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ARTICLES Table of Contents   
Year : 2006  |  Volume : 8  |  Issue : 30  |  Page : 40-44
Hearing loss in young men: Possible aetiological factors

1 Department of Audiology, Karolinska Hospital/Karolinska Institutet, Stockholm, Sweden
2 Dept. of Otolaryngology, Tampere University Hospital, Finland
3 Division of Epidemiology, Norrbacka, Karolinska Hospital/Karolinska Institutet, Stockholm, Sweden
4 Swedish Armed Forces, Sweden

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In the present retrospective register study a very large data base consisting of screening audiograms obtained at military conscription of 18-year-old Swedish men was used. The study group comprised 450,175 men, aged 18 years, tested at conscription to military service. There were nine age groups covering a 24-year period, from 1971 to 1995. This database was compared with a number of different pre- and postnatal factors with possible influence on the hearing function. This ecologic methodology gives tentative clues (but no proof) of possible ototraumatic influences. The hearing capacity was fairly similar during the entire span of the study and only small variations were observed. There was a slight tendency of better hearing capacity in the later age groups, compared with the earlier ones. The mean thresholds of the frequencies 4 and 6 kHz were slightly elevated in 1971, 1976 and, to some extent also in1992. We tried to calculate the levels of leisure noise exposure during the study period. There was no apparent tendency of reduced noise levels, on the contrary the noise levels seemed to increase. The treatment programmes for acute otitis media (AOM) underwent considerable changes during the period from the early fifties to the early eighties, when the participants were pre-school children. One possible explanation for the slight improvement of the hearing capacity could be less ototraumatic influence of AOM. Data about the occurrence of four common epidemic diseases, covering the periods preceding and succeeding the years when the participants were born indicated that influenza and possibly pertussis (whooping cough), constitute putative prenatal risk factors for mild to moderate high frequency hearing loss.

Keywords: Conscripts, ecological method, influenza, middle ear infections, pertussis, screening audiometry

How to cite this article:
Rosenhall U, Pyykko I, Rasmussen F, Muhr P. Hearing loss in young men: Possible aetiological factors. Noise Health 2006;8:40-4

How to cite this URL:
Rosenhall U, Pyykko I, Rasmussen F, Muhr P. Hearing loss in young men: Possible aetiological factors. Noise Health [serial online] 2006 [cited 2023 Jun 3];8:40-4. Available from: https://www.noiseandhealth.org/text.asp?2006/8/30/40/32466

  Introduction Top

Causative factors of hearing loss have been studied, especially regarding moderate to profound hearing loss or total deafness in childhood. [1],[2] Inherited hearing loss has been reported in about half of cases (46-50%) with permanent, most often severe hearing loss in childhood. [3],[4] Other factors are prenatal infections, perinatal influence and postnatal causes like middle ear infections and meningitis. Unknown cause is common, 20% in Parving´s study [1],[2] and 34% in a study from northern Sweden. [3] Moderate to profound hearing loss or total deafness has profound impact on the development of speech and the ability to communicate. Also mild hearing loss might cause problems, but the effects of less pronounced auditory problems in childhood and adolescence are not well known. Aetiological factors causing mild to moderate hearing loss are not well known. High frequency hearing loss of, most cases mild, is common among 13-year-old Swedish schoolchildren (17-20% at 6 kHz), suggesting an early onset of noise induced hearing loss. [5]

The aim of the present study was to investigate possible pre- and postnatal influences on the auditory function of 18-year-old men. The degree of hearing loss studied was mild to, at most, moderate.

  Materials and Methods Top

Study design

The study is ecologic and retrospective and based on information from various registers, as well as scientific reports, historical as well as modern ones. The cited studies have been selected to represent Swedish conditions. Data on hearing capacity was obtained by screening audiograms from conscription of very large numbers of 18-year-old men tested from 1971 to 1995.

Study groups

In Sweden there is (or used to be) compulsory military service for all able men. At age 18 all young men are obliged to show up at one of six conscription centres located at different parts of the country. Nine age cohorts of 18-year old men born from 1953 to 1977 were selected for the study. The men were tested from 1971 to 1995. From 1971 to 1991 every 5 th year was included, from 1991 to 1995 every year. In total 503,689 18-year old men identified in the register of total population at the beginning of the years of conscription from 1971 to 1995. In all 458,910 men were tested with audiometry at conscription examinations, resulting in a drop out frequency of 10.6%. The cohorts varied in size from 55,652 conscripts (participants born in 1963), to 43,841 (participants born in 1977).

All 18-year-old men did not need to appear at the conscription centres during the study period. Exemption from military service was accepted without personal appearance at the centres, provided that a medical certificate issued by a medical doctor could be presented. A number of diagnoses e.g., moderate to pronounced hearing loss, were accepted as reasons for exemption. In 1991, 1.25% of the 18-year old men were exempted from military service because of hearing loss prior to conscription examination without personal appearance. [6] This approximate figure must therefore be added to those presented here in order to get true prevalence figures of hearing loss. For this reason the present investigation concerns mild or at most moderate, hearing impairment.

Conscript audiometry

All conscripts were tested with screening audiometry. Manual screening audiometers (Tegnιr PTA 6) were used up to 1990-91, at that time the manual audiometers were replaced by automatic audiometers (Entomed SA 250). The audiometers were calibrated according to internationally accepted methods. All hearing tests were performed in sound-insulated test rooms. Pure tone levels of the frequencies 0.5, 1, 2, 3, 4 and 6 kHz were determined in 5 dB steps by utilizing the ascending method in both the manual and automatic methods. The screening level 20 dB HL was used. Only air conduction measurements were done and masking of the opposite ear was not performed.

Exposure to ototraumatic factors

The ecologic analysis was performed by estimating exposure to various ototraumatic factors that the participants could have been exposed to during childhood and adolescence. Such patterns of exposure over time are difficult to estimate, but attempts have been done to do so. The studied period includes almost half of the 20 th century (from 1953 to 1995) and substantial changes in the society occurred during this long time.

An important factor with considerable variation during the half century is exposure to noise. Leisure time noise exposure includes noise from loud, amplified music, power tools, noisy toys, firecrackers and motor sports. An estimation of exposure to amplified music was performed by means of comparing two studies from different periods in the same region in western Sweden. [7],[8] Impulse noise from firecrackers and cap guns exceeds the risk levels for hearing loss. [9] The incidence of acoustic trauma due to New Year's firecrackers in different age groups was highest among 19-year-old men in a German study. [10] In a study in Finnish teenagers 51% of the study group estimated to be exposed to noise levels detrimental to hearing acuity. The highest noise exposure came from playing in a band, discos and rock-concerts, motor sports and shooting. [11] In summary, during the period from the fifties to the nineties the leisure time noise exposure has been increasing. The proportion of teenagers beginning the working life already at the age of sixteen, when compulsory school ends, has been decreasing during the study period. In the 70ties 74% of the young men went to senior high school, in the 90ties this figure was 89%. Much effort has also been put into hearing conservation programs during this period. The mean occupational noise exposure is lower today compared to 30 years ago. Because of this the prevalence of hearing loss has decreased in many occupational settings, e.g., in automobile industry. [12] There has also been a strong tendency during the period of fewer employed in extremely noisy sectors as shipyards and mining industry. Accordingly, there is much evidence that the number of teenagers exposed to significant occupational noise has decreased from the Seventies to the nineties. In summary, a considerable number of young men are exposed to significant leisure time noise, an exposure that has increased over the study period. A much smaller percentage is exposed to occupational noise, an exposure that has decreased. We assume that the overall noise exposure during the period seems to have increased for young men during the study period.

Middle ear disease represents another factor with a considerable variability during the study period. The first age cohorts grew up in the early antibiotic era. The treatment for acute otitis media (AOM) was low dose penicillin V, often in combination with tympanotomy (most often without sedation). The present day treatment is different and is characterised by high dose antibiotic treatment, a variety of antibiotics available, but also development of resistant bacterial strains. The pre-antibiotic era in this study is represented by a thesis by Lundgren [13] from southern Sweden and the modern era by an investigation by Ryding et al [14],[15] also from southern Sweden. In Lundgren´s study 448 children were followed up after AOM. [13] In the study by Ryding et al. [14],[15] 113 children were followed up from birth to the age of three years.

Epidemiological data regarding the occurrence of contagious, epidemic diseases in Sweden up to 19 years before the conscription tests could give information of possible pre- and neonatal influence of the hearing of the participants. Information about epidemic diseases was obtained from the Swedish Institute for Infectious Disease Control (SIIDC). There used to be an obligation for medical personnel to report certain common epidemic diseases to the health authorities in each county. Naturally, only patients who consulted a doctor, most often a GP, were reported. Due to limitations of the available epidemiological data we were unable to calculate age specific or age adjusted incidence rates. However, absolute number of cases reported to SIIDC per year is considered a reasonably good indicator of the timing of epidemics of influenza, measles, pertussis, rubella and serous meningitis. While individual records with information an audiometry and personal identification numbers were available in the conscript registry only, aggregated data were available about epidemic diseases. We were thus not able to perform record-linkages between the two information sources. The numbers of reported cases of influenza, pertussis, measles and rubella for each year from 1952 to 1980 are illustrated in [Figure - 1] BD.

Rubella was only reported to SIIDC during the last part of the period, from 1969. In order to obtain information about epidemics of rubella before that year, data from the Military Health Services were used. The number of military servicemen reported to have rubella was used to monitor the disease from 1952 to 1973. There was a very good concordance between the two methods of registration regarding the pattern of rubella epidemics from 1969 to 1973, when both registrations were used [Figure - 1]E. Serous meningitis was also reported, but, with the exception of the year 1957, the reported numbers were small, in most years less than 1,000 cases (annual mean: 670). The two largest peaks were recorded in 1957 (13,162 cases) and in 1973 (2,395 cases).

  Results Top

Conscript audiometry

The hearing of the 18-year-old men belonging to the different birth cohorts was, in general, excellent. Pure tone thresholds for the frequencies 0.5, 4 and 6 kHz are shown in [Figure - 1]A. The mean high frequency hearing (4 and 6 kHz) was slightly poorer in 1971 and 1976 than in the later age cohorts. A small, solitary peak was also observed in 1992. The hearing at 0.5 kHz was the same over the study period.

Noise exposure

The improved hearing function observed in the last two decades has certainly no correlation to changes in noise exposure during the same time. There are no indications that the exposure to noise has decreased among young people. On the contrary, the sound levels seem to have increased during the study period.

Middle ear disease

In Lundgren´s study from the pre-antibiotic era [13] only 68% had normal hearing at the follow up. Half of those with hearing loss had high frequency loss (16%) and half had low- or mid frequency hearing loss. Ryding et al [14],[15] found no or only minor influence on auditory function. A long-term influence of AOM on high frequency loss is possible and could be one explanation for the decreased incidence of hearing loss observed here.

Epidemics of contagious diseases

The situation regarding epidemics of the four common contagious diseases included in the study at the calendar years preceding and succeeding the years of birth of the study subjects is shown in [Figure - 1] B and C. Major outbreak of influenza was registered three times during the study period, in 1957, 1960 and 1969. The first one in 1957 was one of the major pandemics of influenza during the 20 th century, the "Asiatic 'flu", which was highly virulent and contagious. One telling sign of this is that the number of persons with serous meningitis rose dramatically in the year 1957. The cohort born in 1958, the year after this pandemic, had one of the highest prevalence of mild hearing loss in the study. The other outbreaks of influenza were less severe. The influenza epidemic in 1960 occurred between the years of birth of two cohorts in this study (1958 and 1963) and cannot be used to evaluate influenza as a pre- or postnatal risk factor for hearing loss. The third influenza epidemic, in 1969, appeared when those born in 1968 were one year old, with no apparent influence on the hearing. As mentioned, a remarkable peak of serous meningitis was reported to the SIIDC in 1957. The second largest peak was registered in 1973. The conscripts born in 1974 had a slight increase of hearing loss affecting the frequency 6 kHz [Figure - 1].

The annual number of reported cases of pertussis decreased from the late fifties to the late sixties. One important reason is a successful vaccination programme. The frequency of hearing loss also declined during this period. From 1968 to 1976 pertussis was almost totally eliminated. During the last years of the study it appeared again, because of the introduction of a less efficient vaccine. No postnatal increase of the incidence of hearing loss was observed then.

Measles and rubella showed a highly variable course with many outbreaks during the study period. The effect of a vaccination programme for rubella, that started in Sweden in 1972, cannot be recognised in the present study. These diseases cannot be connected to either pre- or postnatal occurrence of mild hearing loss (it must be stressed that all subjects with severe to profound hearing loss had been excluded from this study).

  Discussion Top

There was a tendency in the present study that the hearing had become somewhat better in 18 year-old men in the eighties and nineties compared with the seventies. One explanation is a decrease of the incidence of hearing loss in the last two decades, compared to the first. Another explanation is that the hearing loss cases had become less severe with time or a combination of both explanations. High frequency hearing loss is common among young persons and has above all been attributed to noise exposure. [6],[16] There are, however, no indications that the exposure to noise has decreased among young people. There is a possibility that AOM has an influence of the hearing in the long term, causing low frequency hearing loss (of a conductive) and possibly also high frequency hearing loss (of a sensorineural type). This latter component might provide one explanation for the higher incidence of hearing loss in the earlier study groups.

Among a variety of potential etiologic factors causing hearing loss, infectious diseases (other than AOM) constitute an important, but rather neglected, group. [17] Well-known examples of infections that might cause hearing impairment are rubella, cytomegalovirus infection, bacterial meningitis and mumps. The casual relations between each one of these infections and hearing loss is well recognised. A variety of other infections have also been suspected to cause hearing loss. [18] However, epidemiological evidence of hearing loss of infectious origin are still lacking, except for the diseases mentioned above. Links between influenza and hearing loss have been reported. [19] An animal model, using ferrets, of influenza as a causative agent to hearing loss has been developed. [20] The virulent and contagious influenza that struck the world as a pandemic in 1957, the "Asiatic 'flu", was one of the major pandemics of influenza during the 20 th century. The cohort born in 1958, the year after this pandemic, had the highest frequency of mild hearing loss in the study. This observation indicates a possible prenatal influence on the auditory function of influenza, resulting in an accumulation of mild hearing losses measurable many years later. The other two major outbreaks of influenza epidemic occurred between the years of birth of two cohorts and cannot be used to evaluate influenza as a putative prenatal risk factor for hearing loss.

In the literature pertussis is only sporadically claimed to be a putative cause of hearing loss. [21] In the present study, the occurrence of pertussis seems to be parallel to the incidence of mild hearing loss. Peaks of slight high frequency impairments were seen in the years 1971 and 1976, followed by a decline in subsequent years. Pertussis followed the same pattern with a very low occurrence in the population between 1968 and 1976. The possible influence is therefore probably a prenatal one, especially since the highest peak of the disease occurred the year before the cohort born in 1958, the one with the highest incidence of mild hearing losses in young adult life.

In the present study we have demonstrated slightly poorer high frequency hearing in 18-year old men screened for hearing loss in 1971 and 1976 than in the later age cohorts. Prenatal exposure to influenza and possibly pertussis, may explain the observed variations between the different birth cohorts in occurrence of high frequency hearing loss as described above. However, based on this ecological study we can certainly not rule out other putative risk factors, like changes of life style.

Sensorineural hearing loss in young adults is important to notice, since it might signal auditory problems in later life. Much interest has been focused on aetiological aspects of hearing impairment and why the frequency of hearing loss increases so considerably with increasing age. From this perspective it is motivated to study how mild hearing loss arises and more research aiming to investigate infectious backgrounds of auditory dysfunction is needed.

Results of the present study indicate - but do not prove - that two common epidemic diseases, influenza and possibly pertussis, are hitherto unrecognised pre or early postnatal risk factors for mild hearing loss in young adulthood. Future epidemiological research based on more reliable study designs may shed more light on this issue, which might have public health implications, e.g., regarding vaccination programmes.

  Acknowledgement Top

The contributions of the Swedish National Service Administration for audiometric data from conscription centers and the Swedish Institute for Infectious Disease Control for data concerning epidemic diseases, are gratefully acknowledged.

  References Top

1.Parving A. Hearing disabiolity in childhood - a cross-setional and longitudinal investigation of causative factors. Int J Pediatr Otorhinolaryngol 1993;27:101-11.  Back to cited text no. 1    
2.Parving A. Factors causing hearing impairment: Some perspectives from Europe. J Am Acad Audiol 1995;6:387-95.  Back to cited text no. 2    
3.Sehlin P, Holmgren G, Zakrisson J. Incidence, prevalence and etiology of hearing impairment in children in the county of Vδsterbotten, Sweden. Scand Audiol 1990;19:193-200.  Back to cited text no. 3    
4.Parving A, Stephens D. Propfound permanent hearing impairment in childhood: Causative factors in two European countries. Acta Otolaryngol 1997;117:158-60.  Back to cited text no. 4    
5.Costa OA, Axelsson A, Aniansson G. Hearing loss at age 7, 10 and 13--an audiometric follow-up study. Scand Audiol Suppl 1988;30:25-32.  Back to cited text no. 5    
6.Axelsson A, Rosenhall U, Zackau G. Hearing in 18-year old Swedish males. Scand Audiol 1994;23:129-34.  Back to cited text no. 6    
7.Axelsson A, Lindgren F. Hearing in pop musicians. Acta Otolaryngol 1978;85:225-31.  Back to cited text no. 7    
8.Kδhδri KR. The influence of music on hearing. A study in classical and rock/jazz musicians. Doctorial thesis, G φteborg University: 2002.  Back to cited text no. 8    
9.Hellstr φm PA, Dengerink HA, Axelsson A. Noise levels from toys and recreational articles for children and teenagers. Br J Audiol 1992;26:267-70.  Back to cited text no. 9    
10.Plontke SK, Dietz K, Pfeffer C, Zenner HP. The incidence of acoustic trauma due to New Year's firecrackers. Eur Arch Otorhinolaryngol 2002;259:247-52.  Back to cited text no. 10    
11.Jokitulppo JS, Bj φrk EA, Akaan-Penttilδ E. Estimated leisure noise exposure and hearing symptoms in Finnish teenagers. Scand Audiol 1997;26:257-62.  Back to cited text no. 11    
12.Bruhl P, Davidsson C, Ivarsson A. Noise emission zones in an automobile sheet-metal pressing plant, a 25-year follow-up study at three locations in the plant. Int J Occup Med Environ Health 1996;9:153-62.  Back to cited text no. 12    
13.Lundgren N. The auditory function after otitis media in infancy and earlier childhood. Acta Otolaryngol Suppl 1944;53.  Back to cited text no. 13    
14.Ryding M, Konradsson K, Kalm O, Prellner K. Sequelae of recurrent acute otitis media. Ten-year follow-up of a prospectively studied cohort of children. Acta Paediatr 1997;86:1208-13.  Back to cited text no. 14    
15.Ryding M, Konradsson K, Kalm O, Prellner K. Auditory consequences of recurrent acute purulent otitis media. Ann Otol Rhinol Laryngol 2002;111:261-6.  Back to cited text no. 15    
16.Borchgrevink HM. Effects of noise and blast. Scand Audiol 1990;19:7-18.  Back to cited text no. 16    
17.Davis LE, Johnsson LG. Viral infections of the inner ear: Clinical, virologic and pathologic studies in humans and animals. Am J Otolaryngol 1983;4:347-62.  Back to cited text no. 17    
18.Roizen NJ. Etiology of hearing loss in children. Nongenetic causes. Pediatr Clin North Am 1999;46:49-64.  Back to cited text no. 18    
19.Rantakallio P, Jones P, Moring J, Von Vendt L. Association between central nervous system infections during childhood and adult onset of schizophrenia and their psychoses: A 28-year follow up. Int J Epidemiol 1997;26:837-43.  Back to cited text no. 19    
20.Rarey KE, DeLacure MA, Sandridge SA, Small PA Jr. Effect of upper respiratory infection in the ferret model. Am J Otolaryngol 1987;8:161-70.  Back to cited text no. 20    
21.Catlin FI. Prevention of hearing impairment from infection and ototoxic drugs. Arch Otolaryngol 1985;111:377-84.  Back to cited text no. 21    

Correspondence Address:
Ulf Rosenhall
Department of Audiology, Karolinska Hospital, SE-171 76, Stockholm
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1463-1741.32466

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