hearing damage in the PLD user group.

Despite the potential harmful music listening habits of the last decades, found that “for men and women of a specific age, high-frequency hearing thresholds were lower (better) in 1999–2004 than in 1959–1962. The prevalences of hearing impairment were also lower in the recent survey.” To quantify this, we are talking here about a significant 5 dB difference on average for 6 kHz (the highest frequency measured in the 1959–62 survey) in the age groups above 45 years. In contrast for the youngest age groups (25–34 and 35–44 years) the difference was even larger at approximately 10 dB.

6.3.1

Necrosis and Apoptosis in Noise-Induced Hearing Loss

Cochlear damage following noise exposure occurs through two major routes. The first one is direct mechanical damage, which leads to both hair cell loss through mechanical disruption of the stereocilia and direct damage to supporting and sensory cells ( ). The other route involves biochemical pathways leading to cell death through either apoptosis or necrosis. Apoptosis is an active, energy-requiring process that is initiated by specific pathways in the cell, while necrosis is a passive one requiring no metabolic energy and results in the rupture of the cell body. During necrosis, the cellular content is spilled onto adjacent cells, thereby possibly triggering inflammatory responses. Necrosis and apoptosis are easily distinguishable through differentially activated biochemical processes. The first studies evaluating the type of cochlear cell death following intense noise exposure date back to the mid-1980s. Swollen outer hair cells (OHCs) were observed in cochleae of animals subjected to loud noise (~120 dB SPL). As this is a hallmark of necrosis, it was assumed that necrosis was the major cause of cell death ( ).

Besides necrosis, apoptosis is a key mediator of NIHL. Several biochemical apoptotic markers, such as the caspase cascade, are activated in OHCs after noise trauma ( ). Two important factors seem to determine which cell death pathway is activated following intense noise exposure. The first is sound intensity level. Noises of approximately 115 dB SPL seem to favor necrosis, while only marginally louder noises (~120 dB) seem to favor apoptosis ( ). In this study, two major types of morphological changes of OHC nuclei were noted in the noise-exposed cochleae. One was characterized by formation of chromatin fragments and by shrinkage of nuclei. Another was swelling of OHC nuclei. The finding of nuclear swelling and condensation in the noise-damaged cochleae suggested that two types of nuclear pathologies originated from two distinct biological processes or from a single biological process with two phases of the change. First, in the animals exposed to 110 or 115 dB noise, there was only swelling of nuclei. Second, in this study formation of chromatin fragments and shrinkage of nuclei predominately appeared 3 h after the noise exposure, whereas swelling of nuclei occurred in all the exposed cochleae, particularly in the cochleae obtained 3 and 14 days after the noise exposure. Finally, although both nuclear swelling and condensation coexisted in the animals exposed to 120 dB noise, their distribution along the organ of Corti was different. Considering these differences, concluded that nuclear swelling and nuclear condensation originated from two distinct biological processes leading to cell death. The typical changes of formation of chromatin fragments and shrinkage of nuclei noted in the animals exposed to 120 dB noise are morphologically similar to those nuclear changes described in previous studies for apoptosis, suggesting that apoptotic processes may be involved in intense noise-induced hair cell death (chapter 3 in ).

6.3.2

Delayed Effects of TTS Noise Exposure and Aging

Plastic changes in the auditory system (see chapter: Brain Plasticity and Perceptual Learning ) often result from the loss of cochlear hair cells, regardless whether the loss is induced by mechanical intervention, traumatic noise exposure, or by the application of ototoxic drugs. Damage of hair cells may also result as a consequence of aging. Presbycusis in humans refers to age-related auditory deficits that include a loss of hearing sensitivity and a decreased ability to understand speech, particularly in the presence of background noise. The hearing loss tends to increase with age, with high-frequency losses exceeding low-frequency losses at all ages ( ). Data from large populations screened for noise exposure and otologic disease ( ) show a progressive increase of hearing loss amounting to 20 dB at frequencies below 1 kHz and increasing to 60 dB difference at 8 kHz over the age span from 30 to 70 years. Accumulating auditory stresses during life may lead to presbycusis. The involvement of environmental factors is implied, for example, by the fact that hearing levels are generally poorer in industrialized than in more isolated societies ( ). Prolonged exposure to loud occupational noise has long been recognized as a cause of hearing loss but long-lasting effects, after the noise exposure has stopped, are not clear ( ). Subclinical damage accumulated during employment may place the ear at higher risk for age-related hearing impairment.

wrote a landmark review that we follow here. Survival of ANFs during aging depends on genetic and environmental interactions. Loss of ANFs without associated loss of hair cells is common among mammals during aging and is called primary degeneration. Apparent primary and secondary degeneration (following loss of inner hair cells (IHCs)) of ANFs may occur in the same cochlea ( ), suggesting that age-related ANF and hair cell loss result from independent mechanisms. Primary degeneration of ANFs has been observed in the cochlea of CBA/CaJ mice after moderate noise exposure at a young age ( ). In this study, CBA/CaJ mice were exposed to an 8–16 kHz noise band at 100 dB SPL for 2 h at ages from 4 to 124 weeks and held with unexposed cohorts for postexposure times from 2 to 96 weeks. When evaluated 2 weeks after exposure, maximum threshold shifts in young-exposed animals (4–8 weeks) were 40–50 dB. Animals exposed at at least 16 weeks of age showed essentially no shift at the same postexposure time. However, when held for long postexposure times, these animals showed substantial ongoing deterioration of cochlear neural responses and corresponding primary neural degeneration throughout the cochlea without changes in OHC responses (as measured with DPOAEs). Delayed ANF loss was observed in all noise-exposed animals held 96 weeks after exposure, even in those that showed no NIHL 2 weeks after exposure. Thus, even in the case of clear hair cell loss, true primary versus secondary neuronal loss may be impossible to separate at the early degeneration stage. At the later stages, certain independent mechanisms may contribute to the uncoupling of age-related loss of hair cells and ANFs ( ).

6.3.3

Noise-Induced Permanent Hearing Loss in Animals