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J Am Acad Audiol 6 : 387-395 (1995) Factors Causing Hearing Impairment : Some Perspectives from Europe Agnete Parving Abstract This review concentrates on factors causing permanent hearing impairment in childhood, described in some European studies. The emphasis is on comparative studies, based on strict criteria and terminology upon which longitudinal changes in the pattern of factors causing hearing impairment can be demonstrated in well-defined cohorts of children . The high proportion of 20-39 percent of unknown causes of permanent hearing impairment in childhood reflects a general lack of knowledge about causative factors and systematic etiologic evaluation within pediatric audiology. Future surveillance programs, including examination procedures directed towards causative factors, may see a reduction of the "unknown" category and ultimately may result in prevention of permanent hearing impairment in childhood. Some factors causing hearing impairment in adults are mentioned, including recent studies that show organic toxic solvents as a factor. As well, some controversial findings concerning the relationship between hearing impairment and endocrine disorders such as hypothyroidism and diabetes mellitus are briefly reported . It is concluded that future developments and research in the etiologic field within pediatric and adult audiology may contribute to the delineation of yet unknown damaging factors or reduction of the effect of factors causing hearing impairment - a disorder that ultimately results in adverse effects on the quality of life in all age groups . Key Words: Adults, childhood, etiology, hearing impairment hroughout life, the hearing organ, with its different anatomical areas, may be T affected by numerous factors, resulting in a hearing disorder with an abnormal function of the auditory system . The loss of auditory sensitivity - which in clinical terms is hearing impairment (HI) - may result in reduced abilities of the individual (hearing disability) or in adverse effects on life (hearing handicap) (e .g ., Davis, 1987). A relationship has been established between HI and numerous damaging factors, based on experimental, epidemiologic, and clinical case-control studies, but also by removal of agents resulting in primary prevention in the population or in the individual subject . Factors causing hearing disorders differ according to geography, gender, age, and individual susceptibility to exposed factors. This "Department of Audiology, Bispebjerg Hospital, Copenhagen, Denmark Reprint requests : Agnete Parving, Department of Audiology, Bispebjerg Hospital, DK 2400 Copenhagen NV, Denmark contribution describes some European aspects related to causes of HI . The etiologic classification of HI in this report will be divided according to hearing disorders in childhood, concentrating on permanent HI to such a degree that it requires intervention . Deliberately, no comments and considerations are presented concerning aspects of otitis media with effusion and all its implications for pediatric audiology. In this context, the reader is referred to Chalmers et al (1989) and Haggard and Hughes (1991) . The second part will focus on adults, that is, individuals above the age of 18 years. This section considers studies supporting organic toxic solvents as damaging factors for the hearing organ and describes some controversial findings in subjects with hypothyroidism and diabetes mellitus . HEARING IMPAIRMENT IN CHILDREN M odem pediatric audiology accepts that hearing loss in children is a sign/symptom that should be considered the result of any damaging Journal of the American Academy of Audiology/Volume 6, Number 5, September 1995 factor(s) affecting the hearing organ. Thus, the diagnostic evaluation consists of two major steps: (1) assessment of the HI, its severity, and site of lesion; and (2) evaluation of the causative factors) . Within most European countries, children, upon identification of a permanent HI, will be entered into a surveillance program aimed toward a longitudinal follow-up of the intervention and its effect, especially on the child's speech and language development, social adjustment, and communication skills (European Federation of Audiological Societies, 1993). A diagnostic evaluation program (individualized for each child), including thorough history, (computed tomography/magnetic resonance imaging [MRI] scan), serologic, ophthalmologic, X-ray (CT/MR-scan), pediatric, and genetic examinations, has reduced the category "unknown cause" to only 11 percent in an epidemiologically welldefined cohort born between 1970-1980 (Parving, 1984). Additional or new information on causative factors in the individual child may add to, modify, or change the etiologic diagnosis in the single child; consequently, the etiologic evaluation should be considered a longstanding and dynamic process. These statements are supported by the data in Table 1, which demonstrate the longitudinal aspects of an etiologic evaluation . It should be mentioned that all etiologies are based on strict criteria, and to some degree account for the sensitivity/specificity of different diagnostic procedures . Note that in 1987 an additional 21 children are included in the cohort, reflecting the delayed identification of children with congenital HI (Parving, 1983, 1984, 1988). Table 1 Time of Data Collection Lack of uniform worldwide accepted description of, and criteria for, defining causative diagnosis limits the possibility for comparative studies, both within and between countries. Often the small numbers of subjects in the welldefined reported samples exclude valid statistical analysis and conclusions. An approach toward a diagnostic category based on the interaction between time at insult, causation, and expression has been proposed (Davidson et al, 1988) and implemented (Parving, 1993a), and may solve some of the problems within future comparative and longitudinal investigations . In addition, appropriate sampling of well-defined cohorts based on strict terminology and definition of hearing level is a prerequisite for valid information on the distribution of etiologic factors causing HI . The diagnostic evaluation reflects some important qualitative (i.e., medical audit) aspects' of the pediatric audiologic services offered locally. On a national basis, such data could result in an appropriate planning for allocation of resources within this field. Exchange of information and international collaboration may result in primary prevention of HI, such as vaccination programs or genetic counselling. 1980-1990 Cross-sectional Data In a geographically well-defined cohort of children born between 1980-1990 and provided with hearing aids, the prevalence rate of different factors causing the HI was described. The proportion of the etiologies within the sample was calculated as shown in Table 2 (Parving, 1993a) . Cohort Born 1970-1980 1982 Program Etiologies N Fetal infection Hereditary hearing loss (no associated abnormalities) Natal/neonatal complications Ototoxic drugs Meningitis Various genetic syndromes Chromosomal aberrations Malformations of ears Meniere's disease Otitis media sequelae Unknown cause Total 19 32 16 27 16 14 2 3 6 2 2 1 2 18 16 32 117 27 2 3 9 2 2 2 4 Revision 1987 N % N 22 43 19 37 20 50 14 36 16 14 14 10 - 31 22 23 138 17 24 19 12 117 11 5 16 8 2 Hearing Impairment/Parving Table 2 Prevalence Rate (1/1000) of Different Factors Causing HI (N = 181), Calculated on Basis of Total Age-matched Target Group (N = 95,912) Prenatal causes Inheritance Fetal infection Malformation Perinatal causes Postnatal causes Otitis media Meningitis Unknown cause N Prevalence Rate (1/1000) Proportion of Etiology (%) 99 84 9 6 17 28 22 6 37 1 .03 0 .88 0 .09 0 .06 0 .17 0 .29 0 .23 0 .06 0 .38 55 46 5 3 9 15 12 3 20 Table 3 Cross-sectional Longitudinal Data from the Copenhagen Area Cohort Prenatal causes Genetic Fetal infection Malformation Perinatal causes Postnatal causes Otitis media Meningitis Head injury Unknown cause Cohort 1970-1980 (N = 186) 1980-1990 (N = 181) N N 95% Cl 94 65 25 4 27 12 5 6 51 69 27 6 15 7 - 99 84 9 55 85 9 NS S S 17 28 22 6 9 15 - NS 49 26 37 20 NS 1 S = significant, NS = not significant . The causative factors in this sample were categorized according to Davidson et al (1988) . The table shows that prenatal causes are most frequent, and that inheritance is the overall dominating factor accounting for 46 percent . Perinatal and postnatal factors account for 9 percent and 15 percent, respectively. Twenty percent had not been classified as to etiology at the time of data collection (January 1992). When performing cross-sectional longitudinal comparisons based on retrospective data, the definitions and criteria for the comparison must be identical in order to evaluate true differences in the causes of hearing disorders in children . However, a change in prevalence due to a cohort effect (e .g., rubella epidemic) may change the overall prevalence and thus influence and change the proportion of different causes within the sample . In addition, the period of sampling and the age of the children, that is, the time of evaluation, is crucial, especially in small samples, and should always be considered . With this in mind, a comparison of two cohorts of children provided with hearing aids and born between 1970-1980 (evaluated January 1982) and 1980-1990 (evaluated January 1992) shows an increase in the prevalence of 23 percent, that is, 1.5/1000 in the 1970-1980 cohort (N = 186/121,544 age-matched children) and 1.9/1000 in the 1980-1990 cohort (N =181/95,912 age-matched children). The change may in part be due to changes in the criteria for provision of hearing aids . However, when controlling for that factor, a true increase in the prevalence of 19 percent was demonstrated . The increase resulted in changes in the pattern of factors causing HI, as shown in Table 3 . There was a significantly higher proportion of HI caused by inheritance in the 1980-1990 cohort, whereas there was a significant reduction in the proportion of etiologies associated with fetal infections . These inversely related changes result in no significant changes overall in the prevalence of prenatal causes, but emphasize that a more detailed evaluation of the causes in the different categories according to time of insult is necessary. This development in the causes of HI throughout a 10-year period in the described area is compatible with the increase of immigrants in the target population, having different cultural and religious backgrounds (Parving, 1993a, b) . Thus, the results seem to document the strong relationship between demography and disease. Some additional longitudinal information on the causes of HI can be obtained from a cohort of subjects born between 1960-1970, who were living in Copenhagen (data collection in January 1991). Any comparative analysis to the cohorts born between 1970-1980 and 1980-1990 is vulnerable due to the age factor. For valid comparison, the 1960-1970 cohort should have been evaluated in January 1972, and the retrospective sampling based on clinical records results in prevalence underestimates and lack of information (Parving and Christensen, 1993). A reanalysis of the data can, however, control for the criterion "provision of hearing aids," and thus a sample of N =125 was evaluated and categorized according to Davidson et al (1988) . The population of those between 20-30 years in 1991 comprised N = 110,504, yielding an estimate of 1 .1/1000 adults provided with a hearing aid. Due to the shortcomings in the original sampling, the prevalence rate may represent a substantial underestimate, but it may also reflect the changing attitude towards hearing aid rehabilitation, Journal of the American Academy of Audiology/Volume 6, Number 5, September 1995 which became increasingly more acceptable throughout the 1970s and 1980s due to improvements in both the technical and cosmetic aspects of hearing instruments . The causes of the HI in the 1960-1970 cohort are listed in Table 4. To facilitate comparison of information on the longitudinal cross-sectional data, the causes of the HI in the birth cohorts of the 1970s and 1980s cohorts are also included . Due to uncertainty concerning the 1960-1970 cohort, no comparative statistical analysis has been included . Some Additional European Data In 1977, the member countries of the European Community performed a survey of a cohort of hearing-disabled children born in 1969 (Martin et al, 1981). The survey had many objectives, including to "determine the cause of deafness" and "define the size of the group in which the cause is reported to be unknown." The survey demonstrated that, among those with sensorineural HI, the cause could be ascribed to fetal rubella infection in 16 percent, varying from 12-20 percent between countries, while genetic causes accounted for only 9 percent of the HI . Although the survey was confined according to geography and birth cohort, and the criteria for hearing level (>_ 50 dB HI in the better hearing ear averaged across the audiometric frequencies of 500, 1000, and 2000 Hz) was strictly defined, the most reliable result obtained is - according to the present author's evaluation - the proportion of 42 percent of unknown etiology of the HI . Based on the survey, it was recommended that there should be more detailed research into the etiology of the HI in children with a supposed unknown cause. Table 4 Prenatal Genetic Fetal infection Malformation Perinatal Postnatal Otitis sequelae Meningitis Head injury Unknown 390 10-Year Birth Cohorts 1960s (N = 125) 1970s (N = 186) 1980s (N= 181) N N % N 94 84 9 6 27 12 22 6 49 51 99 55 15 7 17 28 9 15 26 37 20 55 49 2 4 25 14 3 8 3 31 44 65 25 4 20 11 5 6 1 25 Recent epidemiologic figures on HI in childhood from two European countries (England and Denmark) have shown that the prevalence rate of 2/1000 of children with permanent HI, requiring hearing aids in identical birth cohorts, is fairly similar within both the compared health authority districts within countries and also between the two countries (Davis and Wood, 1992 ; Parving 1993b; Davis and Parving, 1994). A direct comparison between the proportion of different diagnostic categories could not be performed between countries. However, when family history and the neonatal intensive care unit status of the children were considered significant, differences in the factors causing HI were found between the two countries. This was not the case, however, between districts within the same country (Parving, 1993a ; Davis and Parving, 1994). Although a European survey has not been' carried out, numerous data on the etiology of hearing disorders in children have been reported from several European countries and districts (e .g ., Kankkunen, 1982 ; Newton, 1985 ; Das, 1988 ; Hirsch, 1988 ; Lenzi and Zaghis, 1988 ; Dias and Andrea, 1990 ; van Rijn and Cremers, 1991 ; Vanniasegaram et al, 1993). An attempt has been made - whenever allowed by the available data - to organize some of the reported etiologies according to generally recognized categories (Davidson et al, 1988). The result may be seen in Table 5. It is important to understand that major differences in the inclusion criteria, definition of samples, age of the children, and definition of hearing level are present, thereby excluding a detailed direct comparative analysis . A cautious interpretation supports the notion that prenatal causes are most frequent in different parts of Europe with genetic factors, dominating and varying from 20-46 percent within the samples listed in Table 5 . Although this is not new information, it is important due to the rapid development of the field of molecular genetics . Future research within this area may provide clinicians with additional valuable information, probably resulting in a reduction of unknown cause and improved counselling and prevention of genetic HI (O'Malley and Ledley, 1993 ; Ryan et al, 1993). In Table 6, the frequency of unknown cause in some European studies suggests that the category comprises 20-39 percent of all individuals with HI . Although this represents an improvement compared to the 42 percent reported in the European survey (Martin et al, 1981), the high proportion of unknown cause in Hearing Impairment/Parving Table 5 Factors Causing Hearing Impairment in Childhood* Newton, 1985 (N= 111 ; > 25 dB HL) N Prenatal Genetic factors Fetal infection Malformations Various Perinatal Postnatal Otitis media sequelae Meningitis Measles/mumps Ototoxicity Various van Rijn, 1989 (N = 162 ? 35 dB HL) N % 43 33 15 N 46 64 9 2 14 14 5 15 9 11 6 8 1 3 4 1 Dias and Andrea, 1990 (N = 1024x; dB HL ?) 201 93 26 19 143 50 52 41 16 Vanniasegera m, et al 1993 (N= 101 ; >_ 50 dB HL) N 33 14 16 40 8 16 2 4 1 48 16 8 1 *The table should be read in conjunction with Table 6. 'In 10 subjects with conductive and 93 with perceptive HI, the etiology is known but not categorized . the samples supports the idea of a general ignorance about factors causing damage to the hearing organ in childhood. 111 1977-1980 39 been reported (Church and Gerking, 1988), and the ototoxicity and teratogenic effects of drugs are now often considered (Barr, 1982 ; Scott and Griffiths, 1994). Finally, noise exposure, even from infant toys (Jerger, 1994), or from the environment, may represent a hazard to the hearing of children. In fact, fetal noise exposure has been suggested as a causative factor (Lalande et al, 1986); however, the supportive evidence is scarce and fairly speculative. To the author's knowledge, a causal relationship between fetal infection with human immunodeficiency virus and HI has not yet been established, but some reports demonstrate auditory dysfunction in HIVaffected subjects (Real et al, 1987 ; Birchall et al, 1992). Since the virus is neurotropic, a fetal viral infection may affect the hearing organ and cause auditory dysfunction, resulting in a prenatal cause of HI . However, a sensorineural HI in HIV-infected subjects may be caused by other infectious agents or by sequels from encephalitis/meningitis; thus, the auditory dysfunction may be categorized as postnatal. Future research within this problem may support the speculations . 1568 Not defined 32 Concluding Remarks 162 1960-1975 34 1024 Not defined 27 181 1980-1990 20 101 Not defined 29 It seems likely that significant differences are present in the prevalences of causes of childhood HI among the European countries, considering the differences in the national child populations. However, in order to further document this, identical definitions and strict criteria for etiologic diagnosis, including intrinsic and extrinsic factors, Future Etiologic Perspectives A constant clinical awareness towards etiologic diagnosis may yield additional or new information on future diseases causing HI in children . Through such diligence, a likely relationship between HI and fetal alcohol syndrome has Table 6 Proportion (%) of Unknown Cause in Different European Reports Investigated (N) Martin et al, 1981 (EEC) Kankkunen,1982 (Sweden) Parving, 1984, 1988 (Denmark) Newton, 1985 (England) Lenzi and Zaghis, 1988 (Italy) van Rijn, 1989 (Holland) Dias and Andrea, 1990 (Portugal) Parving, 1993 (Denmark) Vanniasegaram et al, 1993 (England) Birth Unknown Cohorts Category (YO (°/0) 2988 1969 42 179 1970-1980 16 117/138 1970-1980 11/17 Journal of the American Academy of Audiology/Volume 6, Number 5, September 1995 should be introduced . The sensitivity and specificity of diagnostic tests and procedures should be evaluated, etiologic diagnostic programs implemented, and performance ensured of all pediatric units. As true changes in the causes of HI have been documented over time, a continuous monitoring of the causes should be performed, and this may result in preventative measures, nationally and internationally. CAUSES OF HEARING IMPAIRMENT INADULTS umerous factors, intrinsic and extrinsic N known and unknown - may affect the hearing organ in adults and result in permanent, predominantly sensorineural HI throughout life . The strong correlation between HI and age, gender (intrinsic factors), noise exposure, otitis media, and ototoxic drugs (extrinsic factors) has long since been established and known, and will not be concentrated upon in this context (e .g ., reviews by Davis, 1987 ; Henderson et al, 1993 ; Nadol, 1993 ; Scott and Griffiths, 1994). Throughout the last decade, lifestyle factors, such as diet, alcohol, and smoking, have also been emphasized (e .g ., Axelsson and Lindgren, 1985 ; Sikora et al, 1986 ; Dengerink et al, 1987 ; Stephens et al, 1991); however, the findings are controversial and much disputed, and it seems fair to state that major uncertainties still exist concerning lifestyle and HI . Solvent Exposure and HI Continuous exposure to organic toxic solvents has been accepted as a factor causing damage to the brain, resulting in cognitive dysfunctions or even severe degrees of dementia (Axelsson et al, 1980 ; Hein et al, 1990). This relationship has in some European countries been recognized by the political and administrative authorities, and may be based on legislation resulting in compensation, if the exposure can be ascribed to the occupational environment . An involvement of cranial nerves after organic solvent exposure has been demonstrated, including vestibular function (Odkvist et al, 1980, 1987). Moreover, an accumulation of animal (e .g ., Pryor et al, 1987 ; Sullivan et al, 1989 ; Johnson, 1994) and human studies (Barregard and Axelsson, 1984 ; Jacobsen et al, 1993 ; Morata et al, 1993) support the notion that toxic solvents represent a factor contributing to the development of HI . The exact mechanisms behind the damaging effect of organic solvents or solvents in combination with other damaging factors is 392 not fully understood, but a synergistic effect in rats between noise and organic solvents has been supported (Johnson, 1994), whereas an additive effect in humans has been suggested (Jacobsen et al, 1993 ; Morata et al, 1993). Among Brazilian workers within printing and painting manufacturers, a case-control study demonstrated significant differences between the prevalence of high-frequency HI in unexposed subjects (i .e ., 8%), combined noise and toluene exposure (i .e ., 53%), noise only exposure (i .e ., 26%), and organic solvent only exposure (i.e ., 18%) . The study estimated an adjusted relative risk of HI 4 times greater for the noise group, 11 times greater for the combined noise and solvent exposure group, and 5 times greater for the solvent only exposure group (Morata et al, 1993). In a Danish epidemiologic study, the relationship between self-assessed hearing problems and occupational exposure to solvents was investigated using a cross-sectional design with 3284 participating male subjects, aged 53-74 years. The study demonstrated that exposure to organic solvents for 5 years or more resulted in an adjusted relative risk for HI of 1 .4 (95% CI 1.1-1 .9) without exposure to noise. The factors adjusted for were age, noise trauma, chronic middle ear infection, and a family history of HI . The prevalence of HI was 24 percent in subjects not exposed to organic solvents, and the attributable risk from solvent exposure was 9.6 percent. Exposure less than 5 years had no effect on hearing ability. In contrast to the study by Morata et al (1993), the Danish study showed no additional effect from organic solvents to noise exposure, which was by far the most hazardous factor to hearing ability. Although some controversies between the mentioned studies exist, it seems likely that a moderate adverse effect on hearing sensitivity in humans is caused by toxic organic solvents, which should be accounted for and prevented in the working environment. Disorders in Endocrine Glands Hypothyroidism Since 1907, a relationship between acquired hypothyroidism and reduced hearing sensitivity has been claimed (Kemp, 1907), often based on single case stories or upon small, uncontrolled samples treated with L-thyroxine, demonstrating improvements in hearing sensitivity (Ritter and Lawrence, 1960 ; Sachdev and Hall, 1975). These findings have been disputed (de Vos, Hearing Impairment/Parving 1963 ; Post, 1964), and, more recently, case-control studies in subjects above and below the age of 60 years have failed to demonstrate an effect of thyroid hormone on the hearing ability in subjects with acquired hypothyroidism (Parving et al, 1983, 1986). In addition, no evidence for a causal relationship between hypothyroidism and hearing disability was found using an epidemiologic approach (Parving et al, 1993). Experimental animal studies showing morphologic and functional abnormalities cannot be disregarded; however, many animal experiments have concentrated on congenital hypothyroidism, which originates in the developing ear and thus is completely different from hypothyroidism acquired in adulthood. Thus, no morphologic or specific histologic abnormalities were demonstrated in the temporal bones from elderly subjects dying with untreated myxoedema (Parving et al, 1986 ; Hald et al, 1991), and, in addition, no deposition of neutral or acid glycosaminoglycans could be found in postmortem examinations of the brain from two subjects (Hald et al, 1991). However, as the thyroid gland is an essential regulator of cellular metabolism, the claimed relationship between hypothyroidism and HI based on treatment with L-thyroxine may be due to improved cellular mechanisms in the organ of Corti, or in the neurogenic tissue of the cochlear nerve, or in a combination of these. The continuing demonstration of improvements in hearing ability in hypothyroid patients upon treatment should perhaps be explained by a better cooperation in psychoacoustic testing, when the patient is euthyroid, and thus in a better, general health condition . Although the pathoanatomical literature is scarce on this subject, the hypothesized functional relationship between HI and acquired hypothyroidism in adults is strongly supported by preliminary findings showing a lack of morphologic and histologic abnormalities in the temporal bones and brains from such patients . Diabetes Mellitus The claim of a causal relationship between HI and diabetes mellitus is also controversial in clinical, epidemiologic, and histologic studies (e .g., Jorgensen and Buch, 1961 ; Friedmann et al, 1975 ; Taylor and Erwin, 1978 ; Gibbin and Davis, 1981 ; Parving et al, 1990, 1993 ; Ferrer et al, 1991 ; Triana et al, 1991 ; Rust et al, 1992). Some of the conflicts derived from clinical studies may be ascribed to the pronounced heterogeneity of diabetic patients in the investigations and/or to lack of strict criteria for HI and/or to less sophisticated techniques for assessment of hearing disorders in the past . In a case-control study including only subjects with long- and short-term insulin-dependent diabetes mellitus, pure-tone audiometry failed to demonstrate a relationship between HI and diabetes mellitus when adjusted for age and sex, whereas the results of auditory brainstem response showed prolonged latencies of the I-V intervals in 40 percent of the long-term patients and in 5 percent of the short-term patients (Parving et al, 1990). This supported previous findings by Donald et al (1981) and Fedele et al (1984), and a subsequent study including MRI and neuropsychological testing showed signs of damage to the central nervous system and supported the hypothesis of a diabetic encephalopathy (Collier et al, 1988 ; Pozzessere et al, 1988) including the central auditory pathways (Dejgaard et al, 1991). However, so far, histologic studies of the brains, temporal bones, or central auditory pathways from the investigated subjects have not been reported, and the causal relationship between diabetes mellitus and HI - whatever the site of lesion should still be a subject for future investigations and dispute . Concluding Remarks Concerning factors causing HI in adults, the intentions were to briefly summarize some evidence for extrinsic factors, such as toxic organic solvents that are likely to cause damage to the hearing organ, and point out the highly controversial findings within hypothyroidism and diabetes mellitus, to which some of the author's own research has contributed. Other investigations, both mentioned and unmentioned, are highly acknowledged by the author, who apologizes for both deliberate exclusions of references and for ignorance. 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