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Noise and Military Service: Implications for Hearing Loss and Tinnitus 2 Noise-Induced Hearing Loss The purpose of this chapter is to provide background material on noise-induced hearing loss to facilitate understanding of the evidence on noise-induced hearing loss in military personnel presented in Chapter 3. The chapter begins with a general discussion of the structure and function of the auditory system, with particular emphasis on the periphery, and the impact of noise on the peripheral auditory system. The effects of noise on hearing thresholds are reviewed next, followed by a review of the time course for the development of hearing loss from noise exposure. Next, exogenous and endogenous risk factors that may alter an individual’s susceptibility to noise-induced hearing loss are reviewed. This is followed by a discussion of national and international standards that have been developed to estimate the amount of noise-induced hearing loss to be expected from a given noise exposure and to separate the effects of noise from age-related changes in hearing. MECHANISMS AND MODELS OF NOISE-INDUCED HEARING LOSS Structure and Function of the Hearing Apparatus In humans and other mammals, the auditory system consists of the external, middle, and inner ears (Figure 2-1), as well as the central auditory pathways in the brain. Sound waves enter the external ear through the pinna, travel through the external ear canal, and strike the eardrum. The external ear boosts high-frequency (2000–5000 Hz in humans) sound en-
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Noise and Military Service: Implications for Hearing Loss and Tinnitus FIGURE 2-1 Semi-schematic drawing of the human ear. Sound waves enter the pinna, travel through the external ear canal, and strike the eardrum, setting it in motion. Motion of the eardrum sets the middle ear bones (malleus [M], incus [I], and stapes [S]) in motion and ultimately generates pressure waves in the fluids of the inner ear. Sensory cells in the hearing portion of the inner ear (i.e., cochlea) are then stimulated. When the fibers of the cochlear nerve are stimulated by the sensory cells, auditory information is transmitted to the brain. SOURCE: Modified from Brödel (1946). ergy by about 20 dB before it strikes the eardrum (Shaw, 1974). The eardrum vibrates when sound waves strike it, setting the middle-ear bones (malleus, incus, stapes) (Figure 2-1) in the air-filled middle-ear cavity in motion. The base of the stapes is fitted into the oval window of the hearing portion of the fluid-filled inner ear, the cochlea. Movement of the stapes sets up pressure waves in the fluids inside the cochlea, which contains the organ of Corti, the sensory organ for hearing, spiraling from base to apex. The primary sensory receptors for hearing, the inner hair cells, are found within the organ of Corti as are the outer hair cells, which primarily facilitate the sensory response of the inner hair cells. The pressure waves within the cochlea vibrate the basilar membrane and the attached organ of Corti (Figure 2-2). Specific sound frequencies vibrate specific places along the length of the cochlea, with high-frequency sound causing maximum vibration in the base of the cochlea and low-frequency sound causing maximum vibration in the apex. In addition, as the intensity of sound increases, the
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Noise and Military Service: Implications for Hearing Loss and Tinnitus FIGURE 2-2 Cross-section of one turn of the spiral-shaped cochlea. The organ of Corti (outlined by the black dashed line) is attached to the flexible basilar membrane and is surrounded by large fluid spaces (i.e., scala vestibuli, endolymphatic space, scala tympani). The organ of Corti contains sensory cells (i.e., inner and outer hair cells) that respond to pressure waves in the fluid spaces by releasing neurotransmitter from their bases. The nerve fibers that terminate on the hair cell bases are extensions of the auditory neurons. The nerve fibers conduct auditory information to the brain when the hair cells release neurotransmitter. TM = tectorial membrane. SOURCE: Modified from Davis and Associates (1953). amplitude of basilar membrane vibration also increases, although in a nonlinear, compressive manner over much of its operating range. The mechanical activity of the basilar membrane leads to mechanical stimulation of the inner and outer hair cells. From the surface of each hair cell, thin hair-like processes (stereocilia) project into the overlying gelatinous tectorial membrane (Figure 2-2). Movement of the basilar membrane and organ of Corti relative to the tectorial membrane deflects the stereocilia and opens ion channels in the hair cells. Channel opening depolarizes the hair cells so they release a neurotransmitter from their bases. This conver-
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Noise and Military Service: Implications for Hearing Loss and Tinnitus sion of mechanical energy from basilar membrane vibration to neuro-electrical energy by the sensory cells in the organ of Corti is a process involving high levels of metabolic activity. The nerve fibers connected to the hair cells, primarily the inner hair cells, are excited by the neurotransmitter and transfer the auditory information to the brain. Effects of Noise on Hearing The magnitude of hearing loss that results from excessive exposure to noise depends on factors associated with the exposure (e.g., sound pressure level [SPL], duration, type of noise, and frequency), as well as the characteristics of the individual being exposed (e.g., susceptibility to noise damage, age, prior history of hearing/ear damage). In the next section, we examine the influence of the type of noise in greater detail. Impulse/Impact Noise High-level, short-duration noise can arbitrarily be categorized as impulse noise, which is the product of explosive devices (e.g., gunfire), or impact noise, which is generated by the forceful meeting of two hard surfaces (e.g., a hammer to a nail, impact wrenches). The typical measures of impulse noise are the initial peak level and the duration of the first over-pressure. This is the A-duration and is less than 1 millisecond (msec) for handguns and several msec for large cannons. For impact noise, the two principal descriptors are the highest peak in a series of successive peaks (reverberations) and the so-called B-duration, the duration from the highest peak level to a point in time when the reverberations have decayed either 10 or 20 dB. B-durations range from 50 to 300+ msec. The distinction between impulse and impact noise becomes blurred in many real-life situations because impulse noise can reflect off the ground, or other surfaces, and the reflections add to the initial impulse noise, creating a large, more complicated waveform that is best described using the B-duration (Hamernik and Hsueh, 1991). Impulse noise creates several special hazards to the auditory system. First, the high peak levels associated with gunfire (140–190 dB pe SPL)1 may damage the cochlea by causing rapid mechanical failure and injury (Henderson and Hamernik, 1986). A series of rapidly occurring impulses 1 As noted in Chapter 1, various metrics have been used in the literature to quantify the sound levels associated with impulse and impact noise, including dBP and dB pe SPL. Sound levels for steady-state noise, on the other hand, are more commonly expressed as dBA. Since simple conversions among these various metrics are not possible, the committee chose to report sound levels using the specific metric employed in the studies reviewed.
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Noise and Military Service: Implications for Hearing Loss and Tinnitus can be partially attenuated by the acoustic reflex, a reflexive contraction of the middle-ear muscles, while isolated impulses reach the cochlea before the activation of the acoustic reflex. Thus, intense explosions may result in large cochlear lesions and significant hearing losses. This damage is termed “acoustic trauma,” and hearing at most frequencies may be affected (e.g., Ward and Glorig, 1961). Additional symptoms include a sense of fullness in the ears, speech sounding muffled, and a ringing in the ears (i.e., tinnitus) (Kraus, 1959; Ward and Glorig, 1961). Although some recovery of hearing takes place after an acoustic trauma episode, the individual is often left with a severe, permanent hearing loss (Ward and Glorig, 1961; Van Campen et al., 1999). Exposure to impulse noise can result in acoustic trauma from a limited number of exposures, including a single exposure, but can also result in conventional noise-induced hearing loss from extended periods of exposure to impulse noise over many weeks, months, or years. The relationship between noise-induced hearing loss and the peak amplitude of an impulse or impact noise is complicated. Systematic research with the chinchilla has shown that at the lower range of exposure to impulse noise (< 140 dB pe SPL) or impact noise (< 115 dB pe SPL), the chinchilla develops a hearing loss that is proportional to the total energy of the exposure (peak level × number of impulses). However, above these peak sound pressure levels, the auditory system is damaged primarily by the large displacements caused by high peak levels. The dividing line between the “energy” and “peak-level” behavior is referred to as the “critical level.” It should be noted that the critical levels of about 140 dB SPL for impulse noise and 115 dB SPL for impact noise are general approximations for the chinchilla. The actual critical level is dependent on the specific waveform of the impulse and impact noise (Henderson and Hamernik, 1986). Based on across-species comparisons from chinchillas to humans, the critical levels for humans are likely to be approximately 10 dB higher than those observed in chinchillas. However, because of the high risk of hearing loss from high-level impulses and the variability in subsequent noise-induced hearing loss, a more conservative criterion of 140 dB SPL has been adopted for humans. Below the critical level, hearing loss grows by the rate of approximately 1–3 dB of hearing loss for each dB of increase in peak level. However, above the critical level, hearing loss grows 3–7 dB for each dB increase in the level of the impulse or impact noise. This accelerated growth of hearing loss with increase in peak sound pressure level above the critical level is one of the factors that make high-level impulse and impact noise particularly dangerous (Henderson and Hamernik, 1986). Impulse and impact noise also present a heightened risk when either occurs with other steady-state background noise (approximately 85–95
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Noise and Military Service: Implications for Hearing Loss and Tinnitus dBA). Experimental studies with laboratory animals have shown that exposure to combinations of relatively benign impact and steady-state noise can lead to multiplicative interactions with hearing loss and cochlear damage, with the effects of the combined exposure being greater than the simple additive effects of impulse or continuous noise (Hamernik et al., 1981). Lei et al. (1994) have developed a metric, based on the distribution of noise levels during exposure, that captures the extra hazard to hearing associated with such combined exposures in laboratory animals. Intermittent and Continuous Exposures to Steady-State Noise Exposure to less intense noise (i.e., < 90 dBA) for short durations (i.e., ≤ 24 hrs) may result in a mild (< 30 dB) temporary hearing loss (Mills et al., 1970; Melnick, 1976). A noise-induced temporary hearing loss, or temporary threshold shift (TTS), is characterized by an increase in the hearing thresholds at some frequencies immediately following exposure, depending on the frequencies comprising the noise and its intensity. The threshold shift generally disappears within 24–48 hours after the exposure terminates (Mills et al., 1970; Melnick, 1976). Typically, exposure to more intense noise (> 90 dBA) or moderate noise for longer durations (> 24 hours) results in a larger amount of TTS (i.e., > 40 dB). In these cases, postexposure improvement of thresholds may continue for 30 days or longer, but in general, thresholds will not return to preexposure values. The individual likely will be left with a residual permanent threshold shift (PTS) (Taylor et al., 1965; Mills and Talo, 1972; Mills, 1973; Henderson et al., 1974a; Henderson and Hamernik, 1982). Hearing loss that results from exposure to sound with energy spread across a wide range of frequencies, such as many broad-band noises and impulses common to most industrial and military settings, is typically characterized by a gradual increase in threshold as frequency increases. Typically, the hearing loss abruptly reaches a maximum between 3000 and 6000 Hz, followed by a return toward normal hearing at still higher frequencies. This particular pattern of hearing loss, as illustrated in Figure 2-3, is typically referred to as the “noise-notch” audiogram. It is a clinical hallmark often used to distinguish noise-related high-frequency hearing loss from that associated with other etiologies, such as ototoxic medications or aging. Several mechanisms have been offered to explain the extra vulnerability of the higher frequencies to the damaging effects of a broad-band noise, including better transmission of the higher frequencies through the outer and middle ears to the inner ear (e.g., Saunders and Tilney, 1982; Rodriguez and Gerhardt, 1991) and specific vascular (e.g., Axelsson and Vertes, 1982) or metabolic (e.g., Thalmann, 1976) vulnerabilities of this region of the cochlea. However, none of these mechanisms can fully explain
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Noise and Military Service: Implications for Hearing Loss and Tinnitus FIGURE 2-3 Illustration of a typical noise-notch audiogram. Average audiogram (n = 450 ears) from Cooper and Owen (1976) shown here. Error bars at 250 and 8000 Hz represent ±1 standard deviation and were the only standard deviations reported by the authors of this study for the average pure-tone thresholds at individual frequencies. The dashed line connecting thresholds at 1000 and 8000 Hz provides a visual representation of the Notch Index (NI) metric. all of the features of the increased vulnerability of the 3000–6000 Hz region of the cochlea to noise damage. Although the group data from Cooper and Owen (1976) in Figure 2-3 reveal a clear decrease in hearing from 1000 Hz to 4000 Hz followed by a return toward better hearing at still higher frequencies (8000 Hz), a pattern that typifies a noise notch, this is not always readily apparent for individual data. Discerning a noise notch in the pattern of hearing loss may be especially challenging in older adults for whom age-related hearing loss is super-imposed on a preexisting noise notch (see pp. 62–63). As a result, there
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Noise and Military Service: Implications for Hearing Loss and Tinnitus have been attempts to define the presence or absence of a noise notch more objectively than by simply relying on visual inspection of the pattern of hearing loss in the high frequencies, the latter approach not being particularly reliable (e.g., McBride and Williams, 2001a,b). One such approach to objectively define the presence or absence of a noise notch was advocated initially by Coles et al. (2000) and further refined by Dobie and Rabinowitz (2002). A graphic demonstration is provided by drawing a line to connect the hearing thresholds at 1000 and 8000 Hz, as illustrated by the dashed line in Figure 2-3. Having thresholds between 1000 and 8000 Hz (especially those at 2000, 3000, and 4000 Hz) that fall at or below the dashed line is thought to indicate the presence of a high-frequency notch in the hearing loss. Dobie and Rabinowitz (2002) describe a corresponding metric, referred to as the notch index (NI), that is simply the mean of the hearing thresholds at 1000 and 8000 Hz subtracted from the mean of the hearing thresholds at 2000, 3000, and 4000 Hz. Values of NI greater than 0 dB are thought to indicate the presence of a notch, whereas those less than 0 dB do not. For the hearing thresholds displayed in Figure 2-3, the notch index is 12 dB and is consistent with poorer hearing thresholds at 2000–4000 Hz than at 1000 and 8000 Hz. Other approaches to objective determination of the presence or absence of a noise notch have been described previously (e.g., Gates et al., 2000). The simplicity of the notch index and similar metrics is appealing, although additional research is needed to establish its reliability, as well as sensitivity and specificity in the identification of noise-induced hearing loss in the general population. In summary, there are four key acoustic parameters of a given noise exposure that determine the type and amount of the resulting hearing loss. These are the sound pressure level of the noise, the duration and temporal pattern of the exposure (hours/day, impulses/day, number of years), the type of noise (steady-state, impulse/impact, blast), and the spectral content of the noise. Knowledge of values for each of these four parameters is necessary, but not sufficient, to fully assess the hazard of a given exposure to hearing. Although there can be some variation in the audiometric pattern of hearing loss for pure-tone thresholds following exposure to noise, the hallmark of noise-induced hearing loss is a characteristic noise notch in the audiogram that typically occurs between 3000 and 6000 Hz. Effects of Noise on the Structure of the Hearing Apparatus Acoustic trauma can occur following exposure to very intense noise, typically blasts > 150 dBA. Humans experiencing blasts at very high sound levels (~ 180 dB SPL) may suffer damage to the middle ear, including hemorrhage in or perforation of the eardrum and fracture of the malleus (Davis et al., 1949; Hirsch, 1968; Ward, 1973; Henderson et al., 1974b;
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Noise and Military Service: Implications for Hearing Loss and Tinnitus Roberto et al., 1989). If the eardrum does not rupture during such an intense exposure, the organ of Corti is likely to rupture off the basilar membrane (Ward, 1973; Henderson et al., 1974a,b; Roberto et al., 1989). When a portion of the organ of Corti ruptures, it does not reattach to the basilar membrane. Rather, it eventually degenerates. As noted, the hearing loss associated with acoustic trauma often is severe and spans a wide range of frequencies, much broader than that represented by the high-frequency, noise-notch pattern of hearing loss associated with other types of noise exposures. Because sound levels in areas free from reflective surfaces, known as free fields, decay 6 dB per doubling of distance from the sound source, a key factor in such exposures may be the proximity of the individual to the blast. For example, consider two individuals, A and B, such that A is located 1 meter from a blast and the sound level recorded at that location was 160 dBA. Individual B, on the other hand, is located 32 meters from this same blast. Assuming that the blast can be modeled as a point source in a free field, the sound level at the location occupied by B will be 130 dBA. Whereas A may experience acoustic trauma from such a blast, including the development of a severe hearing loss affecting a wide range of frequencies, this will be much less likely for B, who might, through repeated such exposures over time, develop the more common noise-notch pattern of hearing loss. Importantly, individuals A and B may each subsequently report having heard a loud blast in a case history, but the hazard to hearing will be much greater for individual A, who is closer to the blast. Observations from Operation Iraqi Freedom suggest that even when personnel are close enough to suffer a blast injury that results in medical evacuation, four out of ten such individuals escape without permanent hearing loss, although many do experience acoustic trauma resulting in a severe or profound hearing loss (Chandler, 2005). Individuals with mild or moderate permanent noise-induced hearing losses typically have some structural damage in their cochleas. The damage may initially involve scattered loss of sensory cells, primarily outer hair cells, in the organ of Corti (undamaged sensory cells shown in Figures 2-2 and 2-4, part A). Permanent noise-induced hearing loss may also result in damage to or destruction of other important structures in the cochlea, including fibrocytes in the spiral ligament and limbus and cells of the stria vascularis (Liberman and Mulroy, 1982; Hirose and Liberman, 2003) (Figure 2-2). In humans and other mammals, outer hair cells are usually the first type of sensory cell to be damaged or destroyed by excessive noise (Bredberg, 1968; McGill and Schuknecht, 1976) (Figure 2-4, part B). With larger permanent hearing losses, the degeneration involves both outer and inner hair cells (Bredberg, 1968; Liberman and Mulroy, 1982; Bohne and Harding, 2000) (Figure 2-4, part C). With severe permanent hearing losses,
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Noise and Military Service: Implications for Hearing Loss and Tinnitus FIGURE 2-4 Drawings of the organ of Corti showing: (A) undamaged organ of Corti where all inner hair cells (IHC) and outer hair cells (OHC 1, 2, 3) are present; (B) beginning noise damage where 3 outer hair cells are missing (arrows); (C) moderate noise damage where 11 outer hair cells and 1 inner hair cell are missing (extent of loss indicated by arrows); and (D) severe noise damage where an entire portion of the organ of Corti is absent and is replaced on the basilar membrane (BM) by an undifferentiated, squamous epithelium. Nerve fibers to the area are also missing. TM = tectorial membrane. SOURCE: Modified from an original painting by David Bellucci.
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Noise and Military Service: Implications for Hearing Loss and Tinnitus a variable amount of the organ of Corti (i.e., both sensory and supporting cells) is missing. In these cases, an undifferentiated layer of squamous epithelium covers the basilar membrane where the organ of Corti degenerated, and the nerve fibers that originally innervated the missing sensory cells also disappear (Johnsson and Hawkins, 1976; McGill and Schuknecht, 1976; Bohne and Harding, 2000) (Figure 2-4, part D). The time course of cell degeneration and scar formation in the cochlea following a damaging noise exposure can be determined from animal studies only. A number of studies have shown that outer hair cells often begin to degenerate during an exposure. Additional outer hair cells, as well as inner hair cells and various supporting cells, may degenerate for days to a few weeks following termination of the exposure. While the various cells are degenerating, scars are forming in the organ of Corti. Phalangeal scars, formed from supporting-cell processes, replace missing hair cells, and squamous epithelial scars, formed from supporting cells on the basilar membrane, replace degenerated portions of the organ of Corti. Nearly all scar formation is completed by 1 month postexposure (e.g., Stockwell et al., 1969; Bohne, 1976; Fredelius, 1988; Wang et al., 2002). Although there are some exceptions, especially for high-intensity, low-frequency sounds (e.g., Jerger et al., 1966; Burdick et al., 1978; Mills et al., 1983), good consistency has been observed in human and animal studies between the frequency content of the exposure stimulus and the location in the cochlea experiencing the greatest damage or injury (e.g., Johnsson and Hawkins, 1976; Moody et al., 1976). For narrow-band stimuli, the maximum cochlear insult is often one-half to one octave higher in frequency than the exposure stimulus (Ward, 1973). For broad-band noises and impulses, much more commonly encountered in military and industrial settings, the damage is greatest in the high-frequency (i.e., basal) portion of the cochlea (e.g., Gravendeel and Plomp, 1959; Ward, 1973; Ylikoski and Ylikoski, 1994). Furthermore, these differences in location of the greatest cochlear damage are accurately reflected in the pattern of hearing loss. For example, the noise-notch pattern of hearing loss (Figure 2-3) is associated with underlying damage to the sensory cells in the basal portion of the cochlea; that is, the portion of the cochlea tuned to those frequencies. In addition, as suggested by the sequence of illustrations shown in Figure 2-4, there is also a positive correlation between the amount of damage at a particular location in the cochlea and the severity of the hearing loss measured for a frequency associated with that location, although this correlation is believed to be weaker for low-frequency sounds (e.g., Bredberg, 1968). The pattern of hearing loss measured following noise exposure provides valuable information about the extent and severity of the underlying damage, especially in the middle and high frequencies following exposures to broad-band sounds.
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Noise and Military Service: Implications for Hearing Loss and Tinnitus FIGURE 2-6 Age-related hearing loss for men (ISO-1999, database A, top panel) and hypothetical progression of noise-induced hearing loss with increased length of exposure in years (bottom panel). The bottom panel displays hypothetical NIPTS in dB, as well as the noise-only hearing loss data plotted in dB HL.
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Noise and Military Service: Implications for Hearing Loss and Tinnitus hearing loss at 8000 Hz. This demonstrates the characteristic noise-notch pattern of hearing loss in which the notch is located at 6000 Hz. As noted previously, the notch location varies with the noise exposure and across individuals experiencing the same noise exposure, but it is generally located at 3000, 4000, or 6000 Hz. A noise notch located at 6000 Hz was chosen for illustration purposes in the bottom panel of Figure 2-6 because of the frequent appearance of notches at this frequency in the data on military noise-induced hearing loss reviewed subsequently in Chapter 3. Perhaps, therefore, the pattern of hearing loss across frequency can assist in determining how much, if any, of an older adult’s hearing loss can be attributed to prior noise exposure. That is, rather than just considering the hearing threshold at one frequency for the two 70-year-old individuals, A and B, in our previous example, one of whom had no prior noise-induced hearing loss and the other who had sizable noise-induced hearing loss, perhaps the presence or absence of a noise notch will assist in sorting this out. To examine the impact of aging on the pattern of hearing loss across frequency, the additivity model of ISO-1999 and ANSI S3.44 was applied to the two sets of data in the top and bottom panels of Figure 2-6. The top panel was assumed to represent a “pure” age-related hearing loss for each age decade, and the bottom panel was interpreted as four different degrees of noise notch developed in four young men during the first few years of noise exposure (rather than the progression of noise-induced hearing loss over time, as originally indicated). The case represented by the “45-dB notch” has a threshold at 4000 Hz that is about 40 dB HL and is representative of individual A in our previous examples. Individual B, on the other hand, was assumed to have no noise-induced hearing loss, and thresholds for this individual would be best represented by the age-only curves (“no notch”) depicted in the top panel of Figure 2-6. Figure 2-7 illustrates the combined effects of noise (noise notches of various depths) and age (50-, 60-, 70-, and 80-year-olds) that result from using the ISO/ANSI additivity model to combine the sets of hearing thresholds from the two panels of Figure 2-6. When examining the predictions for each age, clear notching is visible in patterns of hearing loss for those individuals with initial noise-notch patterns at ages 50 and 60 years, but appears to be absent at ages 70 and 80 years. The other clear trend with age is the convergence of all the hearing losses by the age of 80 years. Hearing losses that differed by about 50 dB in the high frequencies for 50-year-olds differ by about half that much for 80-year-olds. Thus, there is less difference in pattern of hearing loss by the time these individuals reach their 70s and 80s, and the severity of the loss no longer differs as much among these individuals. As a result, two individuals who have similar hearing thresholds when measured at 70 or 80 years of age may have had entirely different patterns of hearing loss as young adults and throughout much of their
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Noise and Military Service: Implications for Hearing Loss and Tinnitus FIGURE 2-7 Illustrations of the combined effects of aging (top panel from Figure 2-6) and noise exposure (bottom panel from Figure 2-6) using the ISO-1999/ANSI S3.44 model for additivity. Each panel depicts the combined hearing loss for a separate decade (50-, 60-, 70-, or 80-year-old men). adult lives. Once again, this underscores the critical importance of measuring hearing thresholds periodically (preferably annually) for individuals exposed to noise and, ideally, before and after employment or military service. With only the hearing thresholds from a much later stage in life, it is virtually impossible to discern how much, if any, of an individual’s hearing loss can be attributed to noise exposure or for how long this hearing loss might have been present.
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Noise and Military Service: Implications for Hearing Loss and Tinnitus With regard to the estimation of noise-induced hearing loss, the following represents a summary of the main points of this section of the chapter: Without measurement of pure-tone thresholds prior to and following a given exposure to noise, it is impossible to document the effects of that exposure on hearing or to know what portion of the hearing loss in an older individual is due to earlier noise exposure. ISO-1999 and ANSI S3.44 provide estimates of median values and range of variation in noise-induced hearing loss for a given noise exposure. Predictions are best for the noise-induced hearing loss that results from continuous or intermittent exposures to steady-state noise at levels between 75 and 100 dBA for 8 hours per day (for an assumed 5-day work week) for periods of 10 to 40 years. Age-related hearing loss occurs at several of the same frequencies for which noise-related hearing loss occurs, and the measured thresholds are presumed to be a combination of these two forms of hearing loss. Combined effects of noise and age on hearing thresholds range from energy summation to decibel summation. The combined effects of noise and age included in ISO-1999 and ANSI S3.44 lie somewhere between these two extremes. FINDING: The evidence from cross-sectional studies of noise-induced hearing loss in humans is sufficient to conclude that daily time-weighted average noise exposures greater than approximately 85 dBA for 8 hours for periods of many years pose a hazard to human hearing and that the hazard increases as the time-weighted average exposure exceeds this value. FINDING: The evidence is not sufficient to determine the probability of acquiring a noise-induced hearing loss, or to estimate the magnitude of the noise-induced hearing loss, that a specific individual is likely to experience from a given noise exposure. REFERENCES ANSI (American National Standards Institute). 1996. ANSI S3.44 Determination of Occupational Noise Exposure and Estimation of Noise-Induced Hearing Impairment. New York: Acoustical Society of America. Aran JM, Hiel H, Hayashida T, Erre JP, Aurousseau C, Gulhaume A, Dulon D. 1992. Noise, aminoglycosides, and diuretics. In: Dancer AL, Henderson D, Salvi RJ, Hamernik RP, eds. Noise-Induced Hearing Loss. St. Louis, MO: Mosby Year Book. Pp. 188–195. Axelsson A, Vertes D. 1982. Histological findings in cochlear vessels after noise. In: Hamernik RP, Henderson D, Salvi R, eds. New Perspectives on Noise-Induced Hearing Loss. New York: Raven Press. Pp. 49–68.
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Representative terms from entire chapter: