Causes of Hearing Loss in the Australian community
Injury to the auditory system and consequential hearing loss through excessive noise exposure is a global pandemic. Industrial noise exposure is the greatest cause of noise induced hearing loss (NIHL). Hearing protective devices are able to effectively suppress noise to within safe levels, however most available devices also reduce speech intelligibility. Frost and Sullivan (2002). Litigation has recently been mandated in Australian industries to ensure the use of hearing protective devices. A report by researchers Wilson et al. (1998) illustrates that “a noise component was associated with 37% of people with hearing loss. That is, for 37% people with a hearing loss, noise was responsible for at least part of their hearing loss. The most common sources of noise injury are workplace noise and recreational noise (personal stereos, domestic use of power tools and motor sports), although the attributable fractions for each have been debated. (Acess Economics, 2006). The total financial cost of NIHL was estimated at $11.75 billion in 2005, which was 1.4% of GDP or $200 for every Australian (Frost & Sullivan, 2005). In many industrialised countries it is considered the biggest compensatable occupational hazard. There are hidden costs associated with noise and these include the detrimental effects on work attendance, staff turnover, employee quality and productivity. NIHL is the greatest preventable cause of hearing loss.
Audiological examination of individuals with NIHL will typically show a characteristic notch at 4 KHz. Martin & Martin (1993, as cited in Rappaport & Provencal, 2002) describe the proposed mechanisms underlying this 4 KHz notch. These include “the acoustic resonance of the external auditory canal, mechanical injury caused by severe motion of the basilar membrane, metabolic exhaustion of activated cells, vascular narrowing causing ischemia, and ionic poisoning from interruption of the chemical gradients of the inner ear.”
Initial exposure to excessive noise will produce a temporary hearing threshold shift that will persist for a limited period of time. Prolonged or high intensity exposure may cause a permanent threshold shift with irreparable sensori-neural hearing loss. The insidious nature of a noise injury is that the consequential permanent hearing loss is usually delayed and cumulative.
A primary initiative is educating people of the damaging effects of excessive noise exposure and how to appropriately protect their hearing in their respective environments. WorkSafe occupational health and safety regulations ensure hearing conservation programs are implemented in Australian Industries. The noise exposure limits imposed by the regulations are an 8 hour average of 85
dB(A) Leq and a peak noise level of 140 dB(C) at the employee’s ear position. (WorkSafe, 2007). Litigation should increasingly focus on recreational noise hazards such as restrictions at concerts or in orchestral settings. As described by TechEnclave (2007), “the damage to your ears depends both on the noise level and time of exposure. Prolonged exposure to any noise above 85 dB can cause gradual hearing loss. Stereo rock music can have levels of 110 – 125 dB and rock concerts between 110 – 140 dB and at such levels regular exposure of more then 1 minute risks permanent hearing loss.” Also described is that all combinations of headphones/earphones and MP3 players generate potentially harmful sound levels. Twelve minutes at 102 dBA to seven hours at 86 dBA will exceed the occupational noise limit. You will exceed the limit in just one minute if you played heavy metal or pop music at full volume levels of 114 dBA. “At these sound levels exposure for longer durations can pose a risk of immediate, serious and permanent hearing loss.” TechEncave (2007, p.4) Litigation is beginning to address this problem by restricting the maximal output levels of personal listening devices and public music events.
Technological advances in hearing protection include the use of ear plugs with graded attenuation levels and frequency responses. For example musician’s ear plugs have a flat frequency response allowing the natural preservation of acoustic content whilst attenuating the signal to within safe and comfortable listening levels. Innovations in electronic hearing protection have produced two main categories; products that improve short range communication in noisy environments, whilst attenuating harmful sounds to with safe and comfortable limits and products that provide entertainment during work and play. Such devices can be called Noise Canceling Ear Muffs or Active Ear Muffs. A manufacturer and supplier of such products is the Elvex Corporation. On their website they explain that “The technology used is not noise cancellation but rather different compression and filtration techniques. Also FM radio earmuffs are included in the electronic hearing protection category.” (Elvex, 2006,p.1) Quality non electronic ear muffs range in price from about $30 to $130, whilst electronic muffs typically range from $50 to $500 Australian dollars depending on the quality and purpose of use.
Intensified education and litigation applied holistically to noise abatement will help reduce the incidence of NIHL. A commonwealth program should investigate a full range of industries to identify noise hazards. Suitable noise abatement strategies could then be advocated. The costs of implementing suitable noise management programs would vary depending on industrial requirements and incentives provided for timely compliance.
According to the World Health Organisation (WHO) Chronic middle ear infection is the main cause of mild to moderate hearing impairment in children. As described by Dhooge et al. (2003, cited on the ASHA website 2007) “Otitis Media (OM) is an inflammation of the middle ear that is usually associated with the build up of fluid. The fluid may or may not become infected. Symptoms, severity and frequency, and the length of the condition may vary. At one extreme is a single short period of thin, clear, non infected fluid without any pain or fever but with slight decrease in hearing ability, whilst the other extreme can be repeated bouts with infection, thick “glue-like” fluid and possible complications such as permanent hearing loss.” A fluctuating conductive hearing loss usually accompanies OM and can have a lifetime of impact due to the impairment of hearing during the critical years of speech and language development. A report by Zinkus & Gottlieb (cited in Anderson et al. 1979) describe that “children with histories of severe chronic otitis media during the first three years of life, suffer subsequent educational retardation, as well as significant lowering of verbal intelligence. Additionally it has been observed in Australia that severe recurrent otitis media in early childhood resulted in later problems of articulation, deficiencies in connected speech and in the use of phoneme combinations.”
As described by Dhooge et al. (2003), “Seventy five percent of children experience at least one bout of OM by their 3rd birthday and almost half of these children will have 3 or more infections during their first 3 years of life.” It is so common in young children because the eustachian tube, a passage between the middle ear and the back of the throat, is smaller and nearly horizontal in children than in adults and is easily blocked by conditions such as large adenoids and infections. Until the eustachian tube changes in size and angle as the child grows, children are more susceptible to otitis media.
Poor living conditions found in many inland indigenous communities increase the likelihood of children perpetuating a Chronic Suppurative Otitis Media (CSOM) disease cycle. A spectrum of risk factors include; overcrowding, lack of appropriate washing facilities and clean water, poor hygiene, inadequate parental care, malnutrition, social problems such as alcoholism, smoking and sub-optimal access to appropriate health care facilities. Risk to young infants is greatly increased by exposure to contagious siblings, in larger families with more infectious siblings and in those that attend day care. Infants that aren’t breast fed fail to acquire maternal antibodies through breast milk and are left with an immature immune system. Those who experience their first episode of Acute Otitis Media (AOM) before six months of age are also prone to recurrent episodes. (Henderson et al., cited in Mathews,1992).The WHO has indicated that a prevalence rate of greater then 4% in a defined population of children is a massive health problem requiring urgent attention. CSOM effects up to 40% of children living in some aboriginal communities.
Pathogens usually consist of multiple bacterial species that colonize the naso-pharynx. Frequent exposure of infants to contagious siblings usually results in otitis media becoming established as early as 1 to 4 weeks after birth. AOM can leads to an acute perforation of the tympanic membrane, with purulent discharge. Some episodes of AOM can resolve completely without treatment over a period of hours or days, however the associated middle ear effusion (MEE) needs days or weeks to resolve. Untreated episodes of AOM can also lead to a more persistent otitis media with effusion (OME). Chronic OME can lead to an immobilization of the tympanic membrane and a thickening of the fluid in the middle ear known as “glue ear”. Consequently a conductive hearing loss is sustained. CSOM is diagnosed on the basis of persistent or recurrent purulent otorrhoea. CSOM is rare in children with access to good medical care. (Mathews et al. 1992)
Dr Alastair Mackendrick explains that the incidence of middle ear disease tends to naturally decrease by 5 to 6 years of age and usually resolves by the early teens. Repeated perforations can eventually result in a chronic perforation. The longer the perforations persist the greater the likelihood of permanent damage to the middle ear structures and the contribution of a sensori-neural hearing loss. Although the tympanic membrane often heels, some perforations may remain.
Dr A.J. Mackendrick, (personal communication, August 3rd, 2007)
As stated by Dr Coates et al. (2002), “In the aboriginal population the best predictor of an impending perforation is a bulging tympanic membrane.” Other signs and symptoms of acute otitis media such as pain, fever, irritability or redness of the tympanic membrane may be absent or go unnoticed. Due to the lack of signs and symptoms parents may not see their child as being unwell and consequently their children remain untreated. To date the hearing needs of aboriginal children are not being adequately met. Dr Coates indicates that there needs to be greater access to therapy, hearing aids, special teachers, classroom sound-field systems and other rehabilitative programs. Funds from the Commonwealth hearing health services program need to redistributed such that indigenous ear health programs receive a more equitable share. As described by Coates et al. (2002), “The Commonwealth needs to reform the provision of rehabilitative services and coordinate approaches to sound-field amplification in schools he government need to reform the provision of health care services.”
The incidence and impact of otitis media varies across regional distributions of indigenous communities. Rural communities generally have a lower socioeconomic status then urban communities and a corresponding higher incidence of middle ear disease. In central Australia in 1982 a screening of aboriginal school age children showed 53% had significant hearing losses in one or both ears compared with 11% in non aboriginal school aged children. Of those with hearing losses 32% had perforated drums. An average hearing loss above 30 dB was present in between 34% – 65% of these children in different communities compared with only 8% in non-aboriginal school aged children. 12% had hearing losses in the better ear of between 40 – 50 dB. Quinn. (1983, as cited in Mackendrick, 1999).
A survey conducted by Kelly, and Weeks (1991) in 3 aboriginal communities showed a similar incidence of perforations and hearing loss in the rural communities. Urban aboriginals in the survey had 50% less ear problems than rural aboriginals, but still a much higher incidence then non-aboriginal populations. As stated by Dr Mackendrick (1999), “the long term effects of recurrent infection is significant hearing loss in a high proportion of cases, as well as a significant incidence of cholesteotoma. It has been accepted practice by many clinicians to manage suppurative otitis media medically and wait for spontaneous healing of perforations, which does occur in a high proportion of cases.”
Increased socio-economic status has seen Broome in W.A. grow substantially over the last 20 years. There has been a large reduction in the incidence of middle ear disease with enhanced access to fresh water, hygiene, nutrition, greater parental care and medical services. Episodes of OM have become less acute or “less florid”. These lower grade form of OM have resulted in a decline of perforations and the suppurative forms of otitis media (SOM), However as the effusion remains longer the incidence of “glue ear” has correspondingly increased. This has predisposed to the greater incidence of retraction pockets leading to cholesteotoma. The incidence of cholesteotoma has been reported to be as high as 10 % in cases of Chronic OM. Specialist services to Broome should be increased to remediate these emerging problems.
Remediation of the problem would require an intensive holistic approach aimed at improving the overall living conditions of afflicted indigenous communities. Developing infrastructure to provide better housing, access to education, medical services and fresh water could initiate the process. Strategies to address the social problems of alcoholism, passive smoking and domestic violence would be necessary. Such changes would facilitate improved parental care, hygiene, promote breast feeding, nutrition and general well-being. The cost of developing such infrastructure would run into the millions of dollars per annum.
Medical initiatives include increasing primary health care for the detection and management of ear disease, the widespread use of vaccines such as the polysaccharide, polyvalent pneumococcal and new pneumococcal conjugate vaccine. Where primary health care interventions have failed timely referral to Otolaryngologists for assessment and surgical interventions can improve hearing outcomes. The effectiveness of antibiotics remains controversial and high and prolonged courses of antibiotics are required. Optimal use of topical applications is also beneficial. Along with ear toileting with benadine solution, topical application of anti-biotics can be pumped into the middle ear. (Mackendrick, 1999).
Future research should focus on the best use of preventive strategies and interventions including educational, medical, surgical and audiological initiatives. A current initiative is the Office for Aboriginal and Torres Strait Islanders Health Hearing Program. A flying medical service exists where children in isolated towns such as Balgo, Billi Luna and Buesk are flown to Broome for specialist intervention.
Presbycusis is a term used to describe a deterioration of auditory function with advancing age and could be considered the most universal cause of hearing loss. All major divisions of both the peripheral and central auditory mechanisms are susceptible to deterioration. It typically manifests as a bilateral hearing loss of frequencies above 2 KHz and progressively affects lower frequencies. According to Sussman (2000), most people over the age of 50 slowly loose some ability to hear. Presbycusis is not just caused by physiological age related changes it may simply be the result of a build up of wax in the ear or progressive damage to the inner from infection, disease, injury and loud noise.
Hearing loss as a result of viral or bacterial infection is also common. For example the measles virus may produce a moderate to severe bilateral hearing loss with the potential vestibular involvement as well. Rigorous screening and vaccinations can minimize the risk of hearing loss from such microbes. Various drugs can be ototoxic causing hearing and balance disorders. Rappaport & Provencale (2002) explain that antibiotics such as aminoglycosides (e.g. gentamicin) as well as chemotherapeutic agents (e.g., cis-platinum). Whenever these drugs are used there should be a program of audiologic screening. Also renal function should be considered a cofactor for the development of such ototoxicity.
The majority of hearing loss in the Australian population is acquired rather then congenital. The human auditory system has evolved with a wide dynamic range and is highly sensitive. It is vulnerable to the high intensity impulse sounds and persistent high intensity sound prevalent in modern industrialized society. The worldwide pandemic of NIHL needs to be addressed. Generating awareness through education and litigation has initiated the process however such measures need to be broadened and intensified. The WHO advocates a hearing impairment and deafness control strategy within their department of chronic diseases and health promotion. In Australia initiatives are gathering momentum in addressing the problems of chronic middle ear disease in indigenous communities.
References
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CRC Hear and the Victorian Deaf Society (2006, Feb). Listen Hear! The Economic Impact and Cost of Hearing Loss in Australia. Retrieved August 11th 2007, from
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American Speech-Language-Hearing Association Causes of Hearing Loss in Children (1997 – 2007)
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Victorian WorkCover Authority: WorkSafe. (2007). Occupational Health & Safety (Noise) Regulations 2004. Retreived August 14, 2007, from http://www1.worksafe.vic.gov.au/vwa/home.nsf/pages/so_noise_legis
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Kelly, H.A. & Weeks, S. Ear Disease in Three Aboriginal Communities in Western Australia. Medical Journal of Australia. Vol. 154. Feb. 1991 240 – 245.