4
Tinnitus

Tinnitus is a perceived sound that cannot be attributed to an external sound source (Eggermont, 2003). It is a subjective phenomenon, perceivable only by the person who is experiencing it.1 The committee was asked to review the evidence regarding noise levels that can cause tinnitus and other risk factors for tinnitus.

This chapter first provides a brief overview of the features of tinnitus, its impact on individuals with the condition, and approaches to its clinical assessment and treatment. Some of the issues that arise in studying tinnitus are noted, and basic data on its occurrence in the general population are presented. The major portion of the chapter focuses on a review of epidemiological data on the relationship between tinnitus and noise exposure, hearing loss, and other risk factors. Important features of studies reviewed by the committee are summarized in Table D-6 in Appendix D. The chapter

1  

Tinnitus is distinct from other acoustic events that can be generated in the head or neck regions and reach perception. Some of these events include vascular pulsations, palatal and intratympanic myoclonus, patulous Eustachian tube, jugular outflow syndrome, and cervical crepitus. Although these effects have been referred to as “objective tinnitus” (see Hazell, 1995), the term “somatosounds” (Anonymous, 1981) better describes these phenomena. Use of the term somatosounds provides a clearer distinction between acoustic events generated within the body and the completely subjective perception of tinnitus.

The condition referred to as “pulsatile tinnitus” can be a somatosound or a neural event induced within the brain, usually by a dilated arterial loop affecting the auditory nerve (De Ridder et al., 2005). However, this phenomenon is not related to tinnitus associated with noise exposure, and the specifics of this distinction are beyond the scope of the committee’s report.



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Noise and Military Service: Implications for Hearing Loss and Tinnitus 4 Tinnitus Tinnitus is a perceived sound that cannot be attributed to an external sound source (Eggermont, 2003). It is a subjective phenomenon, perceivable only by the person who is experiencing it.1 The committee was asked to review the evidence regarding noise levels that can cause tinnitus and other risk factors for tinnitus. This chapter first provides a brief overview of the features of tinnitus, its impact on individuals with the condition, and approaches to its clinical assessment and treatment. Some of the issues that arise in studying tinnitus are noted, and basic data on its occurrence in the general population are presented. The major portion of the chapter focuses on a review of epidemiological data on the relationship between tinnitus and noise exposure, hearing loss, and other risk factors. Important features of studies reviewed by the committee are summarized in Table D-6 in Appendix D. The chapter 1   Tinnitus is distinct from other acoustic events that can be generated in the head or neck regions and reach perception. Some of these events include vascular pulsations, palatal and intratympanic myoclonus, patulous Eustachian tube, jugular outflow syndrome, and cervical crepitus. Although these effects have been referred to as “objective tinnitus” (see Hazell, 1995), the term “somatosounds” (Anonymous, 1981) better describes these phenomena. Use of the term somatosounds provides a clearer distinction between acoustic events generated within the body and the completely subjective perception of tinnitus. The condition referred to as “pulsatile tinnitus” can be a somatosound or a neural event induced within the brain, usually by a dilated arterial loop affecting the auditory nerve (De Ridder et al., 2005). However, this phenomenon is not related to tinnitus associated with noise exposure, and the specifics of this distinction are beyond the scope of the committee’s report.

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Noise and Military Service: Implications for Hearing Loss and Tinnitus concludes with a discussion of tinnitus in the context of military service and a proposal for monitoring tinnitus among U.S. military personnel. BACKGROUND Tinnitus is often referred to as “ringing in the ears,” reflecting a characterization of the sound that individuals commonly report. Other descriptions of the perceived sound include buzzing, hissing, whistling, and humming (e.g., Alberti, 1987; Stouffer and Tyler, 1990; Mrena et al., 2002). Reports of other characteristics of tinnitus also vary. Tinnitus induced by noise exposure, for example, is often described as high-pitched (e.g., Melinek et al., 1976; Man and Naggan, 1981; Cahani et al., 1983; Alberti, 1987; Chermak and Dengerink, 1987; Stouffer and Tyler, 1990), whereas tinnitus associated with Ménière’s disease2 has been described as a low-pitched sound (NRC, 1982). Tinnitus can be transient or persistent. Some studies define persistent or prolonged tinnitus as lasting at least 5 minutes (e.g., Coles, 1984; Parving et al., 1993; Palmer et al., 2002; Sindhusake et al., 2003b). Persistent tinnitus can be perceived continuously (all or most of the time) or occasionally. A given episode of tinnitus may also resolve, with new episodes possible in the future. Tinnitus is considered a symptom rather than an illness (NRC, 1982). It is associated with many conditions, including noise exposure and noise-induced hearing loss. Among the other conditions that may cause or be accompanied by tinnitus are presbycusis, Ménière’s disease, otosclerosis, head injury, cerebellar-pontine angle tumors, otitis media, meningitis, dental disorders, and exposure to certain medications (e.g., salicylates, aminoglycoside antibiotics, and some chemotherapy agents) (Lockwood et al., 2002). It is not always possible to identify a precipitating cause of tinnitus. A survey of tinnitus patients found that only 54 percent attributed their tinnitus to a particular cause (Stouffer and Tyler, 1990). The onset of tinnitus is described by some as gradual and by others as sudden (Axelsson and Barrenas, 1992). In a population-based study of older adults, 55 percent of participants with tinnitus reported a gradual onset, 24 percent reported a sudden onset, and the remainder did not know (Sindhusake et al., 2003b). Uncertainty about the onset of tinnitus can make the identification of a precipitating cause challenging. Individuals differ in their susceptibility and reaction to tinnitus. The reasons for these differences are not known but are likely related both to 2   Ménière’s disease is a disorder of the inner ear affecting balance and hearing (the audio-vestibular system), characterized by abnormal sensations of movement (vertigo), dizziness, loss of hearing in one or both ears, and tinnitus.

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Noise and Military Service: Implications for Hearing Loss and Tinnitus the magnitude and quality of the perceived tinnitus and to the psychological makeup, life experiences, and current stress factors of the individual. The mechanisms underlying tinnitus are not completely understood. Generally, it is reasonable to presume that the involvement of central components of the auditory system “results in” the perception of sound. In addition, if there is an emotional reaction to the tinnitus, other areas of the central nervous system that are involved in emotionally charged events, such as the amygdala, are activated (e.g., Aggleton and Mishkin, 1986; LeDoux, 2000; see Cacace, 2004, for a review). The actual site of the origin of the tinnitus could be anywhere in the auditory system but likely includes the auditory periphery in many if not most cases. Other areas in the brain that relate to vision, touch, and movement can also affect tinnitus in some instances (Baguley, 2002; Cacace, 2003; Eggermont, 2003). As tinnitus is usually accompanied by hearing loss, similar mechanisms are likely involved. Experimental studies of noise-induced tinnitus present a relatively homogeneous and consistent body of research. (This is in contrast to pharmacological manipulations to induce tinnitus, which result in more varied effects.) In these studies, noise exposure results in cochlear hair cell damage (see Chapter 2). Perhaps surprisingly, spontaneous neural activity arising from the auditory nerve is lost or significantly diminished following noise damage. However, increases in spontaneous neural activity have been found in brainstem and cortical regions. For example, following exposure to intense sound, the dorsal cochlear nucleus has been implicated in consistently producing and/or modulating hyperactive neural activity, which may serve as a trigger or generator site for tinnitus (Kaltenbach et al., 2005). A common hypothesis for tinnitus in this instance is a “release from inhibition,” and in some instances, this may contribute to reactive changes (reorganization) at more central locations in the auditory system. Thus, tinnitus might be initiated by a discontinuity in the spontaneous activity across auditory nerve fibers with different characteristic frequencies, which may result in the reduction of lateral inhibition and produce changes in tonotopic maps in the auditory cortex (e.g., Muhlnickel et al., 1998; Salvi et al., 2000; Eggermont, 2003; see Eggermont and Roberts, 2004, for a review). This supposes that the effects of noise exposure and subsequent hearing loss disrupt the delicate balance between excitation and inhibition in the central auditory pathways. The possibility that the onset of noise-induced tinnitus might be delayed by months has been raised because studies in laboratory animals have shown that degenerative processes initiated by the noise exposure continue in central auditory pathways after termination of the exposure (Kim et al., 1997; Morest et al., 1998). Although degenerative changes in afferent pathways will most likely not affect auditory thresholds, it is possible that they

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Noise and Military Service: Implications for Hearing Loss and Tinnitus could contribute to other central processes such as tinnitus. The time required for this reorganization might vary across individuals and potentially could be a long-term process. However, as the interval between a noise exposure and the onset of tinnitus lengthens, the possibility that tinnitus will be triggered by other factors increases. A more complete understanding of the mechanisms by which tinnitus is generated will be needed before the existence of delayed onset of noise-induced tinnitus can be confirmed or rejected. Impact of Tinnitus Most people with tinnitus report few problems, but for some individuals, tinnitus can be a life-altering experience. The adverse effect of tinnitus can impair psychological well-being and the ability to function in social and professional settings (Stephens and Hallam, 1985; Wilson et al., 1991; Tyler, 1993; Meric et al., 1998). For those affected, problems occur with their emotional health, hearing, sleep, and concentration (Axelsson and Sandh, 1985; Mrena et al., 2002; Tyler et al., 2004). Tinnitus has also been reported to induce fear, frustration, anger, irritability, and anxiety (Erlandsson et al., 1991; Halford and Anderson, 1991; Dineen et al., 1997; Andersson et al., 2001; Mrena et al., 2002; reviewed in Erlandsson, 2000). Depression or depressive symptoms may be contributing factors for some individuals who experience serious distress from tinnitus (Erlandsson, 2000; Dobie, 2003). A potential link to suicide has been suggested for severe cases, but depression or other relevant factors may exist (Jacobson and McCaslin, 2001). For some people, the impact of tinnitus may be worse than the impact of an accompanying hearing loss (Salmivalli, 1967; Axelsson and Barrenas, 1992; Mrena et al., 2002). Clinical Assessment and Treatment Currently, the assessment of tinnitus involves psychoacoustical measures and self-reporting by patients. Psychoacoustical assessment of tinnitus attributes, such as pitch and loudness, and validated questionnaires offer a standardized basis for characterizing the perceived magnitude of tinnitus and its impact. In addition, these measures can help in identifying treatment needs, selecting treatment approaches, and monitoring the status of tinnitus over time. In psychoacoustical testing, patients compare the perceived pitch and loudness of their tinnitus with defined sounds presented under controlled conditions (for reviews, see Tyler, 2000; Vernon and Meikle, 2003; Henry, 2004). Self-report questionnaires widely used to assess the impact of tinnitus include the Tinnitus Handicap Questionnaire (Kuk et al., 1990), the Tinnitus Reaction Questionnaire (Wilson et al., 1991), and the Tinnitus

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Noise and Military Service: Implications for Hearing Loss and Tinnitus Handicap Inventory (Newman et al., 1996). (For reviews, see Erlandsson, 2000; Tyler, 1993, 2000; Noble, 1998; Wilson and Henry, 2000.) See Box 4-1 for examples of questions from these assessment instruments. The quality, pitch, and loudness of tinnitus influence the subjective annoyance (as they do for all sounds), but other factors can also be important. The degree of annoyance caused by tinnitus is influenced by both the characteristics of the tinnitus and an individual’s personality (Axelsson and Sandh, 1985; Dauman and Tyler, 1992). Some people with tinnitus do not seek treatment, but others do. Axelsson and Ringdahl (1989) found that of the survey respondents who described their tinnitus as always present, 25 percent felt an “urgent” need for treatment. Of those who experienced tinnitus “often,” 6 percent reported an urgent need for treatment. In a population-based study of older adults, 37 percent of those who had tinnitus had sought care and 6 percent received some form of treatment (Sindhusake et al., 2003b). Among a group of workers with tinnitus and newly detected hearing loss, 14 percent consulted a physician (Phoon et al., 1993). For people with tinnitus who do seek treatment, a thorough evaluation includes a comprehensive medical examination of body systems with spe- BOX 4-1 Sample Questions from Questionnaires Used to Assess the Impact of Tinnitus Tinnitus Handicap Questionnaire (Kuk et al., 1990) Subjects rate their agreement with 27 items using a scale from 0 (strongly disagree) to 100 (strongly agree). I do not enjoy life because of tinnitus Tinnitus causes me to avoid noisy situations I think I have a healthy outlook on tinnitus Tinnitus Reaction Questionnaire (Wilson et al., 1991) Subjects rate 26 items, using a 5-point scale (0 = not at all; 1 = a little of the time; 2 = some of the time; 3 = a good deal of the time; 4 = almost all of the time). My tinnitus has made me unhappy My tinnitus has made me feel tense My tinnitus has interfered with my ability to work Tinnitus Handicap Inventory (Newman et al., 1996) Subjects report their endorsement of 25 items (yes, sometimes, no). Because of your tinnitus is it difficult for you to concentrate? Does your tinnnitus make you angry? Do you feel that you have no control over your tinnitus?

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Noise and Military Service: Implications for Hearing Loss and Tinnitus cial attention to the head, neck, cranial nerves, medications, drug use, and psychiatric history (e.g., depression) (Tyler and Babin, 1986; Shulman, 1997; Dobie, 2003). Tinnitus associated with certain medical conditions (e.g., tumors and some infections) may resolve when those conditions are treated. No current form of treatment can eliminate tinnitus arising from many other causes, but some treatments may lessen the adverse impact of tinnitus. Treatment approaches being used include counseling, counseling combined with sound therapies, antidepressants and other medications, electrical stimulation at the ear, and transcranial magnetic stimulation over specific areas of the brain (e.g., Hazell and Wood, 1981; Hazell, 1995; Dobie, 1999; Dauman, 2000; Sweetow, 2000; Vernon and Meikle, 2000; Wilson and Henry, 2000; Young, 2000; Jastreboff and Jastreboff, 2003; Plewnia et al., 2003; Rubinstein et al., 2003; Tyler and Cacace, 2004; Tyler et al., 2004; Kleinjung et al., 2005). ISSUES IN STUDYING TINNITUS A significant advance in exploring mechanisms of tinnitus has been research on the development of behavioral animal models of tinnitus (e.g., Jastreboff et al., 1988a,b; Bauer et al., 1999; Bauer and Broznoski, 2001; Heffner and Harrington, 2002; Bauer, 2003; Lobarinas et al., 2004; Moody, 2004). Experimental work has been instrumental in gaining insight into the anatomical loci and neural codes for noise-induced tinnitus (e.g., increases in spontaneous neural activity, bursting, synchronous discharges among different neurons) by combining behavioral verification with detailed physiologic recordings (e.g., Kaltenbach et al., 2004a; for a review, see Kaltenbach et al., 2004b). Experimental studies have also been conducted with humans, but such studies must be designed to protect subjects from permanent injury. Temporary tinnitus has been elicited in response to well-defined noise exposures (e.g., Loeb and Smith, 1967; Chermak and Dengerink, 1987; George and Kemp, 1989). It is not clear, however, that this transient tinnitus is comparable to the more persistent form that is the source of concern in most epidemiological and clinical studies. Furthermore, the experimental noise exposures may not be representative of “real-world” noise exposures. Epidemiological studies are the most common means of assessing the prevalence of tinnitus in the population and determining the factors that are associated with higher rates of tinnitus. However, these observational studies do not permit random assignment of subjects to exposures of interest. Most studies of tinnitus are cross-sectional rather than longitudinal. Documentation of past exposures to noise and other risk factors is rarely available. With retrospective reports, the timing and magnitude of those exposures or their comparability across study participants cannot be determined.

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Noise and Military Service: Implications for Hearing Loss and Tinnitus Furthermore, with no objective basis for detecting or characterizing tinnitus, studies have used various definitions of tinnitus and different methods to elicit reports on whether and how tinnitus was experienced. OCCURRENCE OF TINNITUS Little is known about the incidence of tinnitus, that is, the number of new cases that develop in a population during a given period. Tinnitus can arise without a distinctive precursor (Alberti, 1987; Stouffer and Tyler, 1990; Axelsson and Prasher, 2000), and retrospective assessments of the timing of its onset are vulnerable to recall errors. A rare prospective, population-based assessment of the incidence of tinnitus among older adults (ages 48–92 years at baseline) in Beaver Dam, Wisconsin, found that 6 percent developed tinnitus over a 5-year period (Nondahl et al., 2002). The incidence of tinnitus in this older population was not associated with age or gender. Several reports offer some perspective on the prevalence of tinnitus in the United States (see Table 4-1). Data from national surveys during the 1990s (Adams et al., 1999; Hoffman and Reed, 2004) showed prevalence rates for adults (ages 18 or 20 years and older) ranging from 4 to 8 percent. An earlier prevalence estimate from a nationally representative health examination survey conducted in the United States in 1960–1962 found that 6 percent of adults (ages 18–79 years) reported what was classified as “severe” tinnitus and 27 percent had “mild” tinnitus (Roberts, 1968). The study of older adults in Beaver Dam (Nondahl et al., 2002) found that 9 percent of men and 8 percent of women reported “significant tinnitus,” which was defined in the study as tinnitus experienced during the past year that the respondent rated as at least moderately severe or as causing problems getting to sleep. Overall, 2 percent of the study participants reported that their tinnitus was severe (Nondahl et al., 2002). With an alternative definition of tinnitus (“buzzing, ringing, or noise in your ears in the past year that usually lasts longer than 5 minutes”), the prevalence estimate was 18 percent at a 5-year follow-up of this population (Nondahl et al., 2004). Studies in Europe and Australia, using various definitions of tinnitus and study populations of various ages, have produced prevalence estimates ranging from about 10 to 15 percent in people 20 years of age and older and from 14 to 30 percent in people 50 years of age and older (see Table 4-1). Whether age is an independent risk factor for tinnitus is unclear. The prevalence of tinnitus is generally higher at older ages, but the rates at the oldest ages are not always the highest (see Table 4-1). A multivariate analysis of a subset of the data collected in a 1994–1995 study of U.S. adults found significant age-related differences in the prevalence of tinnitus. Compared with those ages 20–24 years, the likelihood of having tinnitus was

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Noise and Military Service: Implications for Hearing Loss and Tinnitus greatest for persons ages 65–74 years (odds ratio [OR] 4.08, 95% confidence interval [CI] 3.25–5.12) (Hoffman and Reed, 2004). In contrast, an analysis of Norwegian data on the prevalence of “bothersome tinnitus” showed no significant age-related differences for women and a significant difference for men only for the age group 45–54 years (OR 1.30, 95% CI 1.06–1.60) (Hoffman and Reed, 2004). In these cross-sectional studies, the possibility of underlying differences among age cohorts must be considered along with any effects of aging or tinnitus risk factors, such as hearing loss, that may themselves be related to age. Multivariate analyses are also available from two community-based studies limited to older adults. One study (study population ages 48–92 years) found a significant reduction in the likelihood of having tinnitus with increases in age (OR 0.84, 95% CI 0.78–0.90) (Nondahl et al., 2002). The other study (study population ages 55 years and older) found no significant difference in tinnitus prevalence by age (Sindhusake et al., 2003b). TINNITUS AND NOISE EXPOSURE Tinnitus may occur following a single exposure to high-intensity impulse noise, long-term exposure to repetitive impulses, long-term exposure to continuous noise, or exposure to a combination of impulses and continuous noise (Loeb and Smith, 1967; Chermak and Dengerink, 1987; Metternich and Brusis, 1999; Temmel et al., 1999; Stankiewicz et al., 2000; Mrena et al., 2002). To assess the association between tinnitus and noise exposure, the committee reviewed reports from studies of the general population, workers in high-noise environments, military personnel, and persons who experienced acoustic trauma. These studies are described in the next several sections. The discussion concludes with summary observations drawn from across these study populations and the committee’s findings regarding tinnitus and exposure to noise in general, as well as impulse noise in particular. Tinnitus and Noise Exposure in the General Population Population-based studies provide a mixed picture of the association between noise exposure and tinnitus. In such studies, quantitative data on noise doses or noise levels are not available. Noise exposure is commonly represented by indicators such as occupation or qualitative characterizations of the level of workplace noise. A multivariate analysis of U.S. data from a special supplement to the 1994 National Health Interview Survey found that veterans of military service had an increased likelihood of having chronic tinnitus (has lasted for at least 3 months) compared with those who had not served in the military (OR 1.29, 95% CI 1.17–1.43) (Hoffman and Reed, 2004). In this study

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Noise and Military Service: Implications for Hearing Loss and Tinnitus TABLE 4-1 Prevalence of Tinnitus in Adults by Age Group, from Selected Studies Study N U.S. Health Examination Survey, 1960–1962 6,672 National Study of Hearing, United Kingdom, 1980–1986 34,050 Gothenberg, Sweden, 1989 2,556 U.S. National Health Interview Survey: Hearing Supplement, 1990 59,343 U.S. National Health Interview Survey: Disability Supplement, 1994–1995 99,435 Epidemiology of Hearing Loss Study, Beaver Dam, Wisconsin, 1993–1995 3,737 Nord Trøndelag Hearing Loss Study, Norway, 1996–1998 47,410 Blue Mountains Hearing Study, Australia, 1997–1999 2,015 NOTES: Definitions of tinnitus used in each study: U.S. Health Examination Survey: Noticed ringing in the ears or bothered by other funny noises at any time over the past few years and bothered “quite a bit” by the noise (severe tinnitus). Age groups are 18–34, 35–44, 45–54, 55–64, 65–74, 75–79. National Study of Hearing: “Prolonged spontaneous tinnitus” that lasts for more than 5 minutes and occurs not only after loud sounds. Gothenberg, Sweden: An ear noise that occurs often or always and sounds like a peep, chirping, roaring, wind blowing in the trees, etc. U.S. National Health Interview Survey, Hearing Supplement: Having been bothered by ringing in the ears or other funny noises in the head in the past 12 months. population, 29 percent of veterans and 15 percent of nonveterans reported having chronic tinnitus. Similar rates were seen in data from a 1990 supplement to the National Health Interview Survey: 21 percent of veterans and 14 percent of nonveterans reported “bothersome” tinnitus (Hoffman and Reed, 2004). (Measures of the statistical significance of the difference were not presented.) In age- and gender-adjusted comparisons between occupational groups, the 1994 data showed a marginally significant elevation in the prevalence of tinnitus among skilled and unskilled workers compared with professionals (OR 1.18, 95% CI 1.00–1.39), but no significant differences between professionals and other occupational groups. These analyses of the National Health Interview Survey data used responses obtained only from direct self-reporting on tinnitus and excluded proxy responses. In the 1990 data, one-third of the reports had come from proxy respondents. The effect on the results of any selection biases associated with reporting (the respondents themselves or proxy respondents) is not known.

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Noise and Military Service: Implications for Hearing Loss and Tinnitus Prevalence (%) Age (years) Total Adult 20–29 30–39 40–49 50–59 60–69 70–79 ≥80 ≥50 3 4 6 9 12 11 — 10 6 6 7 10 13 16 14 14 14 10 8 6 9 19 20 21 — 20 14 5 6 7 10 13 13 14 12 8 1 2 4 6 8 9 8 8 4 — — — 7 10 9 6 8 — 10 10 12 17 20 24 23 20 15 — — — 28 33 31 25 30 — U.S. National Health Interview Survey, Disability Supplement: Now have a ringing, roaring, or buzzing in the ears that has lasted for at least 3 months (chronic tinnitus). Epidemiology of Hearing Loss Study: Buzzing, ringing, or noise in the ears in the past year of at least moderate severity and/or tinnitus that caused difficulty in falling asleep (significant tinnitus). Nord Trøndelag Hearing Loss Study: Bothered by ringing in the ears. Blue Mountains Hearing Study: Experienced any prolonged (lasting 5 minutes or longer) ringing, buzzing, or other sounds in the ears or head within the past year. SOURCES: Roberts (1968); Sindhusake et al. (2003b); Hoffman and Reed (2004). The data from Norway on bothersome tinnitus showed a significantly higher likelihood of having the condition among both men and women who had been exposed to loud noise at work (“difficult to have a conversation”) for more than 5 hours per week (Tambs et al., 2003; Hoffman and Reed, 2004). The odds ratio for men exposed for more than 15 hours per week was 1.70 (95% CI 1.53–1.87) compared with men who had not been exposed to loud noise at work. Frequent exposure to impulse noise significantly (and similarly) increased the likelihood of having tinnitus for both men and women. For men, the odds ratio for a history of exposure to impulse noise was 1.78 (95% CI 1.61–1.96). Tinnitus was significantly related to occupational noise exposure among working-age British men (Palmer et al., 2002). The prevalence of tinnitus was 13 percent for those who had worked in a noisy job for more than 10 years and 5 percent for men with no noise exposure: an age-adjusted rate ratio of 2.6 (95% CI 2.0–3.4). Earlier British data also showed rates of

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Noise and Military Service: Implications for Hearing Loss and Tinnitus tinnitus that were about twice as high among persons reporting having worked in a noisy environment for more than 6 months (24 percent) as among those who had not worked in noise (14 percent) (Medical Research Council’s Institute of Hearing Research, 1981). The pattern was similar across three broad age groups (< 40 years, 40–60 years, and > 60 years), with tinnitus rates of 22–33 percent for those who had worked in noise and 11–18 percent for those who had not. Among the older adults in the Beaver Dam study, major occupation, history of occupational noise exposure, and hunting history were not associated with a higher likelihood of having tinnitus (prevalence) or developing tinnitus (incidence) (Nondahl et al., 2002). It is important to note that many people were retired at the time of the initial examination and therefore were no longer exposed to occupational noise. In the similarly designed Australian study, however, the prevalence of tinnitus was significantly related to the severity of work-related noise exposure (Sindhusake et al., 2003a). Compared with unexposed participants, the relative risk of having tinnitus was 1.39 (95% CI 1.13–1.72) for participants exposed to “tolerable noise” and 1.53 (95% CI 1.13–2.06) for those exposed to high levels of occupational noise (“unable to hear speech”). Similarly, a Swedish study of two cohorts of older men (Rosenhall and Karlsson, 1991) found a significant association at age 70 years between tinnitus and more than 10 years of occupational noise exposure. Tinnitus and Noise Exposure in Industrial Populations Studies of industrial populations offer an opportunity to quantify noise levels in the workplace and in some cases to estimate workers’ noise doses. Three studies drew on large datasets from audiometric surveillance programs. Only one small study reported a comparison with workers who had not been exposed to noise. Some studies excluded workers with other risk factors for tinnitus, including evidence of ear disease. Among 110,647 noise-exposed Austrian industrial workers, 7 percent reported having tinnitus (Neuberger et al., 1992). Workers with a history of ear disease and other risk factors for tinnitus were included in the analysis. Minimum noise exposure was 4-hour daily exposure to levels greater than 85 dBA for at least 6 months. Median noise levels were 90 dBA, with 6 percent of workers exposed to levels higher than 100 dBA. No association was found between the prevalence of tinnitus and the type of noise exposure (i.e., continuous versus impact/impulse noise). Although 7 percent of the workers were described as exposed to impact noise, it was noted that impact noise may not have been distinguished from continuous noise if unweighted peak levels were less than 145 dB (Neuberger et al., 1992).

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Noise and Military Service: Implications for Hearing Loss and Tinnitus prospective studies, including studies of younger adults, are needed to learn more about the relation between hearing loss and the incidence of tinnitus. FINDING: The evidence is sufficient to conclude that hearing loss (hearing thresholds greater than 25 dB HL at one or more audiometric frequencies between 250 and 8000 Hz) is associated with a higher prevalence of tinnitus. FINDING: The evidence is not sufficient to determine precisely the magnitude of the risk of tinnitus associated with hearing loss. OTHER RISK FACTORS Clinical and epidemiological studies have shown that tinnitus is associated with exposure to a variety of factors in addition to noise and hearing loss. The committee identified one study that examined the combined effect of noise exposure and smoking on the prevalence of tinnitus (Palmer et al., 2004). In this British postal survey (n = 10,418), smoking did not have a significant effect on the prevalence of persistent tinnitus (present “most or all of the time in the past 12 months”) after age and duration of occupational noise exposure were taken into account. Other studies have examined tinnitus and smoking without specific consideration of possible interactions with noise exposure. Some found no association between smoking and tinnitus (Chung et al., 1984; Nondahl et al., 2002; Sindhusake et al., 2003a), but a multivariate analysis of data for Norwegian adults found a significantly higher prevalence of tinnitus for both men and women who had smoked for at least 5–15 years, compared with those who had never smoked (Hoffman and Reed, 2004). Studies of the effect of noise in combination with other factors on the prevalence of tinnitus were not identified. Reviewed briefly here are findings on the association between tinnitus and factors other than noise and hearing loss. The statistically significant associations are summarized in Table 4-5. A prospective study of the incidence of tinnitus in older adults found a substantial increase in risk associated with otosclerosis and more modest increases in risk associated with a history of head injury (Nondahl et al., 2002). In the same study, higher concentrations of serum cholesterol were associated with a marginally significant increase in the risk of tinnitus. Cross-sectional, population-based studies have found statistically significant associations with a higher prevalence of tinnitus for a history of head injury (Nondahl et al., 2002; Hoffman and Reed, 2004), severe neck injury (Sindhusake et al., 2003a), and cardiovascular disease (Nondahl et al.,

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Noise and Military Service: Implications for Hearing Loss and Tinnitus TABLE 4-5 Health and Socioeconomic Factors Associated with a Significant Increase or Decrease in Incidence or Prevalence of Tinnitus Significant Risk Factors Incidence of Tinnitus Epidemiology of Hearing Loss Study, Beaver Dam, Wisconsin OR (95% CI) Otosclerosis 8.85 (1.42–55.14) Total serum cholesterol 1.042 (1.004–1.080) Cardiovascular disease   History of head injury 1.55 (1.08–2.22) Hospitalized for head injury   History of middle ear infection History of sinus infection History of severe neck injury History of migraine Self-reported health status: Excellent Very good Good Fair Poor Smoking Never 0 to < 5 yrs ≥ 5 and < 15 yrs ≥ 15 yrs Annual income $0–9,999 $10,000–19,999 $20,000–34,999 $35,000–49,999 $50,000+ Residence Northeast Midwest South West NOTES: OR = odds ratio, RR = relative risk, CI = confidence interval. SOURCES: Nondahl et al. (2002); Sindhusake et al. (2003a); Hoffman and Reed (2004).

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Noise and Military Service: Implications for Hearing Loss and Tinnitus Prevalence of Tinnitus U.S. National Health Interview Survey: Disability Supplement OR (95% CI) Nord Trøndelag Hearing Loss Study, Norway (men only) OR (95% CI) Epidemiology of Hearing Loss Study, Beaver Dam, Wisconsin OR (95% CI) Blue Mountains Hearing Study, Australia RR (95% CI)     1.45 (1.05–2.00) 1.56 (1.21–2.02)     1.43 (1.26–1.62)           1.35 (1.05–1.73) 1.30 (1.08–1.57) 1.34 (1.04–1.73) 1.28 (1.06–1.56) 0.58 (0.52–0.65)   0.79 (0.72–0.87) 1.00 1.63 (1.46–1.80) 2.36 (2.10–2.65) 0.78 (0.68–0.88) 1.00 1.28 (1.14–1.43) 1.50 (1.04–2.16)       1.00 1.26 (1.00–1.58) 1.22 (1.07–1.38) 1.19 (1.09–1.30)     1.56 (1.36–1.78) 1.22 (1.08–1.39) 1.20 (1.06–1.36) 1.05 (0.92–1.20) 1.00       1.00 1.20 (1.03–1.39) 1.16 (1.00–1.35) 1.48 (1.26–1.72)      

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Noise and Military Service: Implications for Hearing Loss and Tinnitus 2002). Middle ear infection, sinus infection, and migraine have also been associated with higher rates of tinnitus in older adults (Sindhusake et al., 2003a). In cross-sectional studies of noise-exposed workers, higher rates of tinnitus have been found among subjects with a history of head injury or ear diseases compared to those without a history of those conditions (e.g., Neuberger et al., 1992; Phoon et al., 1993). Fair or poor self-reported health status was associated with a significantly higher prevalence of tinnitus compared with reported good health (Hoffman and Reed, 2004). The same analyses found a significant reduction in tinnitus risk for persons reporting very good or excellent health. Clinical evidence shows that certain medications can induce tinnitus, but at the population level, studies of older adults did not show a significantly higher prevalence of tinnitus associated with past exposure to ototoxic medications (Sindhusake et al., 2003a) or regular use of aspirin (325 mg at least twice a week for more than 3 months) (Nondahl et al., 2002; Cruickshanks, 2005). In an analysis of the sample of National Health Interview Survey data, modest increases in the likelihood of having tinnitus were associated with lower income and residence in other regions compared to the Northeast. Education level was not associated with significant differences in tinnitus prevalence (Hoffman and Reed, 2004). TINNITUS AND U.S. MILITARY PERSONNEL Tinnitus that is determined to have been incurred during or aggravated by military service (“service connected”) is compensable as a disability by the Department of Veterans Affairs. At the end of fiscal year 2003, tinnitus was the third most common disability, with 242,610 cases among veterans receiving compensation for any form of service-connected disability (Veterans Benefits Administration, 2004a). Until May 1999, it was necessary to establish that persistent tinnitus had resulted from service-connected head injury, concussion, or acoustic trauma (Henry et al., 2004; Veterans Benefits Administration, 2004b). Since then, recurrent tinnitus associated with any condition incurred in or aggravated by military service has been compensable (Henry et al., 2004; Veterans Benefits Administration, 2004b). Despite the fact that tinnitus is compensable, the committee found little indication that the services monitor the presence or absence of tinnitus among military personnel during active duty. The forms that summarize service members’ medical histories (DD Form 2807-1, DD Form 2807-2, Standard Form [SF] 93) and the results of their periodic physical examinations (DD Form 2808, SF 88) capture information on hearing, including pure-tone thresholds and use of hearing aids, but do not include questions

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Noise and Military Service: Implications for Hearing Loss and Tinnitus about tinnitus. Similarly, the forms used by the services’ hearing conservation programs (see Chapter 5 and Appendix G) to record the results of audiometric testing and reports on the use and distribution of hearing protection devices include no question about the presence or absence of tinnitus. However, the opportunity does exist for reports of tinnitus volunteered by service members or solicited by medical or audiology personnel to be recorded on these forms. Perhaps the only current source of limited but explicit documentation of tinnitus is the post-deployment health assessment questionnaire (DD Form 2796). A requirement for post-deployment health assessments was established in 1997 (DoD, 1997), and the current version of the assessment form with the questions on noise exposure and tinnitus dates from April 2003. Only personnel who are deployed would have the opportunity to complete the form. Without systematic documentation of the tinnitus status of military personnel, it is not possible to determine whether service members have tinnitus at the time they enter or leave military service or when during military service tinnitus might have developed. In the absence of systematic information about tinnitus, it is not possible for the services to identify tinnitus hazards that might be different from those for noise-induced hearing loss. The committee strongly suggests that the Department of Defense add monitoring of tinnitus to both its routine health surveillance and the audiologic surveillance that is part of the services’ hearing conservation programs. One approach might be the addition of questions to the forms used to report medical history (DD Form 2807-1) or the results of medical examinations (DD Form 2808) and to the forms used by the hearing conservation programs to record reference audiograms (DD Form 2215) and periodic and termination audiograms (DD Form 2216). Tinnitus surveillance might begin with audiologic assessments at entry into and separation from military service. Basic questions, such as “Do you have any ringing or buzzing in your ears or head?” and “When did you first notice the ringing or buzzing?” could be considered as a way to begin to obtain information about tinnitus during military service. At this time, however, there is no generally accepted and validated question, or set of questions, that can be recommended for use in tinnitus surveillance. Factors that may deserve consideration in defining tinnitus for a monitoring program include persistence of episodes (e.g., longer than 5 minutes), regularity of occurrence (e.g., perceived all the time, perceived several times per week, perceived only after exposure to loud noise), and level of annoyance. The Department of Defense and the military services should explore the merits of various approaches to tinnitus surveillance.

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Noise and Military Service: Implications for Hearing Loss and Tinnitus Tinnitus and hearing loss are both associated with exposure to high levels of noise. Although the factors that result in tinnitus are not as easy to predict as those that result in hearing loss, doses of noise (and risk factors) that are considered hazardous for hearing may also be tinnitus hazards. Consequently, the precautions regarding noise-exposure limits and the use of hearing protection may help prevent tinnitus as well as hearing loss. The scope of the hearing conservation programs of the military services could appropriately be broadened to encompass the prevention of tinnitus as well as hearing loss—thus “hearing loss and tinnitus prevention programs.” REFERENCES Adams PF, Hendershot GE, Marano MA. 1999. Current estimates from the National Health Interview Survey, 1996. Vital and Health Statistics, Series 10, No. 200. Hyattsville, MD: National Center for Health Statistics. Aggleton JP, Mishkin M. 1986. The amygdala: Sensory gateway to the emotions. In: Pultchik R, Kellerman H, eds. Emotion, Theory, Research, and Experience. Vol. 3. New York: Academic Press. Pp. 281–289. Alberti PW. 1987. Tinnitus in occupational hearing loss: Nosological aspects. Journal of Otolaryngology 16(1):34–35. AMSA (Army Medical Surveillance Activity). 2004. Responses to Selected Questions on DD 2796 Post Deployment Health Assessments, Since 01-Jun-2003. Data provided to the Institute of Medicine Committee on Noise-Induced Hearing Loss and Tinnitus Associated with Military Service from World War II to the Present, Washington, DC. Andersson G, Vretblad P, Larsen HC, Lyttkens L. 2001. Longitudinal follow-up of tinnitus complaints. Archives of Otolaryngology–Head and Neck Surgery 127(2):175–179. Anonymous. 1981. Definition and classification of tinnitus. In: Evered D, Lawrenson G, eds. Tinnitus. Ciba Foundation Symposium 85. London, England: Pitman Books Ltd. Pp. 300–302. Attias J, Reshef I, Shemesh Z, Salomon G. 2002. Support for the central theory of tinnitus generation: A military epidemiological study. International Journal of Audiology 41(5):301–307. Axelsson A, Barrenas M-L. 1992. Tinnitus in noise-induced hearing loss. In: Dancer AL, Henderson D, Salvi RJ, Hamernik RP, eds. Noise-Induced Hearing Loss. St. Louis, MO: Mosby Year Book. Pp. 269–276. Axelsson A, Prasher D. 2000. Tinnitus induced by occupational and leisure noise. Noise Health 2(8):47–54. Axelsson A, Ringdahl A. 1989. Tinnitus—A study of its prevalence and characteristics. British Journal of Audiology 23(1):53–62. Axelsson A, Sandh A. 1985. Tinnitus in noise-induced hearing loss. British Journal of Audiology 19(4):271–276. Baguley DM. 2002. Mechanisms of tinnitus. British Medical Bulletin 63:195–212. Bauer CA. 2003. Animal models of tinnitus. Otolaryngology Clinics of North America 36(2):267–285. Bauer CA, Brozoski TJ. 2001. Assessing tinnitus and prospective tinnitus therapeutics using a psychophysical animal model. Journal of the Association for Research in Otolaryngology 2:54–64. Bauer CA, Brozoski TJ, Rojas R, Boley J, Wyder M. 1999. Behavioral model of chronic tinnitus in rats. Otolaryngology–Head and Neck Surgery 121:457–462.

OCR for page 116
Noise and Military Service: Implications for Hearing Loss and Tinnitus Cacace A. 2003. Expanding the biologic basis of tinnitus: Crossmodal origins and the role of neuroplasticity. Hearing Research 175:112–132. Cacace AT. 2004. The limbic system and tinnitus. In: Snow JB, Jr., ed. Tinnitus: Theory and Management. Hamilton, Ontario, Canada: BC Decker. Pp. 162–170. Cahani M, Paul G, Shahar A. 1983. Tinnitus pitch and acoustic trauma. Audiology 22(4):357–363. Chermak GD, Dengerink JE. 1987. Characteristics of temporary noise-induced tinnitus in male and female subjects. Scandinavian Audiology 16(2):67–73. Christiansson BA, Wintzell KA. 1993. An audiological survey of officers at an infantry regiment. Scandinavian Audiology 22(3):147–152. Chung DY, Gannon RP, Mason K. 1984. Factors affecting the prevalence of tinnitus. Audiology 23(5):441–452. Coles RR. 1984. Epidemiology of tinnitus: (1) Prevalence. Journal of Laryngology and Otology 9(Suppl.):7–15. Coles RRA. 1996. Epidemiology, aetiology and classification. In: Reich GE, Vernon JA, eds. Proceedings of the Fifth International Tinnitus Seminar 1995. Portland, OR: American Tinnitus Association. Cruickshanks K. 2005. Comments. E-mail to J. Durch, Institute of Medicine, June 13. Dauman R. 2000. Electrical stimulation for tinnitus suppression. In: Tyler RS, ed., Tinnitus Handbook. San Diego, CA: Singular Publishing Group. Pp. 377–398. Dauman R, Tyler RS. 1992. Some considerations on the classification of tinnitus. In: Aran J-M, Dauman R, eds. Proceedings of the Fourth International Tinnitus Seminar, Bordeaux, France. Amsterdam, The Netherlands: Kugler & Ghedini Publications. Pp. 225–229. De Ridder D, Ryu H, De Mulder G, Van de Heyning P, Verlooy J, Moller A. 2005. Frequency specific hearing improvement in microvascular decompression of the cochlear nerve. Acta Neurochirurgica 147(5):495–501. Dineen R, Doyle J, Bench J. 1997. Audiological and psychological characteristics of a group of tinnitus sufferers, prior to tinnitus management training. British Journal of Audiology 31(1):27–38. Dobie RA. 1999. A review of randomized clinical trials in tinnitus. Laryngoscope 109(8): 1202–1211. Dobie RA. 2003. Depression and tinnitus. Otolaryngologic Clinics of North America 36(2): 383–388. DoD (Department of Defense). 1997. Department of Defense Instruction 6490.3: Implementation and Application of Joint Medical Surveillance for Deployments. Washington, DC: Department of Defense. Eggermont JJ. 2003. Central tinnitus. Auris Nasus Larynx 30 (Suppl 1):S7–S12. Eggermont JJ, Roberts LE. 2004. The neuroscience of tinnitus. Trends in Neuroscience 27:676–682. Erlandsson SI. 2000. Psychological profiles of tinnitus patients. In: Tyler RS, ed. Tinnitus Handbook. San Diego, CA: Singular Thompson Learning. Pp. 25–57. Erlandsson SI, Rubinstein B, Axelsson A, Carlsson SG. 1991. Psychological dimensions in patients with disabling tinnitus and craniomandibular disorders. British Journal of Audiology 25(1):15–24. Gabriels P, Monley P, Guzeleva D. 1996. Noise-exposed workers: Is tinnitus being ignored? In: Reich GE, Vernon JA, eds. Proceedings of the Fifth International Tinnitus Seminar 1995. Portland, OR: American Tinnitus Association. Pp. 373–380. George RN, Kemp S. 1989. Investigation of tinnitus induced by sound and its relationship to ongoing tinnitus. Journal of Speech and Hearing Research 32(2):366–372.

OCR for page 116
Noise and Military Service: Implications for Hearing Loss and Tinnitus Griest SE, Bishop PM. 1996. Evaluation of tinnitus and occupational hearing loss based on 20-year longitudinal data. In: Reich GE, Vernon JA, eds. Proceedings of the Fifth International Tinnitus Seminar 1995. Portland, OR: American Tinnitus Association. Pp. 381–394. Halford JB, Anderson SD. 1991. Anxiety and depression in tinnitus sufferers. Journal of Psychosomatic Research 35(4-5):383–390. Hazell JWP. 1995. Models of tinnitus: Generation, perception, clinical implications. In: Vernon JA, Møller AR, eds. Mechanisms of Tinnitus. Boston: Allyn and Bacon. Pp. 57–72. Hazell JWP, Wood SM. 1981. Tinnitus masking—a significant contribution to tinnitus management. British Journal of Audiology 15(4):223–230. Heffner HE, Harrington IA. 2002. Tinnitus in hamsters following exposure to intense sound. Hearing Research 170:83–95. Henry JA. 2004. Audiological assessment. In: Snow JB, Jr., ed. Tinnitus: Theory and Management. Hamilton, Ontario, Canada: B.C. Decker. Pp. 220–236. Henry JA, Schechter MA, Regelein RT, Dennis KC. 2004. Veterans and tinnitus. In: Snow JB, Jr., ed. Tinnitus: Theory and Management. Hamilton, Ontario, Canada: B.C. Decker. Pp. 337–355. Hoffman HJ, Reed GW. 2004. Epidemiology of tinnitus. In: Snow JB, Jr., ed. Tinnitus: Theory and Management. Hamilton, Ontario, Canada: B.C. Decker. Pp. 16–41. Jacobson GP, McCaslin DL. 2001. A search for evidence of a direct relationship between tinnitus and suicide. Journal of the American Academy of Audiology 12(10):493–496. Jastreboff PJ, Jastreboff MM. 2003. Tinnitus retraining therapy for patients with tinnitus and decreased sound tolerance. Otolaryngology Clinics of North America 36(2):321–336. Jastreboff PJ, Brennan JF, Coleman JK, Sasaki CT. 1988a. Phantom auditory sensation in rats: An animal model for tinnitus. Behavioral Neuroscience 102:811–822. Jastreboff PJ, Brennan JF, Sasaki CT. 1988b. An animal model for tinnitus. Laryngoscope 98: 280–286. Kaltenbach JA, Zacharek MA, Zhang, Frederick S. 2004a. Activity in the dorsal cochlear nucleus of hamsters previously tested for tinnitus following intense tone exposure. Neuroscience Letters 355:121–125. Kaltenbach JA, Zhang J, Zacharek MA. 2004b. Neural correlates of tinnitus. In: Snow JB, Jr., ed. Tinnitus: Theory and Management. Hamilton, Ontario, Canada: B.C. Decker. Pp. 141–160. Kaltenbach JA, Zhang J, Finlayson P. 2005. Tinnitus as a plastic phenomenon and its possible neural underpinnings in the dorsal cochlear nucleus. Hearing Research 206:200–226. Kamal AA, Mikael RA, Faris R. 1989. Follow-up of hearing thresholds among forge hammering workers. American Journal of Industrial Medicine 16(6):645–658. Kim J, Morest DK, Bohne BA. 1997. Degeneration of axons in the brainstem of the chinchilla after auditory stimulation. Hearing Research 103:169–191. Kleinjung T, Eichhammer P, Langguth B, Jacob P, Marienhagen J, Hajak G, Wolf SR, Strutz J. 2005. Long-term effects of repetitive transcranial magnetic stimulation (rTMS) in patients with chronic tinnitus. Otolaryngology–Head and Neck Surgery 132:566–569. Kuk FK, Tyler RS, Russell D, Jordan H. 1990. The psychometric properties of a tinnitus handicap questionnaire. Ear and Hearing 11(6):434–445. LeDoux JE. 2000. Emotion circuits in the brain. Annual Review of Neuroscience 23:155–184. Lobarinas E, Sun W, Cushing R, Salvi R. 2004. A novel behavioral paradigm for assessing tinnitus using schedule-induced polydipsia avoidance conditioning (SIP-AC). Hearing Research 190(1-2):109–114.

OCR for page 116
Noise and Military Service: Implications for Hearing Loss and Tinnitus Lockwood AH, Salvi RJ, Burkhard RF. 2002. Tinnitus. New England Journal of Medicine 347(12):904–910. Loeb M, Smith RP. 1967. Relation of induced tinnitus to physical characteristics of the inducing stimuli. Journal of the Acoustical Society of America 42(2):453–455. Man A, Naggan L. 1981. Characteristics of tinnitus in acoustic trauma. Audiology 20(1): 72–78. Medical Research Council’s Institute of Hearing Research. 1981. Epidemiology of tinnitus. In: Evered D, Lawrenson G, eds. Tinnitus. Ciba Foundation Symposium 85. London, England: Pitman Books Ltd. Pp. 16–34. Melinek M, Naggan L, Altman M. 1976. Acute acoustic trauma—a clinical investigation and prognosis in 433 symptomatic soldiers. Israel Journal of Medical Sciences 12(6):560–569. Meric C, Gartner M, Collet L, Chery-Croze S. 1998. Psychopathological profile of tinnitus sufferers: Evidence concerning the relationship between tinnitus features and impact on life. Audiology and Neuro-Otology 3(4):240–252. Metternich FU, Brusis T. 1999. [Acute hearing loss and tinnitus caused by amplified recreational music.] Laryngorhinootologie 78(11):614–619. Moody DB. 2004. Animal models of tinnitus. In: Snow JB, Jr., ed. Tinnitus: Theory and Management. Hamilton, Ontario, Canada: B.C. Decker. Pp. 80–95. Morest DK, Kim J, Potashner SJ, Bohne BA. 1998. Long-term degeneration in the cochlear nerve and cochlear nucleus of the adult chinchilla following acoustic overstimulation. Microscopy Research and Technique 41:205–216. Mrena R, Savolainen S, Kuokkanen JT, Ylikoski J. 2002. Characteristics of tinnitus induced by acute acoustic trauma: A long-term follow-up. Audiology and Neuro-Otology 7(2): 122–130. Muhlnickel W, Elbert T, Taub E, Flor H. 1998. Reorganization of auditory cortex in tinnitus. Proceedings of the National Academy of Sciences 95(17):10340–10343. Neuberger M, Korpert K, Raber A, Schwetz F, Bauer P. 1992. Hearing loss from industrial noise, head injury and ear disease. A multivariate analysis on audiometric examinations of 110,647 workers. Audiology 31(1):45–57. Newman CW, Jacobson GP, Spitzer JB. 1996. Development of the tinnitus handicap inventory. Archives of Otolaryngology–Head and Neck Surgery 122(2):143–148. Noble W. 1998. Self-Assessment of Hearing and Related Functions. London, England: Whurr. Nondahl DM, Cruickshanks KJ, Wiley TL, Klein R, Klein BE, Tweed TS. 2002. Prevalence and 5-year incidence of tinnitus among older adults: The Epidemiology of Hearing Loss Study. Journal of the American Academy of Audiology 13(6):323–331. Nondahl DM, Cruickshanks KJ, Wiley TL, Klein R, Klein BE, Tweed TS. 2004. Comment on tinnitus in older adults from the Blue Mountains Study by Sindhusake et al. and comparison with tinnitus data from the Epidemiology of Hearing Loss Study. International Journal of Audiology 43(1):60. NRC (National Research Council). 1982. Tinnitus—Facts, Theories, and Treatments. Committee on Hearing, Bioacoustics, and Biomechanics. Working Group 89 (McFadden D, chair). Washington, DC: National Academy Press. Palmer KT, Griffin MJ, Syddall HE, Davis A, Pannett B, Coggon D. 2002. Occupational exposure to noise and the attributable burden of hearing difficulties in Great Britain. Occupational and Environmental Medicine 59(9):634–639. Palmer KT, Griffin MJ, Syddall HE, Coggon D. 2004. Cigarette smoking, occupational exposure to noise, and self reported hearing difficulties. Occupational and Environmental Medicine 61:340–344.

OCR for page 116
Noise and Military Service: Implications for Hearing Loss and Tinnitus Parving A, Hein HO, Suadicani P, Ostri B, Gyntelberg F. 1993. Epidemiology of hearing disorders. Some factors affecting hearing. The Copenhagen Male Study. Scandinavian Audiology 22(2):101–107. Phoon WH, Lee HS, Chia SE. 1993. Tinnitus in noise-exposed workers. Occupational Medicine (London) 43(1):35–38. Plewnia C, Bartels M, Gerloff C. 2003. Transient suppression of tinnitus by transcranial magnetic stimulation. Annals of Neurology 53(2):263–266. Roberts J. 1968. Hearing status and ear examination: Findings among adults, United States, 1960–1962. Vital and Health Statistics. Series 11, No. 32. Washington, DC: Department of Health, Education, and Welfare. Robertson RM, Page JC, Williams CE. 1978. The Prevalence of Hearing Loss Among Selected Navy Enlisted Personnel. NAMRL-1251. Pensacola, FL: Naval Aerospace Medical Research Laboratory. Rosenhall U, Karlsson AK. 1991. Tinnitus in old age. Scandinavian Audiology 20(3):165–171. Rubertone M (U.S. Army). 2004. RE: Cross Tabulation Help. E-mail to R. Erdtmann, Institute of Medicine, November 4. Rubertone M (U.S. Army). 2005. RE: Clarification on Tables Provided. E-mail to R. Erdtmann, Institute of Medicine, March 2. Rubinstein JT, Tyler RS, Johnson A, Brown CJ. 2003. Electrical suppression of tinnitus with high-rate pulse trains. Otology and Neurotology 24(3):478–485. Salmivalli A. 1967. Acoustic trauma in regular army personnel. Clinical audiologic study. Acta Oto-Laryngologica (Suppl 222):1–85. Salvi RJ, Lockwood AH, Burkard R. 2000. Neural plasticity and tinnitus. In: Tyler RS, ed. Tinnitus Handbook. San Diego, CA: Singular Thompson Learning. Pp. 123–148. Shulman A. 1997. Medical evaluation. In: Shulman A, ed. Tinnitus: Diagnosis/Treatment. San Diego: Singular Publishing Group. Pp. 253–292. Sindhusake D, Golding M, Newall P, Rubin G, Jakobsen K, Mitchell P. 2003a. Risk factors for tinnitus in a population of older adults: The Blue Mountains Hearing Study. Ear and Hearing 24(6):501–507. Sindhusake D, Mitchell P, Newall P, Golding M, Rochtchina E, Rubin G. 2003b. Prevalence and characteristics of tinnitus in older adults: The Blue Mountains Hearing Study. International Journal of Audiology 42(5):289–294. Sindhusake D, Golding M, Wigney D, Newall P, Jakobsen K, Mitchell P. 2004. Factors predicting severity of tinnitus: A population-based assessment. Journal of the American Academy of Audiology 15(4):269–280. Stankiewicz C, Przewozny T, Kozlowski J. 2000. [Noise from a car airbag as a cause of acute acoustic trauma.] Otolaryngologia Polska 54(6):775–781. Stephens SD, Hallam RS. 1985. The Crown-Crisp Experiential Index in patients complaining of tinnitus. British Journal of Audiology 19:151–158. Stouffer JL, Tyler RS. 1990. Characterization of tinnitus by tinnitus patients. Journal of Speech and Hearing Disorders 55(3):439–453. Sulkowski W, Kowalska S, Lipowczan A, Prasher D, Raglan E. 1999. Tinnitus and impulse noise-induced hearing loss in drop-forge operators. International Journal of Occupational Medicine and Environmental Health 12(2):177–182. Sweetow R. 2000. Cognitive behavior modification. In: Tyler RS, ed. Tinnitus Handbook. San Diego, CA: Singular Publishing Group. Pp. 297–312. Tambs K, Hoffman HJ, Borchgrevink HM, Holmen J, Samuelsen SO. 2003. Hearing loss induced by noise, ear infections, and head injuries: Results from the Nord-Trøndelag Hearing Loss Study. International Journal of Audiology 42(2):89–105. Temmel AF, Kierner AC, Steurer M, Riedl S, Innitzer J. 1999. Hearing loss and tinnitus in acute acoustic trauma. Wiener Klinische Wochenschrift 111(21):891–893.

OCR for page 116
Noise and Military Service: Implications for Hearing Loss and Tinnitus Tyler RS. 1993. Tinnitus disability and handicap questionnaires. Seminars in Hearing 14:377–384. Tyler RS. 2000. Psychoacoustical measurement. In: Tyler RS, ed. Tinnitus Handbook. San Diego, CA: Singular Publishing Group. Pp. 149–180. Tyler RS, Babin RW. 1986. Tinnitus. In: Cummings CW, Fredrickson JM, Harker L, Krause CJ, Schuller DE, eds. Otolaryngology—Head and Neck Surgery. Vol. 4. St. Louis, MO: C.V. Mosby Co. Pp. 3201–3217. Tyler RS, Cacace AT. 2004. Advances in understanding and treating tinnitus. Tinnitus Today 29(1):8–13. Tyler RS, Noble WS, Preece JP, Dunn C, Witt S. 2004. Psychological treatments for tinnitus. In: Snow JB, Jr., ed. Tinnitus: Theory and Management. Hamilton, Ontario, Canada: B.C. Decker. Pp. 314–325. Van Campen LE, Dennis JM, Hanlin RC, King SB, Velderman AM. 1999. One-year audiologic monitoring of individuals exposed to the 1995 Oklahoma City bombing. Journal of American Academy of Audiology 10(5):231–247. Vernon JA, Meikle MB. 2000. Tinnitus masking. In: Tyler RS, ed. Tinnitus Handbook. San Diego, CA: Singular Publishing Group. Pp. 313–356. Vernon JA, Meikle MB. 2003. Tinnitus: Clinical measurement. Otolaryngologic Clinics of North America 36(2):293–305. Veterans Benefits Administration. 2004a. Veterans Benefits Administration Annual Benefits Report, FY 2003. Washington, DC: Department of Veterans Affairs. Veterans Benefits Administration. 2004b. Written responses to questions from the Institute of Medicine Committee on Noise-Induced Hearing Loss and Tinnitus Associated with Military Service from World War II to the Present, Meeting II, Washington, DC. Wilson PH, Henry JL. 2000. Psychological management of tinnitus. In: Tyler RS, ed. Tinnitus Handbook. San Diego, CA: Singular Publishing Group. Pp. 263–280. Wilson PH, Henry J, Bowen M, Haralambous G. 1991. Tinnitus reaction questionnaire: Psychometric properties of a measure of distress associated with tinnitus. Journal of Speech and Hearing Research 34(1):197–201. Ylikoski ME, Ylikoski JS. 1994. Hearing loss and handicap of professional soldiers exposed to gunfire noise. Scandinavian Journal of Work, Environment & Health 20(2):93–100. Young DW. 2000. Biofeedback training in the treatment of tinnitus. In: Tyler RS, ed. Tinnitus Handbook. San Diego, CA: Singular Publishing Group. Pp. 281–296.