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   Abstract
   Introduction
   Effects of Diffe...
   Mechanisms Behin...
   Concluding Remarks
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INVITED COMMENTARY Table of Contents   
Year : 2009  |  Volume : 11  |  Issue : 45  |  Page : 183-184
Effects of shift work and intermittent noise exposure on hearing: Mechanisms and prophylactic potential

The Research Council of Norway (RCN), Stensberggt 26, 0131 Oslo, Norway

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Date of Web Publication2-Oct-2009
 
  Abstract 

It is well established that intermittent noise exposure characteristically produces less hearing loss than equal energy/intensity continuous noise in animal models. Ongoing different shift work regimes open for direct studies on hearing effects of intermittent noise exposure in man without ethical concern. Amazingly, few such studies are reported. In one recent study in the present volume, noise-exposed employees working 12 hours a day for two consecutive days followed by two days off, the cycle then repeated, had significantly lower permanent hearing loss than employees working nine-hour shifts from 8 am to 5 pm Monday to Friday. This commentary refers to the few studies reported, gives a short overview of the mechanisms behind noise-induced hearing loss and the protective effect of intermittent exposure, and concludes that direct studies in man on the effects of different shift work regimes on occupational hearing loss under specified noise conditions represent a prophylactic potential that calls for increased research activity. Such studies might pave the way for direct use of more optimal intermittent noise exposure regimes in future design of the noise exposure workday/-week and make future hearing conservation programs more effective.

Keywords: Effects, hearing loss, intermittent noise, mechanisms, shift work

How to cite this article:
Borchgrevink HM. Effects of shift work and intermittent noise exposure on hearing: Mechanisms and prophylactic potential. Noise Health 2009;11:183-4

How to cite this URL:
Borchgrevink HM. Effects of shift work and intermittent noise exposure on hearing: Mechanisms and prophylactic potential. Noise Health [serial online] 2009 [cited 2020 Nov 30];11:183-4. Available from: https://www.noiseandhealth.org/text.asp?2009/11/45/183/56209

  Introduction Top


Animal studies show that noise exposure of moderate intensity with intermittent quiet periods produces less hearing loss than equal energy/intensity continuous noise. [1],[2] The protective effect is presumably caused by cochlear recovery between the noise phases. [3] Ongoing different shift work regimes open for direct studies on hearing effects of intermittent noise exposure in man without ethical concern. Based on such studies the distribution of noise exposure during the workday or -week might be optimized, with the potential to reduce occupational noise hazard. Amazingly, few such studies are reported.


  Effects of Different Shift Work Regimes on Noise-Induced Hearing Loss Top


Chou et al[4] report on the "Effects of shift work on noise induced hearing loss (NIHL)" [4] in the present volume of Noise and Health. In this study, noise-exposed employees working 12 hours a day for two consecutive days followed by two days off, the cycle then repeated, had significantly lower permanent hearing loss than employees working nine-hour shifts from 8 am to 5 pm Monday to Friday. Another study showed lower average permanent hearing loss in noise-exposed three-shift workers than in single-shift workers. [5] However, in a third study, the introduction of a 12-hour work shift had no apparent impact on the effectiveness of the hearing conservation program compared with the previous eight-hour shift regime, but the authors assume this might partly be due to inadequate audiometric testing procedures and inadequate use of hearing protection devices. [6] For better understanding of why intermittent noise exposure is less hazardous to hearing than corresponding equal energy continuous noise, one must turn to animal studies.


  Mechanisms Behind Noise-Induced Hearing Loss Top


Animal studies show that both the level and character of noise exposure, the duration and distribution of noise-free periods, blood circulation and other metabolic/chemical processes may be of influence in the production of NIHL. NIHL may be caused by direct mechanical damage as well as more indirect metabolic processes of ionic, ischemic, excitotoxic and free radical origin, resulting in necrosis and/or apoptosis. [7] Beyond a critical level, impulse noise may cause direct mechanical damage in the cochlea. [8] At moderate intensity levels, high-Kurtosis non-Gaussian noise produces significantly more hearing loss than low-Kurtosis Gaussian noise of the same equal energy and spectrum. [9] Intermittent noise causes less damage to the cochlea than continuous noise of the same intensity, thus the damage is not proportional to the total noise energy. [2] Shorter intermittent noise exposure and longer rest periods induce less permanent threshold shift than equal energy noise presented with longer noise cycles and shorter rest periods. [10]

The effects of duration and distribution of noise-free rest periods, on hearing, seem related to the metabolic/chemical mechanisms of damage and recovery in action. The importance of blood circulation (i.e. oxygen availability) on recovery is demonstrated by the finding that hearing loss increases upon administration of carbon monoxide, which expels/blocks oxygen from hemoglobin. [10] Further, individuals with vibration-induced white finger symptoms (i.e. their blood circulation is less tolerant to vibration) also suffer greater permanent hearing loss than people who do not develop such symptoms. [11] Magnesium may limit cochlear damage, presumed to be partly due to its vasodilatator effect. [7] Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are involved in sensory cell and neural death in the peripheral nervous system, and in noise trauma, and may be formed as long as 7-10 days post exposure. [12] Antioxidants administered from three days prior, or one hour, or one, three or five days post exposure reduced ROS/RNS formation, hearing loss and hair-cell damage; early intervention was more effective. [12] A recent review summarizes the underlying mechanisms of NIHL, including sources of ROS generation, pathways of necrotic and apoptotic cell death, antioxidant and pharmacological intervention, and new techniques aimed at interrupting the apoptotic biochemical cascade that results in cell death. [13]


  Concluding Remarks Top


Knowledge of the mechanisms underlying hearing loss is a pre-requisite for prophylactic and therapeutic intervention. The fact that noise-induced damage to hearing develops over time post-exposure by metabolic/chemical mechanisms implies the potential to interfere by chemo-pharmacological agents pre-, per- or post noise exposure. Current knowledge seems still largely insufficient for effective protective and recovery actions.

However, that intermittent noise exposure characteristically produces less hearing loss than equal energy/intensity continuous noise is well established in animal models. Direct studies in man on the effects of different shift work regimes on occupational hearing loss under specified noise conditions represent a prophylactic potential that calls for increased research activity. Such studies might pave the way for direct use of more optimal intermittent noise exposure regimes in future design of the noise exposure workday/-week and make future hearing conservation programs more effective.

 
  References Top

1.Clark WW, Bohne BA, Boettcher FA. Effect of periodic rest on hearing loss and cochlear damage following exposure to noise. J Acoust Soc Am 1987;82:1253-64.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]  
2.Pourbakht A, Yamasoba T. Cochlear damage caused by continuous and intermittent noise exposure. Hear Res 2003;178:70-8.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]  
3.Campo P, Lataye RR. Intermittent noise and equal energy hypothesis. In: Dancer A, Henderson D, Salvi RJ, Hamernik RP, editors. Noise-Induced hearing loss. St. Louis: Mosby Year Book; 1992. p. 456-66.  Back to cited text no. 3      
4.Chou YF, Lai JS, Kuo HW. Effects of shift work on noise induced hearing loss (NIHL). Noise Health 2009;11:185-9  Back to cited text no. 4    Medknow Journal  
5.Holzmόller M, Seibt A, Jakubowski A, Friedrichsen G. Studies on the combined effects of shift work and noise on permanent hearing loss. (In German). Z Gesamte Hyg 1990;36:501-2.  Back to cited text no. 5      
6.Reynolds JL, Royster LH, Pearson RG. Hearing conservation programmes (HCPs): The effectiveness of one company's HCP in a 12-hr workshift environment. Am Ind Hyg Assoc J 1990;51:437-46.  Back to cited text no. 6  [PUBMED]    
7.Sendowski I. Magnesium therapy in acoustic trauma. Magnes Res 2006;19:244-54.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]  
8.Hamernik RP, Turrentine G, Roberto M, Salvi RJ, Henderson D. Anatomical correlates of impulse noise-induced mechanical damage in the cochlea. Hear Res 1984;13:229-47.  Back to cited text no. 8      
9.Davis RI, Qiu W, Hamernik RP. Role of the kurtosis statistics in evaluating complex noise exposures for the protection of hearing. Ear Hear 2009;30:628-34.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]  
10.Chen GD, McWilliams ML, Fechter LD. Intermittent noise induced hearing loss and the influence of carbon monoxide. Hear Res 1999;138:181-91.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]  
11.Pekkarinen J. Noise, impulse noise, and other physical factors: Combined effect on hearing. Occup Med 1995;10:545-59.  Back to cited text no. 11  [PUBMED]    
12.Yamashita D, Jiang HY, Le Prell CG, Schacht J, Miller JM. Post-exposure treatment attenuates noise-induced hearing loss. Neuroscience 2005;134:633-42.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]  
13.Henderson D, Bielefeld EC, Harris KC, Hu BH. The role of oxidative stress in noise-induced hearing loss. Ear Hear 2006;27:1-19.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]  

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Correspondence Address:
Hans M Borchgrevink
The Research Council of Norway (RCN), Stensberggt 26, 0131 Oslo
Norway
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1463-1741.56209

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