WHAT: ARE THE CAUSES, PREVENTION AND TREATMENT OF HEARING LOSS IN

Download Individuals are not protected from other causes of hearing loss just because they are in work. .... journal and will not be further discuss...
1 downloads 443 Views 351KB Size
Download PDF
Love PNG Images
Occup. Med. Vol. 50, No. 7, pp. 492-495, 2000 Copyright © 2000 Lippincott Williams & Wilkins lor SOM Printed in Great Britain. All rights reserved 0962-7480/00

IN-DEPTH REVIEW

What: are the causes, prevention and treatment of hearing loss in the ageing worker? J. Irwin Ninewells Hospital, Dundee, UK Hearing loss is more common in the ageing population as compared to young adults. Individuals are not protected from other causes of hearing loss just because they are in work. Their hearing may therefore be at risk from causes not related to their occupation. Some factors may be synergistically linked to noise exposure, thus increasing the effect of noise on hearing. Although some traumatic and infective causes of hearing loss are amenable to treatment, most occupational hearing loss is not curable once present and rehabilitative measures are the only option. General health and safety measures must be maintained throughout a worker's employment whatever their age. Key words: Elderly; occupational hearing loss; prevention; treatment. Occup. Med. Vol. 50, 492-495, 2000

INTRODUCTION: CAUSES The causes of hearing loss in adults are legion1'2 and obviously workers are not immune from non-occupational causes. There is evidence that some illnesses and their treatments can affect the way in which the ear responds to potentially damaging noise trauma. Occupational noise exposure will be considered later but there are other aspects of the workplace that may affect the ears. Single or multiple episodes of trauma such as skull fracture, direct trauma to the ear, blast injury or barotrauma may affect the middle and/or inner ear. The ageing worker may, in some cases, be more vulnerable to accidents because of slowed reaction time, poor vision, balance or mobility. High quality and wellmaintained general health and safety measures need to be in place and monitored to try to minimize the risk of accident. Working in hot and dusty environments may predispose some employees to otitis externa but ageing individuals are no more at risk than their younger counterparts unless there is some predisposing factor such as diabetes, which is commoner in older people. Occupational noise induced hearing loss has been recognized for hundreds of years and preventative measures have been used for almost as long. For the purposes of this article the natural history of this condition is interesting. Objective studies have only been possible since the introduction of pure tone audiome-

Correspondence to: Dr John Irwin, Area 4, Ninewells Hospital, Dundee DD1 9SY, UK. Tel: +44 (0)1382 633867; e-mail: [email protected]

Downloaded from https://academic.oup.com/occmed/article-abstract/50/7/492/1444386 by guest on 29 August 2018

try.3'4 Initially these were all cross-sectional studies, the progression of hearing loss was estimated by comparing subjects of different ages and length of noise exposure. Burns5 described how the initial effects of noise exposure are seen between 3 kHz and 6 kHz, often at 4 kHz. With time, the dip in hearing around 4 kHz deepens to a maximum and then stops. The thresholds at adjacent frequencies then become involved. Alberti6 also gave a good account of the progression of this condition. The hearing loss at 3 kHz and 4 kHz appears to progress at a steady rate for the first 10 years of exposure but then the rate of progression slows very quickly with little change thereafter. At the other extreme it may take up to 30 years for the 1 kHz threshold to become involved to any great extent but the rate of progress is then rapid. At 2 kHz the most rapid change in threshold occurs between 25 and 35 years. There does seem to be individual variation and there is* a 30 dB difference in threshold at 2 kHz between the 25th and 75th quartiles after 30 years of exposure. The combined effects of noise and age have interested researchers: are the two individual effects simply additive or is there a more complicated interaction? The general consensus seems to have been that there is, at worst, a simple additive interaction and, at best, there is no interaction.6"8 Long-term longitudinal studies following up the same subjects have only been possible recently. These suggest that by the age of 70 years the effects of occupational noise exposure and other acoustic trauma are no longer evident.9'10 This statement also applied to the quartile that demonstrated the greatest effect of noise on hearing (50-60 years) in Hinchliffe's work.10 This means that noise may not cause any additional long term hearing loss. The average exposed individual has a

J. Irwin: Hearing loss in the ageing worker

hearing loss, which occurs at an earlier age than for an average non-exposed individual, but eventually there may well be no difference between the two. However, hearing loss due entirely to the ageing process—presbyacusis—is not as common as generally thought. If older people with hearing loss are properly evaluated, as few as 7-15% are found to have no known cause11'12 and if the aetiology is known, prevention may be possible. It may also be possible to prevent some of the hearing loss that is age related. This means that occupational factors may be the only cause of an individual's hearing loss and that protective measures should be maintained. Is there any synergism between ototraumatic agents? This is well reviewed by Alberti6 who states that there is probably a slight synergy between aminoglycosides at high doses and very loud noises, but if workers are ill enough to be on aminoglycosides they are unlikely to be at work! There is probably no effect from loop diuretics or salicylates. There is, however, a probable slight synergistic effect between vibration and noise. Morata et a/.13 have recently shown that exposure to noise at what is currently 'safe' levels can be damaging if the worker is also exposed to organic solvents. Other recent articles on the aetiology of hearing loss in old age have highlighted the importance of other easily screened for and potentially preventable causes of hearing loss. Brandt et al.i4 found a significant relationship between systolic blood pressure and hearing loss in older subjects. Browning et al} found a similar relationship between plasma viscosity and sensorineural hearing loss. Of more interest is the role of mitochondrial DNA (mtDNA) mutation in sensorineural hearing loss. Ueda et al}6 have studied mtDNA4977 deletions and found a higher incidence in those subjects with hearing loss. This suggests that these cases might be classified as mitochondrial oxidative phosphorylation diseases. This could open the way to new treatment methods.

PREVENTION Standard noise exposure reduction starts with education and includes recreational as well as occupational noise exposure.17 Despite legislation, it is not always possible to persuade workers to use the protection provided. The technique of positive practice overcorrection has been shown to improve user rates, at least in military personnel.18 Design of quieter machinery and provision of comfortable but effective protection are also essential. These aspects are well known to the readership of this journal and will not be further discussed. There are other potential means of preventing hearing loss due both to noise exposure and ageing. This is an exciting and potentially very fruitful area of current research. The exact mechanism of noise induced cochlear damage is being investigated and has been well reviewed by Prasher.19 Glutamate is an excitatory amino acid used as a neurotransmitter in the inner hair cells. Excess noise stimulation leads to an excess of glutamate, which can cause damage to primary auditory dendrites. Downloaded from https://academic.oup.com/occmed/article-abstract/50/7/492/1444386 by guest on 29 August 2018

493

Application of kynurate (a glutamate antagonist) has so far been shown to limit noise damage in guinea pigs. The synaptic damage caused by excitotoxic glutamate release is mediated by a-amino-3-hydroxy-5-methyl-4-isoxazole proprionic acid (AMPA) and kainate receptors and the repair mechanism involves N-methyl-D-aspartate (NMDA) receptors. Nitric oxide (NO) is one of the molecules involved in cell death following NMDAmediated excitotoxic damage in the central nervous system and may be involved in the cochlea. Blockage of NO synthesis in the cochlea could prevent damage from loud noise exposure. Oxygen free-radicals have also been implicated in noise damage. These are released in the hair cells after intense noise exposure and are converted to highly destructive hydroxyl radicals in the stria vascularis. Antioxidants have been shown to prevent TTS after noise exposure. Agents used include allopurinol, lazaroids, a-D-tocopherol and mannitol (see Prasher19). These are all well known and in current use, which could speed up their clinical introduction. Noise exposure leads to an increase in energy consumption in the cochlea. This increase is dependent on magnesium and calcium metabolism and, in particular, damage is worse if magnesium is depleted. Magnesium supplementation has been shown to protect against impact noise (from gunfire) in army personnel. This work has been published by the same group in at least three different sources. 20 " 22 Calcium channel blockers, however, seem to have no effect.23'24 Low level exposure to an acoustic stimulus prior to potentially damaging noise exposure - sound conditioning-seems to toughen the ear and reduce the noise induced hearing loss.25 This seems to be due to a boost in the endogenous antioxidant systems. Sound toughening25 is intermittent pre-exposure to sound levels that cause TTS. This also seems to protect against permanent hearing loss but the mechanism is unknown. Sound conditioning is a simple process and its widespread introduction could prove very interesting. Glial-derived neurotrophic factors (GDNF) have been applied directly to the inner ear to prevent noise damage. Brain-derived neurotrophic factors and neurotrophin-3 provide dose-dependent protection against noise induced hearing loss. Research is exploring the use of viral vectors for gene introduction of these agents into the cochlea before noise exposure (see references 19 and 26).

TREATMENT Outer and middle ear problems are at least theoretically amenable to curative therapy. Occupationally induced otitis externa may be difficult to manage if allergic factors are involved, as repeated exposure will lead to repeated infection. Barriers and removal from the antigen may be necessary. Most traumatic perforations heal spontaneously but myringoplasty may be necessary. The possibility of middle ear reconstruction after trauma is best assessed by an experienced otologist.

494

Occup. Med. Vol. 50, 2000

7. MacRae JH. Noise induced hearing loss and presbyacusis. Audiology 1971; 10: 323-333. 8. Corso JF. Age correction factor in noise-induced hearing loss: a quantitative model. Audiology 1980; 19: 221-232. 9. Health and Safety Executive. A New Look at the Experimental Data on Noise Exposure and Hearing. London: Health and Safety Executive, 1987. 10. Hinchcliffe R. Noise hazards to the general population: hearing surveys reassessed. J Audiolog Med 1999; 8: 113— 121. 11. Stephens SDG. What is acquired hearing loss in the elderly? In: Glendenning F, ed. Acquired Hearing Loss in Elderly People. Stoke on Trent: Beth Johnson Foundation Publications, 1982; 9-26. 12. Iim D, Stephens SDG. Clinical investigation of hearing loss in the elderly. Paper read to the British Society of Audiology, Hull 1985. 13. Morata TC, Dunn DE, Kretschmer LW, Lemasters GK, Keith RW. Effects of occupational exposure to organic CONCLUSION solvents and noise on hearing. ScandJ Work Environ Health 1993; 19: 245-254. Estimates suggest that a total of 600 million people work 14. Brandt LJ, Gordon-Salant S, Pearson JD, et al. Risk factors in potentially hazardous noisy places with about 20 - 30 related to age-associated hearing loss in the speech million of these in both Europe and the US. 3 1 frequencies. J Am Acad Audio! 1996; 7: 152-160. 15. Browning GG, Gatehouse S, Lowe GD. Blood viscosity as a Preventative measures such as design of quieter mafactor in sensorineural hearing impairment. Lancet 1986; 1: chines, reduction of exposure time, and hearing protec121-123. tion are important. Hopefully, the worker who is now 16. Ueda N, Oshima T, Ikeda K, Aoki M, Takasaka T. ageing will have been protected and have no noiseMitochondrial DNA deletion is a predisposing cause for induced hearing loss. It is obvious that this protection sensorineural hearing loss. Laryngoscope 1998; 108: 580must continue throughout the worker's hazardous 584. employment. As other causes of hearing loss are, 17. Alberti PW. Noise induced hearing loss (could easily be hopefully, prevented the ageing worker can look forward prevented). BMJ 1992; 304: 522. to good hearing in old age. The use of sound condition18. Sadler OW, Montgomery GM. The application of positive ing and drugs such as magnesium and antioxidants may practice overcorrection to the use of hearing protection. Am help the prevention of hearing loss. Gene therapy for IndHygAssocJ 1982; 43: 451-454. mitochondrial deletions and for the introduction of intra19. Prasher D. New strategies for prevention and treatment of cochlear neurotrophins seems to be a promising nature noise induced hearing loss. Lancet 1998; 352: 1240-1242. 20. Attias J, Weisz G, Almog S, et al. Oral magnesium intake development. In the meantime, access to high quality reduces permanent hearing loss induced by noise exposure. rehabilitation will allow a reduction in disability and an AmJOtolatyngol 1994; 15: 26-32. improvement in quality of life. 21. Joachims Z, Netzer A, Ising H, et al. Oral magnesium supplementation as prophylaxis for noise-induced hearing loss: results of a double blind field study. Schrifienr Ver WasserBoden Lufthyg 1993; 88: 503-516. REFERENCES 22. Attias J, Joachims Z, Ising H, Bresloff I. Prophylactic effect of magnesium in noise induced hearing loss. In: Prasher D, 1. Irwin J. Causes of hearing loss in adults. In: Kerr AG, Luxon L, eds. Biological Effects of Noise. London: Whurr Stephens SDG, eds. Scott Brown's Diseases of Ear Nose and Publications, 1998; 273-281. Throat. Vol 2. Adult Audiology. 5th edition. Edinburgh: 23. Maurer J, Reichelmann H, Amedee RG, Mann WJ. Butterworth, 1987; 127-156. Diltiazem for prevention of acoustical trauma during 2. Yeoh LH. Causes of hearing disorders. In: Kerr AG, otologic surgery. Journal of Oto-Rhino-Laryngology and its Stephens SDG, eds. Scott Brown' Diseases of Ear Nose and Related Specialities 1995; 57: 319-324. Throat. Vol 2. Adult Audiology. 6th edition. Edinburgh: 24. Maurer J, Mann WJ, Amedee RG. Calcium channel Butterworth, 1997; 2(10)1-2(10)28. blockers for prevention of noise trauma in otologic surgery. 3. Crowden GP. 13th Annual Report of the Industrial Health Journal ofthe Louisiana State Medical Society 1998; 150:400Research Board. London: ???; 1933. 405. 4. Bunch CC. Traumatic deafness. In: Fowler Jr. EP, ed. 25. Canlon B, Borg E, Flock A. Protection against noise trauma Nelson Loose Leaf Medicine of the Ear. New York: Thos by pre exposure to a low-level acoustic stimulus. Hear Res Nelson, 1939; 349-367. 1988; 34: 197-200. 5. Burns W. Noise and Man. 2nd edition. London: John 26. Gao W. Therapeutic potential of neurotrophins for treatMurray, 1973; 223-228. ment of hearing loss. Mol Neurobiol 1998; 17: 17-31. 6. Alberti PW. Noise and the ear. In: Kerr AG, Stephens SDG, 27. Feghali JG, Lefebvre PP, Staekker H, et al. Mammalian eds. Scott Brown's Diseases of Ear Nose and Throat. Vol 2. auditory hair cell regeneration/repair and protection: a Adult Audiology. 5th edition. Edinburgh: Butterworth, review and future directions. Ear Nose and Throat Journal 1987; 594-641. 1998; 77: 276, 280, 282-285.

Sensorineural problems are not yet curable but research into auditory hair cell regeneration is in progress. Cochlea explant in vitro studies and in vivo experiments in rats and guinea pigs using retinoic acid, foetal calf serum and TGF-a, alone or in combination, have proved effective in improving cochleas damaged by ototoxic medication.27 This may lead to intra-cochlear application to treat damage after it has occurred. However, the current mainstay of treatment is rehabilitative rather than curative. This involves amplification in the form of hearing and other aids where needed and should address all of the communication and psychological difficulties caused by the hearing impairment. 28 " 30 This is best dealt with by experts in the field, such as audiological physicians.

Downloaded from https://academic.oup.com/occmed/article-abstract/50/7/492/1444386 by guest on 29 August 2018

J. Irwin: Hearing loss in the ageing worker

28. Hetu R3 Lelande M, Getty L. Psychological disadvantages due to occupational hearing loss as experienced in the family. Audiology 1987; 26: 141-152. 29. Hetu R, Riverin L, Getty L, Lelande M, St-Cyr C. The reluctance to acknowledge hearing difficulties among hearing impaired workers. Br J Audiol 1990; 24: 265276.

Downloaded from https://academic.oup.com/occmed/article-abstract/50/7/492/1444386 by guest on 29 August 2018

495

30. Hetu R, Getty L. The planning of a rehabilitation service for people suffering from occupational deafness. Proceedings of the 5th International Congress on Noise as a Public Health

Problem. Stockholm: Swedish Council for Building Research, 1988; vol. 2: 247-252. 31. Alberti PW. Noise—the most ubiquitous pollutant. Noise Health 1998; 1: 3-5.