Languages:
The SCENIHR opinion states:
3.5. Noise-induced hearing loss and associated impairments
Noise-induced hearing loss (NIHL) accrues progressively and often unnoticed until it has reached a certain degree. The main site of impairment is the outer hair cells of the cochlea, where the damage is irreversible (Bamiou and Lutman 2007). Very high levels of noise exposure can lead to acute mechanical damage to inner and outer hair cells, but this form of damage is very rare. More commonly, there is chronic damage that builds up slowly over time. Since noise-induced hearing loss is irreversible, the main form of treatment is prevention.
Source & ©: SCENIHR,
The SCENIHR opinion states:
3.5.1.Epidemiology of noise-induced hearing loss
Exposure to excessive noise is one major cause of hearing disorders worldwide. The Word Health Organization programme for Prevention of Deafness and Hearing Impairment (WHO 1997, Smith 1998) stated: “Exposure to excessive noise is the major avoidable cause of permanent hearing impairment worldwide. Noise-induced hearing loss is the most prevalent irreversible industrial disease, and the biggest compensatable occupational hazard. More research is needed on basic mechanisms and means of prevention.” In a more recent report WHO states (WHO 2002, Nelson 2005) “Worldwide, 16% of the disabling hearing loss in adults is attributed to occupational noise, ranging from 7% to 21% in the various subregions”. Surveys estimate that noise-induced hearing loss (NIHL) affects 10 to 15 million people in the USA (see Lynch and Kil 2005). In the UK (Palmer et al 2002b) showed that some about 180, 000 people aged 35-64 years were estimated to have severe hearing difficulties attributable to noise at work and for tinnitus this increased to 350,000 people who were seriously affected. In France a survey by the ministry of employment (Sumer: surveillance médicale des risques professionnels 2003, Magaud-Camus 2005) indicates that approximately 7% of employed workers are exposed to excessive noise levels (more than 85 dB(A) for at least 20 hours per week) and about 25 % are exposed to hazardous noise exposures (more than 85 dB(A) but less than 20 hours per week); most exposed workers belong to industry (18%) and, to agriculture and house building (12%). Legally acceptable levels of noise exposure were defined many years ago taking into account the two main physical parameters of acoustic intensity and duration of exposure as used for reference above.
In order to better counteract NIHL a European directive that took effect in February 2006, lowered the first action level (provide protection) to 80 dB(A) (Directive 2003/10/EC, 2003). Acute acoustic trauma from firearms is the most frequent pathology observed in the French army and unfortunately its prevalence increased by about 20 percent in 2006 (BS EN ISO 389-2:1997, 2006).
Although early reviews concluded that leisure noise was unlikely to be a significant threat to hearing compared to occupational noise (e.g. MRC 1986), they noted a need for more good data and research. Since then there have been significant changes in the patterns of noise exposure. Smith et al. (2000) found that the numbers of young people with social noise exposure had tripled (to around 19%) since the early 1980s, whilst occupational noise had decreased.
This increase of risk is consistent with a recent study by Niskar et al (2001), who estimated the prevalence of noise-induced hearing threshold shift among children aged 6-19 years in the third national health and nutrition examination survey of 1988-1994 in the USA. They found that 12.5% had noise-induced threshold shift (NITS) in one or both ears, with higher prevalence in boys (14.2%) compared to girls (10.1%), and in older children aged 12-19 (15.5%) compared to 6-11 year olds (8.5%). 6kHz was the most affected frequency (77.1%) compared to 4 kHz (23.8%) and 3 kHz (14.1%). A single frequency was involved in 88.4% of children. Among children meeting NITS criteria 14.6% had a noise notch for both ears. .No equivalent data exist yet on the European population. In the earlier studies (Davis 1989, Davis 1995, Smith et al 2000) there was no evidence of such notches in 18-25 year old individuals in the UK.
Source & ©:
SCENIHR,
Note: The European Directive 2003/10/EC on
the minimum health and safety requirements regarding the exposure of
workers to the risks arising from physical agents (noise) is
available at:
The SCENIHR opinion states:
3.5.2.Environmental noise exposure levels
In industry settings, the noise levels can average up to 90-125 dB in several areas of work. Outside the workplace, a high risk of hearing impairment arises from attending discos and rock concerts, exercising noisy sports (hunting, sports shooting, speedway) or from exposures to military noise. Children could be exposed to noisy toys as trumpets (92–125 dB SPL), whistles (107-129 dB SPL) and toy weapons (113 - >135 dB SPL) (Plontke et al. 2004).
By their leisure activities individuals expose themselves to noise sources including personal music players which usually generate sounds across a broad frequency range and reaching high sound pressure levels. The equivalent sound levels in discos range from 104.3 to 112.4 dB(A), compared to 75 to 105 dB(A) from personal music players (Serra et al. 2005). The noise dose measures over 4 hours showed an Laeq of 104.3 dB. The nightclubs' average sound level ranged between 93.2 to 109.7 dB(A). Sounds other than noise (such as music) can, at high acoustic levels, be as dangerous for hearing as industrial noise.
There seems to be a trend for increased distribution and use of PMPs, and their improved technical qualities allow for playback without distortion at high levels.
Environmental noise like traffic noise, aircraft noise, construction noise or neighbourhood noise, although sometimes very annoying, does not reach the equivalent levels that can be harmful to hearing. On the other hand, these sources of noise can cause non-auditory effects.
Source & ©:
SCENIHR,
The SCENIHR opinion states:
3.5.3.Exposure – effect relationship
As it was usefully summarised by Lutman et al. (2008), knowledge concerning the relationship between noise exposure and NIHL is based on cross-sectional studies of people exposed to noise, much of which was conducted several decades ago and which concentrated on people exposed continuously to high levels of noise that were more commonplace in the 1950’s and 1960’s. This knowledge is far from complete. Most studies have suffered from the lack of appropriate non-exposed control subjects and longitudinal studies are almost entirely lacking (Lutman and Davis 1996). Authoritative reports have involved large primary studies or have synthesised data from several large primary studies. The seminal study of Burns and Robinson (1970) has been influential in the UK and elsewhere. It formed the basis of the first edition of the international standard ISO 1999 in 1975 and has been embodied in the National Physical Laboratory (NPL) tables that are still used widely for prediction of NIHL in populations exposed to noise. The later version of ISO 1999 in 1990 (ISO 1999:1990) synthesised data from studies in the US as well as from the studies of Burns and Robinson to derive formula for predicting NIHL. An advantage of ISO 1999 (ISO 1999:1990) is that it allows the user to insert different values to account for the effects of age-associated hearing loss. This facility has enabled ISO 1999 to keep up with developing the current understanding of the effects of age on hearing and the recognition that there are important socio-economic factors governing hearing acuity. This is an important achievement because the non-exposed controls used in many studies of NIHL have been drawn from different socio-economic groups than the exposed participants (e.g. office worker, researchers, university staff).
All of the above methods account for the combined effects of age and noise exposure by simple addition of the hearing losses from the two origins, or by a slight modification of simple addition. The modified addition incorporated in ISO 1999 (ISO 1999:1990) slightly reduces the resultant hearing loss compared to simple addition. However, this effect is negligible for combined hearing loss lower than 40 dB and for the present purposes can be ignored.
ISO 1999 allows prediction of the distribution of NIHL to be expected from any cumulative amount of noise exposure. This is combined with (in most cases simply added to) distribution of age-associated hearing loss appropriate to the population in question. This calculated distribution of NIHL allows estimation of the probability that a given magnitude of overall hearing loss will be exceeded. In the context of the present study, noise levels in the range from 80-95 dB(A) are of interests. Based on ISO 1999, the following table (Table 5) shows the extent of NIHL to be expected from a working lifetime of 45 years at daily continuous noise levels of 80, 85, 90 and 95 dB(A). The values are for NIHL at 4 kHz, which is the frequency predicted to give the greatest hearing loss. Values are given for the median and the 5th centile (value exceeded by 5% of population). These data constitute the noise-induced component of hearing loss alone. Note that hearing loss is minimal for exposures at 80 dB(A), even at the 5th centile, and increases at higher levels.
Table 5 : Predicted noise-induced hearing loss (45 years exposure)
Table 6 shows similar data for the much shorter exposure durations of 3 years, which is more relevant to the present opinion. Note that in that case, NIHL is less likely than after 45 years of exposure, as expected. However, the proportion is greater than simply dividing the amount of hearing loss pro rata. To a rough approximation, the magnitude of NIHL after 3 years is 43% of the NIHL after 45 years. The use of this model suggests a departure from the equal energy principle in the direction that more NIHL occurs in the early years of exposure and clearly suggests that preventive measures must be aimed at those who start noise exposure from PMPs when young. Note that at 4 kHz there is more damage earlier; at 1 kHz the damage is less and is later. Hence overall damage to the cochlear can be related to the equal energy principle. ISO 1999 accommodates this trend by assuming that the noise level has to exceed 90dB(A) to affect hearing at 1 kHz and 93 dB(A) to affect hearing at 500 Hz, but 77/78 dB to affect hearing at 4 kHz.
Table 6: Predicted noise-induced hearing loss (3 years exposure)
Until now, we have limited evidence about what exactly makes some subjects more vulnerable than others, but it is well established, that anatomical details play a significant role among other factors.
The relationship between age, noise exposure and prevalence is complex and takes many years to be manifest for a particular cohort. Data from the MRC National Study of Hearing (Davis 1989, Davis 1995) has been re-drawn for the working group to show the prevalence of hearing impairment for men only who have had a zero noise exposure or a measured amount of noise exposure from their occupations. Figure 2 shows the prevalence of three different degrees of hearing impairment as a function of age group (in roughly 20 years age bands). Noise immission has been allocated into three categories. The first is a level at which there would be no danger due to occupational noise, given the level, pattern and duration of occupational noise exposures (<80 dB(A) Lequ 40 for 50 years or less). The second level is 80-89 dB(A) and the third 90-99 dB(A) on same scale equivalence. It is clear from the left panel of Figure 2 that shows the prevalence using the four frequency average threshold (0.5, 1, 2 and 4 kHz) that the 18‑40 age group had no slope at all in terms of the prevalence over noise exposure groups. So there is no relationship at all between the prevalence and noise exposure until the age group of 40–60 when the data show a significant increase across noise exposure groups. This is similar for the oldest age group as well. It may be argued that the effects of earlier damage due to noise appear later, but they are evident at an earlier age in the 4 kHz region of the cochlear that are more susceptible to damage. The data for the 4 kHz threshold alone is shown in the right hand panel and shows that there is indeed a significant effect of noise immission for the youngest age groups at prevalence of at least 25 dBHL for <80 dB(A) Lequ 40 vs 80-89 dB(A) (χ2 = 5.55, p<.0185, df=1), but not for the more disabling levels at 35 and 45 dBHL.
Clearly noise immission from occupational noise at the lowest levels of risk (80-89 dB(A) Lequ 40) affect prevalence of hearing impairment at 25 dBHL+, in younger people aged 18-40 but continue to have a larger impact in older people (for whom the noise has stopped on the whole). As there is no scientific evidence that social noise produces different NIHL levels compared to occupational noise, the model makes clear that at typical noise exposures it will take many years for the exposure to impact on the individual and to be measured in the population. However, 4 kHz seems an excellent frequency at which to measure initial effects.
Source & ©:
SCENIHR,
The SCENIHR opinion states:
3.5.4. Mechanisms of noise-induced hearing loss
3.5.4.1. Overview of pathophysiological effects of noise
At very high acoustic levels as in cases of bomb blast the traumatizing sound can induce mechanical breaks at different parts of the ear such as the eardrum, the ossicles joints and the basilar membrane, these effects being visible with simple optic microscopy. However, in the vast majority of cases acoustic trauma induces less visible damage to the inner ear. A loss of hair cells (the cochlear sensory cells which transform sound into biological processes) has long been the main or only morphological sign of pathology, detected by optic microscopy in specimen obtained after death. It can be observed only in cases of permanent hearing loss and not earlier than several days after acoustic trauma. It is always found in good correlation with the functional (audiometric) measures of hearing loss both for frequency extent and for amount of loss in decibels. The larger the frequency extent of the loss, the wider the loss of hair cells along the cochlea, and, for each sound frequency, the greater the loss in decibels the greater the number of lost hair cells. However, detection of (surviving) hair cells does not mean that they are functional. With the advent of electron microscopy many histological (tissue) and/or cytological (cell) alterations within the cochlea have been observed indicating several different pathological processes occurring more or less simultaneously in the cochlea in response to acoustic trauma. Many of these alterations are not specific for acoustic trauma but represent basic cellular pathological processes which occur in various other diseases of the ear. In early studies a major observed sign was the breaking or fusion of the cilia of hair cells which remains the most specific morphopathology for acoustic trauma. Among the several other alterations observed are: damage to cochlear vasculature associated with altered cochlear blood flow, loss of fibrocytes probably associated with decreased endocochlear potential, rupture of attachments of stereocilia tips to the tectorial membrane, distension or rupture of tip links involved in transduction, damage to pillar cells, swelling or rupture of dendrites below inner hair cells. Excessive noise can induce damage to most cell types in the cochlea, but presently the sequence of these pathological events and their cause/effect relationships remain poorly known.
The histological examination of human temporal bones is a rare opportunity. In recent years only two such histological studies were performed from subjects with a known NIHL, which confirmed a loss of hair cell associated with a degeneration of neural cells with possible signs of alterations of the cochlear vasculature (Rask-Andersen et al. 2000, Nakamoto et al. 2005).
The development of cell and molecular biology provided new insights and investigation tools concerning various pathological cell processes. Among those pathologies associated with excess of free radicals and those involved in apoptosis (or “programmed cell death” proved very fruitful.
The damage of outer hair cells (OHCs) impairs an active, non-linear, biomechanical cochlear feedback process along with a decreasing hearing sensitivity and frequency selectivity. Total OHC loss results in a hearing impairment of 50-70 dB (sensitivity threshold for persisting inner hair cells - IHC), recruitment and a loss of otoacoustic emission (Hamernik et al. 1989, Gao et al. 1992). A decrease in frequency selectivity results in poor speech intelligibility particularly in noisy and/or reverberant environments.
Animal studies have shown that the damage to the cochlea corresponds well with the frequency of the noise (with ½ octave shift toward higher frequencies). However, human exposures to broadband occupational or environmental noise result uniformly in high frequency hearing threshold shift, particularly at the frequencies of 4-6 kHz, regardless of the noise spectrum. This phenomenon can be explained by the anatomical configuration of human external and middle ear and its nonlinear properties.
There are two functional consequences of noise exposure and cochlear lesion to hearing, namely temporary threshold shift (TTS) and permanent threshold shift (PTS) (Plontke et al. 2004).
The most essential parameters for TTS or PTS development include:
- Sound pressure level (SPL) of noise
- The rapidity with which sound levels increase (impulse noise vs continuous noise)
- Exposure time
- Vulnerability of the inner ear
In principle, short exposures to moderately high levels of non-impulse noise, producing reversible changes to the cochlea, result in the TTS; while long exposures (of 4 hours or more in animal experiments) to high levels of noise, producing irreversible changes to the cochlea, result in the PTS. Impulse noise is significantly more harmful than steady-state noise, because the impulses are of very high sound pressure levels (up to 190 dB SPL in the military), and the duration of impulses is too brief that the stapedial reflex (possibly protective contraction of middle ear muscles) has not enough time to conteract, this reflex offers anyhow very little or no protection at high frequencies. However, the relationship between exposure parameters is not as simple as described above. It has been shown that exposure to noise under similar, controlled conditions, in some subjects can result in TTS, while in others in PTS. This finding points to different inter-individual vulnerability of the internal ear.
The vulnerability of the inner ear depends on several environmental and intrinsic factors, like smoking, hypertension, lipids level, age, gender, eye colour and other parameters of anatomy and micro-anatomy some of which are controlled by genetic factors.
Source & ©:
SCENIHR,
The SCENIHR opinion states:
3.5.4.2. Biological processes involved in noise effects
Many research studies have been performed over more than 50 years to understand physiological dysfunctions induced by excessive noise exposure. Over the last five years or so, new and promising data have uncovered several series of factors having a determinant role. The main results are presented below, schematically divided into four categories.
Acoustic factors
In some circumstances an acquired resistance to noise exposure can happen. Exposure to a previous non traumatizing sound may prevent acoustic trauma by a later noise exposure this is known as sound conditioning (Canlon et al. 1988). Liu et al. (2000) further extended earlier findings by showing that low-frequency conditioning sounds could protect from low and middle frequency noise damage. Niu and Canlon (2002) revealed an up-regulation of neurotransmitter release in cochlear efferents in the process of sound conditioning. Cochlear toughening refers to the increased resistance happening over repeated noise exposure in some conditions, in recent experiments Hamernik et al. (2003) further characterized acoustic parameters influencing this phenomenon.
The very long term effects of noise as possibly emerging only at an old age have received contradictory support from several epidemiologic studies (Ferrite and Santana 2005, Lee et al. 2005, Rosenhall 2003, Gates et al. 2000). Very recent experimental data (Kujawa and Liberman 2006) suggest that early noise exposure can render the inner ear more vulnerable to aging. Unnoticeable effects can also occur over years as indicated by small instabilities in cochlear functioning which were observed in students exposed to noise in their leisure-times (Rosanowski et al. 2006).
During the post noise exposure period the presence of loud sounds influences the amount of recovery. Very few studies were devoted to these influences the effective parameters of which are poorly known (Niu et al. 2004, Norena and Eggermont 2005). The beneficial effects of these post-trauma environmental sounds can be quite large and as they are easy to control in humans they have very high potential clinical implications. Epidemiologic data also point to similar significant effects in humans (Abbate et al. 2005).
Environmental factors other than acoustics
Exposure to several chemicals and lowered levels of breathed oxygen were found to increase NIHL. It was observed that chemical asphyxiants potentiated NIHL (Fechter et al. 2000) such as Hydrogen cyanide (Fechter et al. 2002), acrylonitrile (one of the 50 most commonly produced industrial chemicals) (Fechter et al. 2003). Hypoxia, the low oxygen breathing, was found to extend NIHL to all frequencies above those of the noise (Chen and Liu 2005). Smoking was also found a significant risk factor potentiating NIHL in epidemiologic surveys (Burr et al. 2005, Ferrite and Santana 2005, Wild et al. 2005).
Efferent and sympathetic innervations
The efferent and sympathetic innervations of the cochlea (a retrocontrol from the brain to the cochlea) seem to have almost no influence upon the normal functioning of the cochlea as their suppression does not lead to noticeable changes. However, they do influence cochlear reactivity in adverse conditions, and this has been particularly well observed with NIHL. A protective role of the efferent system upon NHIL was uncovered many years ago (Cody and Johnstone 1982). Over the last years significant progress was made regarding exposure parameters leading or not leading to protection (Rajan 2001, Rajan 2003). The predictive value of an efferent response to assess susceptibility to NHIL remains controversial (Maison et al. 2002, Luebke et Foster 2002, Wagner et al. 2005), its involvement in sound conditioning was shown by Niu and Canlon (2002). An influence of the sympathetic cochlear innervation on NIHL was uncovered several years ago (Borg 1982), and later studied. Some experiments (Horner et al. 2001, Giraudet et al. 2002) further extended such observations and pointed to an interaction with the efferent innervation, they also showed modification of cochlear sensitivity to acoustic trauma by anaesthesia or even sedation.
Protective factors
Several newly tested drugs have been proven experimentally to provide protective or reparative properties with regard to NIHL. The pharmacological actions of the drugs are only partly known and many have several metabolic effects and it is difficult to know which of its metabolic properties is involved in NIHL. While recognizing this complexity it is fruitful both for presentation and reasoning to use main pharmacologic categories. Thus drugs are presented here below into five main categories.
Both steroidal and non steroidal anti-inflammatory drugs were found to provide protection against NIHL. Salicylate was found to facilitate recovery from acoustic trauma (Yu et al. 1999), in a later study salicylate in combination with trolox (an anti-NOoxidant) it was shown to decrease NIHL (Yamashita et al. 2005). Corticoids when combined with hyperbaric oxygenation were shown to provide rescue post-trauma in animal experiments (d’Aldin et al. 1999, Lamm and Arnold 1999), this was confirmed and extended by experiments last year in our group (Fakhry et al. 2007. A role of stress and corticosterone in protecting against NIHL was observed (Wang and Liberman 2002). Three recent studies indicate the beneficial action of dexamethasone on NIHL (Takemura et al. 2004, Tahera et al. 2006, Sendowski et al. 2006a) the last publication comes from a laboratory involved in the project.
Anti-oxidants
Over the last three years about twenty publications documented the protective effects of drugs with anti-oxidant properties upon NIHL. These drugs are further somehow differentiated by the authors with regards to their anti-ROS or anti-NOS properties, drugs of both classes were found effective. Approximately 12 different drugs were tested. Some were found repeatedly protective: - N-acetylcysteine (Ohinata et al. 2003, Duan et al. 2004, Kopke et al. 2005), - allopurinol (Franze et al. 2003, Cassandro et al. 2003), - ebselen (Pourbakht and Yamasoba 2003, Lynch et al. 2004), - edaravone (Takemoto et al. 2004, Tanaka et al. 2005) among these at least two are already clinically accepted drugs at least in some countries. Other drugs already clinically accepted as salicylate, vitamin c or vitamin e were also found protective.
Anti-apoptotics
Once NIHL cochlear damage has started as through inflammatory and/or oxidative or other processes apoptotic processes can be triggered and lead to sensory and neural cochlear cell disparition. Five different drugs were reported to be protective aginst NIHL : riluzole (Wang et al. 2002), a peptide inhibitor of c-Jun N-terminal kinase (Wang et al. 2003), calcineurin inhibitors (Minami et al. 2004), all-trans retinoic acid, an active metabolite of vitamin a (Ahn et al. 2005) and, Src-PTK inhibitors (Harris et al. 2005). The potential use of these drugs seems far away at present because of high dose levels needed and low bioavailability with clinical routes of administration.
Neurologic factors
Administration of several neurotrophic factors was found protective against NIHL: - ciliary neurotrophic factor (Zhou et al. 1999), - GDNF and/or NT3 (Yang et al. 2001, Chen et al. 2002), basic fibroblast growth factor (Zhai et al. 2002, Zhai et al. 2004). Modulators of neurotransmission were also found protective: noradrenergic related compounds (Horner et al. 1998, Giraudet et al. 2002), and NMDA blocking agents (Chen et al. 2003, Diao et al. 2005, Ruel et al. 2005).
Miscellani
Hypothermia (Henry 2003), prior heat acclimatation (Paz et al. 2004) and a heat shock protein inducer (Mikuriya et al. 2005) were reported to protect from NIHL, as were also ATP (Sugahara et al. 2004), NO inhibitors (Xiong et al. 2002, Ohinata et al. 2003) and a calcium pump activator (Liu et al. 2002). A special reference must be made to magnesium treatment which was found repeatedly protective (Scheibe et al. 2001, Scheibe et al 2002, Haupt et al. 2003, Attias et al. 2003 , Sendowski et al. 2006b).
Source & ©:
SCENIHR,
This summary is free and ad-free, as is all of our content. You can help us remain free and independant as well as to develop new ways to communicate science by becoming a Patron!
BECOME A PATRON!