Teamwork Approach to Noise-Induced Hearing Loss

**3**

world [3].

**Chapter 1**

**Abstract**

*Alberto Behar*

Noise Exposure

to avoid getting wrong conclusions.

hearing loss prevention

psychological effects [2].

**1. Introduction**

Noise exposure is a basic concept used to assess the risk of noise induced hearing loss in the workplace. It is very important, since loud noise is omnipresent in almost all human activity, especially in industry, construction, mining and transportation. The question to answer is how to determine the risk of a person performing in an environment where the noise levels, duration and frequency content change with time. The answer is obtained by measuring his noise exposure. Although the measurement itself is not complex or difficult, a proper knowledge of what exactly is the noise exposure and how to deal with the measurement result in fundamental

**Keywords:** loud noise, noise induced hearing loss, risk assessment, noise exposure,

Occupational noise is the most common health hazard that is predominant in most workplaces. In a recent survey of working adults in Canada, 42% reported being exposed to hazardous noise levels in the workplace [1]. Exposure to excessive occupational noise can cause permanent hearing loss through sensory-neural damage in the cochlea. In general, hearing is first affected in a specific range of audible frequencies (3000 to 6000 Hz) and then spreads to higher and lower frequencies. Hearing loss is often accompanied by other long-term auditory effects, such as tinnitus (ringing in the ears); increased sensitivity to loud noise; and poorer frequency selectivity (i.e., decreased ability to hear sounds in background noise) compared to individuals with normal hearing. It can also cause other, non-auditory adverse effects, the most common been the cardiovascular (e.g., changes in heart rate, increasing blood pressure). Being a stressor, noise causes also important

Noise levels in the workplace vary in level, duration and frequency content. In general, they are of high levels and are persistent for most of the work shift. They can be continuous, impulsive or interrupted. From the frequency point of view, most are of the wide band type, although they can be rich in high or low

Reduction of the sound levels and, consequently the risk of noise induced hearing loss is the objective of every hearing conservation program in the industrial

The approach to the reduction of the risk follows several steps. The first is finding and recognizing potentially hazardous areas in the workplace. This tends to be done as a result of personal, subjective observations, the principal been difficulties in understanding speech: people ask frequently questions and answers to

frequencies, especially if vibrations are also present in the workplace.

## **Chapter 1** Noise Exposure

*Alberto Behar*

### **Abstract**

Noise exposure is a basic concept used to assess the risk of noise induced hearing loss in the workplace. It is very important, since loud noise is omnipresent in almost all human activity, especially in industry, construction, mining and transportation. The question to answer is how to determine the risk of a person performing in an environment where the noise levels, duration and frequency content change with time. The answer is obtained by measuring his noise exposure. Although the measurement itself is not complex or difficult, a proper knowledge of what exactly is the noise exposure and how to deal with the measurement result in fundamental to avoid getting wrong conclusions.

**Keywords:** loud noise, noise induced hearing loss, risk assessment, noise exposure, hearing loss prevention

#### **1. Introduction**

Occupational noise is the most common health hazard that is predominant in most workplaces. In a recent survey of working adults in Canada, 42% reported being exposed to hazardous noise levels in the workplace [1]. Exposure to excessive occupational noise can cause permanent hearing loss through sensory-neural damage in the cochlea. In general, hearing is first affected in a specific range of audible frequencies (3000 to 6000 Hz) and then spreads to higher and lower frequencies. Hearing loss is often accompanied by other long-term auditory effects, such as tinnitus (ringing in the ears); increased sensitivity to loud noise; and poorer frequency selectivity (i.e., decreased ability to hear sounds in background noise) compared to individuals with normal hearing. It can also cause other, non-auditory adverse effects, the most common been the cardiovascular (e.g., changes in heart rate, increasing blood pressure). Being a stressor, noise causes also important psychological effects [2].

Noise levels in the workplace vary in level, duration and frequency content. In general, they are of high levels and are persistent for most of the work shift. They can be continuous, impulsive or interrupted. From the frequency point of view, most are of the wide band type, although they can be rich in high or low frequencies, especially if vibrations are also present in the workplace.

Reduction of the sound levels and, consequently the risk of noise induced hearing loss is the objective of every hearing conservation program in the industrial world [3].

The approach to the reduction of the risk follows several steps. The first is finding and recognizing potentially hazardous areas in the workplace. This tends to be done as a result of personal, subjective observations, the principal been difficulties in understanding speech: people ask frequently questions and answers to

be repeated. Complaints of excessive noise are also important indications that the noise may be so loud as to create a health risk. This first step is usually performed through a walk-through survey. Sometimes, spot noise level measurements are also done using a sound level meter.

Once the areas with high noise levels have been found, the next step is to quantify the risk. This is done by measuring the noise exposure of individuals or groups of workers working in those areas. This procedure is known as the exposure survey.

Also, the extent of the exposed population (number of exposed persons) is also quantified to find out the magnitud of the problem.

#### **2. Why noise exposure**

Noise exposure is a fundamental concept in assessing the risk from high noise levels.

It is universally accepted that hearing loss occurs as a consequence of long duration exposures to high noise levels. What is usually not too clear is how long the "long duration" is and how high are the "high noise levels". There is no, however discussion regarding that the effect is caused by a combination of both: duration and level. The concept of noise exposure combines both causes and that makes it so important. As mentioned above, in determining the risk of occupational hearing loss, measuring workers' noise exposure is an essential part of any hearing conservation program.

It all derives from an ISO standard [4] that estimates the probability of acquiring noise induced hearing loss after being exposed to a given noise exposure level for different periods of time. As an example, after 40 years of been exposed to 85 dBA for 8 hs a day, 50% of the population will acquire an average of extra 5 dB hearing loss between 500 Hz and 6 KHz, on top of the hearing loss due to age.

On the basis of the above statement, the limit of 85 dBA has been adopted almost internationally for a workday of 8 hs.

#### **3. Standards and definitions**

Reference [5] lists important standards from different institutions, related to noise exposure.

Noise exposure is a complex combination of sound levels a person has been exposed to and the duration of each one of those sound levels [5–8]. The closer analogy is to think in terms of noise energy that enters the persons' ears and damage the delicate organ of hearing. So, two variables are involved there: sound levels and time duration [9].

There are several concepts involved that need to be explained and defined. Their understanding is essential when dealing with this issue.

**Equivalent sound level, Leq, t in dBA** is the first of them. The easier way to understand it is as follows: In real life, sound levels constantly vary with time. They rise when the worker is using a power tool and diminish between operations, while changing continuously. Leq, t is a kind of an "average", constant sound level for the entire period of exposure (working) time, encompassing all "quiet" and "noisy" periods, with the same energy of the real one. It is defined as the value of a noise of constant sou**n**d level that contains the same total A-weighted acoustical energy as the sound of interest. In other words, while the real noise is of a varying sound level, the equivalent has a constant level of the same energy.

**5**

of 8 h).

*Noise Exposure*

been exposed to.

the same.

*DOI: http://dx.doi.org/10.5772/intechopen.95997*

pressure relative to 20 μPa, divided by that time.

working days of different durations can be compared directly. The following formula converts Leq,t into Lex,T:

Where: t is the duration of the actual exposure, in hr. and

different Leq,T and, consequently, different risk of hearing loss.

T is the normalized duration, usually = 8 hr.

exposure for a normalized 8 hs duration will be:

normalized 8 hs duration will be:

Now is the time to clarify the meaning of the letter "t" at the end of the Leq, t. It is there to signify that the Leq in question is for the period of time the worker has

Here we arrive at another important point that needs to be stated: whenever Leq is mentioned, the duration of the exposure (t), should also be stated. Otherwise the Leq has no meaning. This is not too difficult to understand as per the following example: suppose we have two workers. One of them is exposed every day to 90 dBA for 4 hs. The other one is exposed also to 90 dBA, but for 8 hs. It is obvious that the effect to the hearing of the second worker will be larger. In other words even though Leq,4 of the first is equal to the Leq,8 of the second, their effects are not

The numerical definition of Leq, t is as follows: ten times the logarithm (base 10) of the time integral over a stated time, t hours, of the squared A-weighted sound

*Lex Leq* ,T ,t 10 log t / T = + ( ) (1)

**Noise exposure level, Lex, T, in dBA,** is another important measure. This is the one used to predict noise-induced hearing loss as per [4]. It is derived from the measured Leq,t by a simple adjustment to account for the longer or shorter duration of the workday on the workers' hearing. In other words, it answers the following question: what will be the value of Leq,t if the energy that entered the worker's ear during t hs would enter during 8 hs. By calculating Lex,T (with capital T), Leq,t for

As an example, if a worker is exposed to 85 dBA for four hours a day (Leq,4), his

If, on the contrary, he is exposed to 85 dBA for 12 hs (Leq,12), his exposure for a

The above example shows again how two workers with the same Leq,t, have

Mathematically, Lex,T is defined **as** ten times the logarithm (base 10) of the time integral of the squared A-weighted sound pressure relative to 20 μPa for the time actually worked, divided by T hours (usually the standardized shift duration

Finally, it has to be stated that while Leq,t is essentially measured, Leq,T is calculated from the Leq,t value. As it will be described further, the actual measuring instrument, the dosimeter, performs both the measurement and the calculation. Both values, Leq,t and Leq,T can be read on the same device. This greatly simplifies the task of the person performing the noise exposure survey. On the other hand, it can create misunderstandings if the operator does not has clear knowledge of the difference between Leq,t and Leq,T. As mentioned above, the one that is to be used

when assessing the risk of hearing loss is the noise exposure level, Leq,T.

*Lex Leq* ,8 ,4 10 log t / T 85 10 log 4 /8 82 . = + =+ = ( ) ( ) *dBA* (2)

*Lex Leq* ,8 ,12 10 log t / T 85 10 log 12 /8 87 . = + =+ = ( ) ( ) *dBA* (3)

#### *Noise Exposure DOI: http://dx.doi.org/10.5772/intechopen.95997*

Now is the time to clarify the meaning of the letter "t" at the end of the Leq, t. It is there to signify that the Leq in question is for the period of time the worker has been exposed to.

Here we arrive at another important point that needs to be stated: whenever Leq is mentioned, the duration of the exposure (t), should also be stated. Otherwise the Leq has no meaning. This is not too difficult to understand as per the following example: suppose we have two workers. One of them is exposed every day to 90 dBA for 4 hs. The other one is exposed also to 90 dBA, but for 8 hs. It is obvious that the effect to the hearing of the second worker will be larger. In other words even though Leq,4 of the first is equal to the Leq,8 of the second, their effects are not the same.

The numerical definition of Leq, t is as follows: ten times the logarithm (base 10) of the time integral over a stated time, t hours, of the squared A-weighted sound pressure relative to 20 μPa, divided by that time.

**Noise exposure level, Lex, T, in dBA,** is another important measure. This is the one used to predict noise-induced hearing loss as per [4]. It is derived from the measured Leq,t by a simple adjustment to account for the longer or shorter duration of the workday on the workers' hearing. In other words, it answers the following question: what will be the value of Leq,t if the energy that entered the worker's ear during t hs would enter during 8 hs. By calculating Lex,T (with capital T), Leq,t for working days of different durations can be compared directly.

The following formula converts Leq,t into Lex,T:

$$Lex, \mathbf{T} = Leq, \mathbf{t} + \mathbf{10} \log \left( \mathbf{t}/\mathbf{T} \right) \tag{1}$$

Where: t is the duration of the actual exposure, in hr. and

T is the normalized duration, usually = 8 hr.

As an example, if a worker is exposed to 85 dBA for four hours a day (Leq,4), his exposure for a normalized 8 hs duration will be:

$$\text{Lex}, 8 = \text{Leq}, 4 + 10 \log \left( \text{t/T} \right) = 85 + 10 \log \left( 4/8 \right) = 82 \, dBA. \tag{2}$$

If, on the contrary, he is exposed to 85 dBA for 12 hs (Leq,12), his exposure for a normalized 8 hs duration will be:

$$Lex, 8 = Leq, 12 + 10\log\left(t/T\right) = 85 + 10\log\left(12/8\right) = 87\,dBA. \tag{3}$$

The above example shows again how two workers with the same Leq,t, have different Leq,T and, consequently, different risk of hearing loss.

Mathematically, Lex,T is defined **as** ten times the logarithm (base 10) of the time integral of the squared A-weighted sound pressure relative to 20 μPa for the time actually worked, divided by T hours (usually the standardized shift duration of 8 h).

Finally, it has to be stated that while Leq,t is essentially measured, Leq,T is calculated from the Leq,t value. As it will be described further, the actual measuring instrument, the dosimeter, performs both the measurement and the calculation. Both values, Leq,t and Leq,T can be read on the same device. This greatly simplifies the task of the person performing the noise exposure survey. On the other hand, it can create misunderstandings if the operator does not has clear knowledge of the difference between Leq,t and Leq,T. As mentioned above, the one that is to be used when assessing the risk of hearing loss is the noise exposure level, Leq,T.

**Noise dose in %** is another important measure. Although the use of the noise dose is declining lately, many instruments still allow its measurement. The concept is familiar mainly to Occupational Hygienists and commonly used when dealing with hazardous substances. The idea is quite simple: it defines the relation between the amount of a substance absorbed by a person in a given period of time (usually 8 hs) and the maximum allowed by a local jurisdiction. For example, if this limit is set to 85 dBA for an exposure of 8 hs and the actual exposure for the same period of time has been 88 dBA, then his dose will be 200%1 .

The following equation allows for the calculation of Leq,t from a given dose2 :

$$Leq, \mathbf{t} = \mathbf{10} \log \left( \mathbf{D} / \mathbf{10} \mathbf{0} \times \mathbf{8} / \mathbf{T} \right) + L\boldsymbol{\omega} \tag{4}$$

where D = dose in % for 8 h.

T = duration of the daily exposure in hours.

Lc = criterion sound level in dBA3 .

For example, a dose of 100% acquired during 4 hs (using Lc = 85 dBA) will result in

$$Leq, \mathbf{t} = \mathbf{10} \log \left( \mathbf{100} / \mathbf{100} \mathbf{x} \, \mathbf{8} / \mathbf{4} \right) + \mathbf{85} = \mathbf{88} \, dBA. \tag{5}$$

**Criterion level (LC) in dBA** is a constant sound level which, if it continues for the criterion duration (usually 8 hs), will result in the worker's allowable noise exposure. ISO (the International Organization for Standardization), as well as most Canadian provinces [10] and NIOSH (the USA National Institute for Occupational Safety and Health) [11] has adopted LC = 85 dBA for 8 hs.

**Exchange rate** is the increase (decrease) in sound level for which permissible exposure time is halved (doubled)4 . ISO, most Canadian provinces and NIOSH has adopted 3 dB exchange rate. So, for instance, if a person is allowed to have Lex(8) = 85 dBA for 8 hs, he is also allowed to Lex(4) = 88 dBA for 4 hs.

#### **4. Noise exposure measurements**

There are two issues involved in the measurement of Leq,t: one is related to the instrumentation involved and the other deals with the measurement technique and procedures. Although managing the instrument itself is a relatively simple task, the measurement procedure requires basic knowledge of noise as well as practical knowledge regarding where to put the dosimeter, for how long to measure, etc. Measuring noise exposure of groups is more complex and requires some knowledge on statistics to be able to decide how many individuals to sample and for how long.

**7**

**Figure 1.**

*Dosimeters with separate microphones.*

*Noise Exposure*

**4.1 Instruments**

*DOI: http://dx.doi.org/10.5772/intechopen.95997*

Noise exposure can be measured using regular sound level meters and integrating sound level meters. However, there is a device specifically designed to measure Leq,t. It is the **noise dosimeter**. In its basic version it consists of an ¼" diameter microphone connected through a long cord to a container with the battery and the electronic components of the instrument. It also includs a readout device that allows for reading of the measured Leq,t. The microphone is to be attached close to the ear of the person whose exposure will be measured. The rest of the instrument is usually worn on the belt or in the shirt pocket (see photographs in **Figure 1a** and **b).**

1 For this calculation it is assumed that every time the noise exposure increases 3 dB, the exposure is multiplied by two. This is known as "exchange rate" (in this case = 3)

2 As a matter of fact, this calculation is also performed by the dosimeter. Therefore the operator can read the result of the measurement as a Dose as well as Leq,t or Lex,T.

3 Lc is the maximum Lex,T, a person is allowed to be exposed for 8 hs, daily.

4 The two common exchange rates used are 3 dB and 5 dB. Even where the 5 dB exchange rate is required in a Regulation, it is recommended that the 3 dB exchange rate be used as well since it provides a higher degree of protection (for exposure of 8 h) or less).

#### *Noise Exposure DOI: http://dx.doi.org/10.5772/intechopen.95997*

#### **4.1 Instruments**

Noise exposure can be measured using regular sound level meters and integrating sound level meters. However, there is a device specifically designed to measure Leq,t. It is the **noise dosimeter**. In its basic version it consists of an ¼" diameter microphone connected through a long cord to a container with the battery and the electronic components of the instrument. It also includs a readout device that allows for reading of the measured Leq,t. The microphone is to be attached close to the ear of the person whose exposure will be measured. The rest of the instrument is usually worn on the belt or in the shirt pocket (see photographs in **Figure 1a** and **b).**

**Figure 1.** *Dosimeters with separate microphones.*

Recently, manufactures have opted for compact, small size dosimeters called Noise Badges that contain both the microphone and the microprocessor of the instrument. By having the entire instrument in a single body, they eliminate the cord that is a nuisance and also can be a workplace hazard. Measurement results can still be read on the dosimeter itself. Thay can also be transmitted via Bluetooth technology to another device with facilities for recording for future use. This is especially handy when a noise exposure survey is carried out on several workers simultaneously, while each is carrying his own dosimeter. In some models, the receiver is also a charger for the batteries of all instruments. **Figure 2a** and **b** shows Noise Badges from two manufacturers.

There is a wide variety or instruments in the market, able to perform different measurements and calculations. They all belong to the following two basic types of dosimeters: **measuring** and logging.

**Measuring** dosimeters allow for the straight measurement of Leq,t and, eventually calculate Lex,T. Although most allow for reading the results on the instruments themselves, some others relay on a separate measurement device. This is done to keep the results visible to the operators only.

Dosimeters measure sound levels at predetermined intervals of time. **Measuring** dosimeters do not allow for extracting individual readings, just the final results at the end of the measurement period. **Logging** dosimeters, on the contrary, allow for the extraction of individual Leq,t. In such a way one can obtain the entire history of the sound levels at predetermined time intervals. The results can then be downloaded into a computing device and shown as a graph, spreadsheet, etc. By analyzing the partial data, one can follow their variation with time. Then, by knowing where the person was located at different times of the day or what kind of operation he was involved in, one can pinpoint the important noise sources or operations. Noise history is a powerful tool used for the design of noise controls in the workplace.

Another advantage of the logging dosimeters is that by studying the noise history one can determine if there have been abnormal events and then "clean" false results caused from malingering or noises not normal in the particular workplace.

#### **4.2 Measurement techniques**

#### *4.2.1 Individuals*

Measuring Leq,t of individuals using a dosimeter is a relatively simple exercise, generally explained in the manual supplied with the instrument5 . Manuals contain also information on how to care and the main precautions that have to be taken to obtain proper results.

A most important task, often overlooked, is to inform the person(s) under test the reason for testing and how it will be done. In many instances not knowing the "why" and "how" lead to malingering and falls results. Often workers suspect that the instrument will in fact transmit their conversations to the supervisor. In other instances, some individuals created artificially loud noises to show levels that do not exist in reality.

After calibrating the instrument and ensuring that the batteries have enough charge to last during the testing period, the microphone of the dosimeter is attached close to the wearer's ear (generally on the shoulder or close by, and switched on.

**9**

**Figure 2.**

 If the task is repetitive, then the measurement is done during a couple of repetitions, only. However, when the sound levels vary during the shift or if the worker works in different places, the

measurement should last for the entire shift.

*Dosimeters with incorporated microphones (noise badges).*

*Noise Exposure*

*DOI: http://dx.doi.org/10.5772/intechopen.95997*

5 Instructions in this Section are absolutely basics.

*Noise Exposure DOI: http://dx.doi.org/10.5772/intechopen.95997*

#### **Figure 2.**

*Dosimeters with incorporated microphones (noise badges).*

 If the task is repetitive, then the measurement is done during a couple of repetitions, only. However, when the sound levels vary during the shift or if the worker works in different places, the measurement should last for the entire shift.

As mentioned above, if the measurement has been performed for the entire shift, then Lex,T is equal to Lex,t. In other words, the daily reading is his daily noise exposure, Lex,T. If that is not the case, then the Eq. [1] (page YYY) should be used to convert the measured Leq,t in Lex,T.

#### *4.2.2 Groups*

In many instances, there is a need to assess a group of workers that perform identical tasks or are located in the same environment. Providing each one of them with a dosimeter is not necessary or practical. There are procedures to be followed that reduce considerably the number of instruments needed and still obtain reliable, statistically significant results6 .

#### **5. Lex,T for T different of 8 hs**

Noise induced occupational hearing loss is the effect on a person being exposed to high noise levels for extended periods of time. Epidemiological data, used as bases for our present knowledge of hearing loss, were derived from populations working for many years in such high noise environments [12]. This is also the origin of the equal energy theory and the 3 dB exchange rate [13].

As explained above, when the measurement period t is different from T = 8 hs, Eq. 1 is to be used,. The formula is meant for 8 hs long work day where acoustical conditions repeat day after day, month after month, for the assumed 40 active years of a person.

Presently, in many occupations, the duration of the workday is 12 hs a day with several days off to equal to 40 hs a week or 80 hs every two weeks. The question is, shall we still use Eq. 1 with T = 8 hs? No official document exists for such a situation. However, common sense indicate that since the average duration of the workday is still T = 8 hs, (the average over the 2 or the 4 weeks), Eq. 1 is still valid and shall be used.

As an example [14], the total of hs worked by the musicians at the National Ballet of Canada is 350 hs. Therefore, the average Leq,t during their rehearsals/ performances was corrected using Eq. 1 as follows:

$$\text{Lex}, \text{T} = \text{Leq}, \text{t} + 20 \log \text{t} / \text{T} = \text{Leq}, \text{t} + 10 \log 350 / 2000 = \text{Leq}, \text{t} - 7.56 \, dBA \tag{6}$$

Where t = 350 are the actual annual number of hours worked and.

T = 2000 the number of work hours in a year.

We do not really know what happens to ears exposed to 12 hs a day, for a 40 hs week. Nor we know about yearly exposures of less than 2000 hs, that is the average exposure resulting of 8 hs a day, 40 hs a week. We can only assume that the equal energy principle can be extended to cover exposures of different durations.

Using the equal energy principle, one can calculate exposures of different workday duration too. For example, if a worker whose workday is 8 hs and whose exposure measured for 5 hs was Leq,5 = 85 will be.

$$\text{Lex}, \text{T} = \text{Leq}, \text{t} + 20 \log \left( \text{t}/\text{8} \right) = \text{85} + 20 \log \left( \text{5}/\text{8} \right) = \text{83} \, dBA. \tag{7}$$

**11**

**Author details**

Ryerson University, Toronto, Canada

provided the original work is properly cited.

\*Address all correspondence to<EMAIL_ADDRESS>
© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

Alberto Behar

*Noise Exposure*

*DOI: http://dx.doi.org/10.5772/intechopen.95997*

T = 2000 hs and Eq. 1 will be

However, if his workday is t = 12 hs, then

*Lex*,T 85 20 log 12 /8 87 =+ = ( ) *dBA* (8)

*Lex*.T 85 20 log 350 / 2000 77.4 = + = ( ) *dB* (9)

In the case of temporary worker, that performs 350 hs a year, it will be t = 350 hs,

6 See Appendix B in Ref. [9]

However, if his workday is t = 12 hs, then

$$Lex, \text{T} = 85 + 20\log\left(12 \,/\text{8}\right) = 87 \,dBA \tag{8}$$

In the case of temporary worker, that performs 350 hs a year, it will be t = 350 hs, T = 2000 hs and Eq. 1 will be

$$\text{Lex.T} = 85 + 20 \log \left( 350 / 2000 \right) = 77.4 \text{ dB} \tag{9}$$

#### **Author details**

Alberto Behar Ryerson University, Toronto, Canada

\*Address all correspondence to<EMAIL_ADDRESS>
© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

### **References**

[1] Feder K, Michaud D, McNamee J, Fitzpatrick E, Davies H, Leroux T. Prevalence of hazardous occupational noise exposure, hearing loss, and hearing protection usage among a representative sample of working Canadians. Journal of Occupational and Environmental Medicine 2017;59(1):92e113. https://doi. org/10.1097/JOM.0000000000000920.

[2] Vishakha Waman Rawool. Hearing Conservation; (2012), ISBN 978-1- 60406-256-4 (pbk.).

[3] CSA Group. Z1007-16. Hearing Loss Prevention Program Management. Canadian Standards Association, (2016).

[4] ISO 1999. Acoustics — Estimation of noiseinduced hearing loss. International Organization for Standardization, (2013).

[5] ANSI/ASA S12.19-1996 (R2020): Measurement of Occupational Noise Exposure American National Standards Institute (2020)

[6] S1.25-1991 (R2007): Specification for Personal Noise Dosimeters. Acoustical Society of America (2007)

[7] AS/NSZ 1269.1:2005 (R2016): Occupational noise management—Part 1: Measurement and assessment of noise immission and exposure*.* Australia-New Zealand Standard (2016)

[8] ISO 9612:2009: Acoustics — Determination of occupational noise exposure — Engineering method. International Organization for Standardization (2009)

[9] CSA Group. Z107.56-13 Measurement of noise exposure. Canadian Standard Association. (2013).

[10] CCOHS. OSH Answer Fact Sheets. https://www.ccohs.ca/oshanswers/ phys\_agents/exposure\_can.html. Canadian Centre for Occupational Health and Safety. (2020).

[11] NIOSH. Occupational Noise Exposure. National Institute for Occupational Safety and Health. (1998). https://www.cdc.gov/niosh/docs/98- 126/pdfs/98-126.pdf.

[12] Passchier-Vermeer W. Hearing loss due to exposure to steady-state broadband noise, Report no.35. Institute for Public Health Eng, The Netherlands. (1968).

[13] Robinson, D. W. Relations between hearing loss and noise exposure, in Hearing and Noise in Industry, edited by W. Burns and D.W. Robinson. HMSO, London, England. (1970).

[14] Lee J., Behar A., Kunov H., Wong, W. Musicians noise exposure in orchestra pit. Applied Acoustics 66 (2005) 919-931.

**13**

(**Figure 1**).

to hearing loss.

**Chapter 2**

**Abstract**

ototoxicity, co-exposure

**1.1 Noise-induced hearing loss**

experiencing material hearing loss [3, 4].

**1. Introduction**

Occupational Hearing Loss

ototoxic substance and co-existence impact on hearing loss.

Occupational hearing loss received attention after the Industrial Revolution and through World Wars I and II. It currently accounts for the largest portion of occupational diseases, and a third of all hearing loss is due to noise. Occupational hearing losses include noise-induced hearing loss (NIHL), hearing loss caused by ototoxic substances and hearing loss caused by their complex interactions. In the case of NIHL, even when exposed to the same noise, the degree of hearing damage and recovery may vary from person to person, and also be affected by other noise in daily life. Various organic solvents and some heavy metals exposed in workplace are important causes of ototoxic hearing loss, and they are known to have additive or synergistic effects when accompanied by noise. In Korea, NIHL is the most common occupational disease and has been increasing continuously since the 1990s. The number of claims for compensation has also been increasing steadily. However, the developed country including Korea almost never considered the effects of chemicals on the diagnosis and compensation for hearing loss workers. Occupational hearing loss can be prevented through hearing conservation programs. In this chapter, we will introduce the scientific basis of noise induced hearing loss, the impacts of

**Keywords:** occupational hearing loss, noised-induced hearing loss, noise, solvents,

Occupational noise exposure is very common around the world. Up to 25% of workers are exposed to workplace noise above 85 dB(A) (weighted decibel relative to human ear) [1]. Noise-induced hearing loss (NIHL) is the second most common cause of hearing loss after age-related hearing loss (ARHL) and 16% of adult hearing loss is estimated to be caused by workplace noise [2]. In addition, one-third of workers exposed to noise showed audiometric evidence of NIHL, with 16%

The prevalence of NIHL is increasing worldwide. Prevalence in Korea is also increasing, especially over the past 20 years. Cases of accepted compensation for NIHL are more rapidly rising from 2016 than the cases for audiometric diagnosis

Hearing loss is associated with cognitive decline and depression, and now accepted as a risk factor for dementia [5]. Noise from by daily life (subways, electric tools) or hobby (music concerts, sports viewing, hunting, etc.) can also contribute

*Joong-Keun Kwon and Jiho Lee*

### **Chapter 2**

## Occupational Hearing Loss

*Joong-Keun Kwon and Jiho Lee*

#### **Abstract**

Occupational hearing loss received attention after the Industrial Revolution and through World Wars I and II. It currently accounts for the largest portion of occupational diseases, and a third of all hearing loss is due to noise. Occupational hearing losses include noise-induced hearing loss (NIHL), hearing loss caused by ototoxic substances and hearing loss caused by their complex interactions. In the case of NIHL, even when exposed to the same noise, the degree of hearing damage and recovery may vary from person to person, and also be affected by other noise in daily life. Various organic solvents and some heavy metals exposed in workplace are important causes of ototoxic hearing loss, and they are known to have additive or synergistic effects when accompanied by noise. In Korea, NIHL is the most common occupational disease and has been increasing continuously since the 1990s. The number of claims for compensation has also been increasing steadily. However, the developed country including Korea almost never considered the effects of chemicals on the diagnosis and compensation for hearing loss workers. Occupational hearing loss can be prevented through hearing conservation programs. In this chapter, we will introduce the scientific basis of noise induced hearing loss, the impacts of ototoxic substance and co-existence impact on hearing loss.

**Keywords:** occupational hearing loss, noised-induced hearing loss, noise, solvents, ototoxicity, co-exposure

#### **1. Introduction**

#### **1.1 Noise-induced hearing loss**

Occupational noise exposure is very common around the world. Up to 25% of workers are exposed to workplace noise above 85 dB(A) (weighted decibel relative to human ear) [1]. Noise-induced hearing loss (NIHL) is the second most common cause of hearing loss after age-related hearing loss (ARHL) and 16% of adult hearing loss is estimated to be caused by workplace noise [2]. In addition, one-third of workers exposed to noise showed audiometric evidence of NIHL, with 16% experiencing material hearing loss [3, 4].

The prevalence of NIHL is increasing worldwide. Prevalence in Korea is also increasing, especially over the past 20 years. Cases of accepted compensation for NIHL are more rapidly rising from 2016 than the cases for audiometric diagnosis (**Figure 1**).

Hearing loss is associated with cognitive decline and depression, and now accepted as a risk factor for dementia [5]. Noise from by daily life (subways, electric tools) or hobby (music concerts, sports viewing, hunting, etc.) can also contribute to hearing loss.

#### *Hearing Loss - From Multidisciplinary Teamwork to Public Health*

#### **Figure 1.**

*Prevalence of noise-induced hearing loss (D1) and compensated cases in Korea by year (1991 to 2018). Prevalence of noise-induced hearing loss (D1) (in blue bars) and cases for compensation (in red line) have increased from 1991 to 2018. Diagnostic criteria of NIHL in Korea requires hearing loss more than 30 dB on average threshold across 0.5 kHz, 1 kHz, and 2 kHz and more than 50 dB at 4 kHz. If the average threshold exceeds 40 dB, decision for compensation could be made. The compensated cases for NIHL were increasing more sharply since 2016, whereas the diagnosed cases were increasing more steadily. http://www.kosha.or.kr/kosha/ data/healthExamination.do. http://www.moel.go.kr/policy/policydata/view.do?bbs\_seq=20200401401.*

There are jobs where hearing is very important due to the nature of work itself or safety concerns. Hearing loss reduces speech recognition ability in the noisy environment and hearing protection devices (HPDs) also hampers speech recognition in noise. When hearing impaired workers wear a HDPs, their difficulty increases in hearing warning signals. There was association between the severity of hearing loss and the risk of work-related injury requiring hospitalization [6]. Even in the workplace where hearing is less important, hearing loss is a major cause of stress-related sick leave [7]. Economic impact of NIHL on social burden includes lost productivity, absenteeism, reduced income and tax revenues, welfare payment and compensation, special education, vocational rehabilitation programs, and health care [8].

The purpose of this review is to have a comprehensive overview of NIHL including pathophysiology, diagnosis, prevention, and to understand the recently emerging topics on noise-induced cochlear synaptopathy.

#### **1.2 Pathophysiology**

Noise-induced hearing loss is a complex disease caused by the interaction of genetic and environmental factors. It is usually caused by chronic loud noise exposure but also could be caused by transient or repetitive acoustic trauma of very high intensity, resulting in greater damage [9]. The total energy level of noise causing NIHL is determined by the intensity of the noise and the total exposure time. The noise at the same total energy level will cause the same amount of cochlear damage [10].

The inner ear damage caused by noise is divided into temporary threshold shift (TTS) and permanent threshold shift (PTS) depending on the duration of the hearing loss. Hearing loss recovers within 24–48 hours in TTS, while it is irreversible in PTS. Mechanisms of TTS and PTS are considered to be different. Animal study showed that TTS in early life can accelerates age-related hearing loss (ARHL) [11]. However, long-term impact of TTS in human ear is lacking. Pathology of

**15**

*Occupational Hearing Loss*

auditory canal [13].

mechanism of TTS [17].

as a result of silenced auditory nerve fibers [20].

*DOI: http://dx.doi.org/10.5772/intechopen.97109*

noise induced damage is the loss of outer hair cells leading to threshold elevations and poorer frequency discrimination. Main threshold shift occurs at an half octave higher than the frequency of loud noise, with the largest damage at 4 kHz and the smallest at 0.5 kHz [12]. Susceptibility around 4 kHz is associated with the mechanical properties of the middle ear and resonance frequency of external

tion induced by ROS acts as a toxic substance, causing apoptosis [15].

Mechanism of cochlear pathology can be categorized into mechanical and metabolic [12]. Metabolic damage is a major mechanism of NIHL from chronic exposure to noise. Characteristic finding is loss of hair cells as a result of increased free radicals such as reactive oxygen species (ROS) and reactive nitrogen species within cochlear hair cells [14]. Damage starts in outer hair cells in row 2 and 3 of most vulnerable area to noise, possibly as a result of necrosis [15]. Noise releases ROS from mitochondria into cytoplasm of hair cells via release of Ca2+. Cytoplasmic ROS leads to production of pro-inflammatory cytokines and pro-apoptotic factors, finally to apoptosis of hair cells. Free radicals can persist for 7–10 days after cessation of noise exposure, which could induce progressive cochlear damage [16]. Noise-induced ischemia and reperfusion also increase the generation of ROS [14]. Lipid peroxida-

When the noise is extremely loud over 130 dB SPL, mechanical damage could occur via excessive vibrations of the delicate cochlear structures. Breaking or fusion of stererocilia of hair cells are most specific morphopathology. Noise could damage other cochlear structures; damage to cochlear vasculature, loss of fibrocytes, rupture of attachments of stereocilia tips to the tectorial membrane, distension or rupture of tip links, damage to pillar cells, and rupture of dendrites [14]. Noise could crumple pillar cell, decreasing length of the OHC, and detaching stereocilia from tectorial membrane in reversible way, which is understood as a

Recent hot topic on noise-induced damage on auditory system is cochlear synaptopathy. Until recently, noise that does not cause threshold shift was considered safe. However, recent animal experiments have shown that noise exposure that does not cause hair cell loss may damage ribbon synapse between inner hair cell and spiral ganglion neuron [11]. Cochlear inner hair cells (IHCs) are important as mechano-electrical transducer of auditory information. Receptor potential generated by IHCs releases the neurotransmitter at the synaptic end, while outer hair cells work as cochlear amplifier via process of electromotility which increases the vibration of basilar membrane. Synaptic ribbon is specialized electron-dense structure, which is anchored to pre-synaptic membrane only nanometers apart. It contains large pool of "readily releasable" vesicles to finely vary synaptic output continuously in sensory organ of hearing and vision [18]. Thus, damage of ribbon synapse between IHCs and spiral neurons results in improper conveyance of neural information to auditory nerve fiber. Noise causes damage of presynaptic ribbons and postsynaptic nerve terminals showing various degree of swelling. The mechanism of damage for postsynaptic terminal is glutamate-mediated excitotoxicity, while mechanism of ribbon loss is unclear [19]. In cochlear synaptopathy, hearing threshold is normal because OHC is undamaged, but the amplitude of auditory nerve activity decreases

Auditory nerve fibers (ANFs) could be functionally categorized by their spontaneous rate (SR). High-SR ANFs respond to sound at threshold level, whereas low-SR ANFs react to loud sound, follow rapid amplitude changes of acoustic signal, and are considered to have an important role in the hearing in noisy environment due to their larger dynamic range. Low-SR ANF appears to be damaged selectively after noise exposure [20].

#### *Occupational Hearing Loss DOI: http://dx.doi.org/10.5772/intechopen.97109*

*Hearing Loss - From Multidisciplinary Teamwork to Public Health*

There are jobs where hearing is very important due to the nature of work itself or safety concerns. Hearing loss reduces speech recognition ability in the noisy environment and hearing protection devices (HPDs) also hampers speech recognition in noise. When hearing impaired workers wear a HDPs, their difficulty increases in hearing warning signals. There was association between the severity of hearing loss and the risk of work-related injury requiring hospitalization [6]. Even in the workplace where hearing is less important, hearing loss is a major cause of stress-related sick leave [7]. Economic impact of NIHL on social burden includes lost productivity, absenteeism, reduced income and tax revenues, welfare payment and compensation, special education, vocational rehabilitation programs, and

*Prevalence of noise-induced hearing loss (D1) and compensated cases in Korea by year (1991 to 2018). Prevalence of noise-induced hearing loss (D1) (in blue bars) and cases for compensation (in red line) have increased from 1991 to 2018. Diagnostic criteria of NIHL in Korea requires hearing loss more than 30 dB on average threshold across 0.5 kHz, 1 kHz, and 2 kHz and more than 50 dB at 4 kHz. If the average threshold exceeds 40 dB, decision for compensation could be made. The compensated cases for NIHL were increasing more sharply since 2016, whereas the diagnosed cases were increasing more steadily. http://www.kosha.or.kr/kosha/ data/healthExamination.do. http://www.moel.go.kr/policy/policydata/view.do?bbs\_seq=20200401401.*

The purpose of this review is to have a comprehensive overview of NIHL including pathophysiology, diagnosis, prevention, and to understand the recently

Noise-induced hearing loss is a complex disease caused by the interaction of genetic and environmental factors. It is usually caused by chronic loud noise exposure but also could be caused by transient or repetitive acoustic trauma of very high intensity, resulting in greater damage [9]. The total energy level of noise causing NIHL is determined by the intensity of the noise and the total exposure time. The noise at the same total energy level will cause the same amount of

The inner ear damage caused by noise is divided into temporary threshold shift

(TTS) and permanent threshold shift (PTS) depending on the duration of the hearing loss. Hearing loss recovers within 24–48 hours in TTS, while it is irreversible in PTS. Mechanisms of TTS and PTS are considered to be different. Animal study showed that TTS in early life can accelerates age-related hearing loss (ARHL) [11]. However, long-term impact of TTS in human ear is lacking. Pathology of

emerging topics on noise-induced cochlear synaptopathy.

**14**

health care [8].

**Figure 1.**

**1.2 Pathophysiology**

cochlear damage [10].

noise induced damage is the loss of outer hair cells leading to threshold elevations and poorer frequency discrimination. Main threshold shift occurs at an half octave higher than the frequency of loud noise, with the largest damage at 4 kHz and the smallest at 0.5 kHz [12]. Susceptibility around 4 kHz is associated with the mechanical properties of the middle ear and resonance frequency of external auditory canal [13].

Mechanism of cochlear pathology can be categorized into mechanical and metabolic [12]. Metabolic damage is a major mechanism of NIHL from chronic exposure to noise. Characteristic finding is loss of hair cells as a result of increased free radicals such as reactive oxygen species (ROS) and reactive nitrogen species within cochlear hair cells [14]. Damage starts in outer hair cells in row 2 and 3 of most vulnerable area to noise, possibly as a result of necrosis [15]. Noise releases ROS from mitochondria into cytoplasm of hair cells via release of Ca2+. Cytoplasmic ROS leads to production of pro-inflammatory cytokines and pro-apoptotic factors, finally to apoptosis of hair cells. Free radicals can persist for 7–10 days after cessation of noise exposure, which could induce progressive cochlear damage [16]. Noise-induced ischemia and reperfusion also increase the generation of ROS [14]. Lipid peroxidation induced by ROS acts as a toxic substance, causing apoptosis [15].

When the noise is extremely loud over 130 dB SPL, mechanical damage could occur via excessive vibrations of the delicate cochlear structures. Breaking or fusion of stererocilia of hair cells are most specific morphopathology. Noise could damage other cochlear structures; damage to cochlear vasculature, loss of fibrocytes, rupture of attachments of stereocilia tips to the tectorial membrane, distension or rupture of tip links, damage to pillar cells, and rupture of dendrites [14]. Noise could crumple pillar cell, decreasing length of the OHC, and detaching stereocilia from tectorial membrane in reversible way, which is understood as a mechanism of TTS [17].

Recent hot topic on noise-induced damage on auditory system is cochlear synaptopathy. Until recently, noise that does not cause threshold shift was considered safe. However, recent animal experiments have shown that noise exposure that does not cause hair cell loss may damage ribbon synapse between inner hair cell and spiral ganglion neuron [11]. Cochlear inner hair cells (IHCs) are important as mechano-electrical transducer of auditory information. Receptor potential generated by IHCs releases the neurotransmitter at the synaptic end, while outer hair cells work as cochlear amplifier via process of electromotility which increases the vibration of basilar membrane. Synaptic ribbon is specialized electron-dense structure, which is anchored to pre-synaptic membrane only nanometers apart. It contains large pool of "readily releasable" vesicles to finely vary synaptic output continuously in sensory organ of hearing and vision [18]. Thus, damage of ribbon synapse between IHCs and spiral neurons results in improper conveyance of neural information to auditory nerve fiber. Noise causes damage of presynaptic ribbons and postsynaptic nerve terminals showing various degree of swelling. The mechanism of damage for postsynaptic terminal is glutamate-mediated excitotoxicity, while mechanism of ribbon loss is unclear [19]. In cochlear synaptopathy, hearing threshold is normal because OHC is undamaged, but the amplitude of auditory nerve activity decreases as a result of silenced auditory nerve fibers [20].

Auditory nerve fibers (ANFs) could be functionally categorized by their spontaneous rate (SR). High-SR ANFs respond to sound at threshold level, whereas low-SR ANFs react to loud sound, follow rapid amplitude changes of acoustic signal, and are considered to have an important role in the hearing in noisy environment due to their larger dynamic range. Low-SR ANF appears to be damaged selectively after noise exposure [20].

Cochlear synaptopathy could be permanent and lead to a degenerative death of the spiral ganglion neuron [21]. The results of human studies on cochlear synaptopathy are controversial. If the cochlear synaptopathy is confirmed in human subjects, the conventional belief that noise would be safe if it does not cause a threshold shift should be changed [19].

#### **1.3 Individual susceptibility**

Severity of cochlear damage after noise exposure varies among individuals. Genetic factors would account for the different susceptibility up to 50% [22]. In animal study, genetic deficits leading to ARHL predispose the inner ear to NIHL [23]. Single Nucleotide Polymorphism (SNP) is the most common site of genomic mutations. It is estimated that the SNP of K+ recycling gene and heat shock protein (HSP) gene in the inner ear is associated with the sensitivity of NIHL [24, 25].

ISO 1999:2013 model assesses the risk of NIHL with age, gender in addition to intensity of exposed noise and exposure time in years [26]. The prevalence of NIHL is higher in male than in female and racial difference exists with lower prevalence in darker pigmentation [27]. Increasing age, smoking, poor diet, lack of exercise, comorbidity such as diabetes, cardiovascular disease may increase risk of NIHL [28]. Sufficient nutrition helps to preserve high frequency hearing [29].

#### **1.4 Noise exposure levels by occupational group**

The prevalence of hearing loss among noise-exposed workers is various across industries and occupations. Noise exposure is common in industries of mining, construction, manufacturing, forestry, utilities, repair and maintenance, and transportation sectors [2]. Sixty-one percent of the mining workers, 51% of the construction workers, and 47% of the manufacturing workers are exposed to noise [1]. Among workers of the above industry sectors, 20 ~ 25% have a material hearing impairment [30]. In Korea, NIHL was most common in the workers of manufacturing sector, followed by construction sector (**Figure 2**).

#### **1.5 Diagnosis**

Audiometric evidence of NIHL is characteristic notch or bulge between 3 kHz and 6 kHz, mostly worst at 4 kHz, with preserved hearing at 8 kHz and lower frequencies [31]. Notch deepens and widens with continued noise exposure, eventually involving lower frequencies. Hearing aggravates in the first 10–15 years of noise exposure, and then process slows down [17]. The maximum hearing loss from NIHL has been accepted not to exceed 75 dB at higher frequencies and 40 dB at lower frequencies [32]. However, it could reach 80 dB or worse in 2.6% of construction industry engineers [33]. Notch could be observed in 19.9% of persons without history of loud noise exposure, so audiometric notch does not necessarily mean NIHL [3].

Unlike NIHL, the ARHL accelerates over time. Hearing loss in ARHL starts at 8 kHz or higher frequencies and expands to lower frequencies. When NIHL and ARHL coexist, the notch widens and looks like a bulge [34]. As the combined ARHL progresses with advanced age, noise notch may be rarely observed [35]. Sometimes medicolegal opinion is sought about which factor contributes more on the etiology of hearing loss between noise and age. It is impossible to distinguish the allocation of each factor in aged persons.

Hearing in noise may be compromised probably due to cochlear synaptopathy. To quantify damage from noise exposure, speech recognition in quiet and noise is

**17**

*Occupational Hearing Loss*

thy was also suggested [38].

**1.6 Asymmetric NIHL**

**Figure 2.**

*DOI: http://dx.doi.org/10.5772/intechopen.97109*

also recommended [21]. Otoacoustic emission (OAE) can be used as an earlier test before PTA deficit is evident [36]. But recent studies showed that OAE was not more sensitive than PTA in assessing hearing loss caused by long-term exposure to noise [37]. Possibility of middle ear acoustic reflex as a diagnosis of cochlear synaptopa-

*Prevalence of noise-induced hearing loss (D1) according to Korean standard industrial classification. A total of 12,822 cases were diagnosed as NIHL in 2018 in Korea. Among them, NIHL was most commonly reported in manufacturing sector with 9,455 cases, followed by construction, mining, transportation, and business facility management and business support services sectors. http://www.kosha.or.kr/kosha/data/healthExamination.do.*

Noise-induced hearing loss is typically bilateral because noise affects both ears symmetrically. However, it could be asymmetric. Prevalence of asymmetric hearing gap larger than 15 dB in general population is 1% while those of NIHL were reported as 4.7–36% [35]. Left ear was more affected, especially in male [39, 40]. Lateral difference was most prominent in 3–6 kHz [41]. The firefighters and public safety workers may no longer be able to carry their duties because asymmetric hearing disturbs to distinguish sound direction and causes work-related risk [42].

There are two theories about mechanism of lateral asymmetry. One is head shadowing effect that makes noise level affecting each ear unequal [43]. Another is that left ear is more susceptible to noise damage for physiological reasons. It involves a less sensitive acoustic reflex in left side and a stronger protective auditory

MRI scan should be performed to rule out vestibular schwannoma in asymmetric hearing loss. Medicolegal decision of asymmetric NIHL is quite unconvincing. According to Robinson's criteria, if there is no evidence of NIHL in the better ear, patients can be declined compensation [45]. Whereas, Fernandes et al. insisted that comment should be made on the causation as being noise-induced, if there is no

The prevalence of tinnitus among noise-exposed workers is 24%, which is much higher than that of the general population [47]. Tinnitus is bilateral in majority of

efferent system of the right olivocochlear bundle [44, 45].

other cause to explain the asymmetry [46].

**1.7 Tinnitus and hyperacusis**

#### *Occupational Hearing Loss DOI: http://dx.doi.org/10.5772/intechopen.97109*

#### **Figure 2.**

*Hearing Loss - From Multidisciplinary Teamwork to Public Health*

should be changed [19].

**1.3 Individual susceptibility**

mutations. It is estimated that the SNP of K+

**1.4 Noise exposure levels by occupational group**

ing sector, followed by construction sector (**Figure 2**).

Cochlear synaptopathy could be permanent and lead to a degenerative death of the spiral ganglion neuron [21]. The results of human studies on cochlear synaptopathy are controversial. If the cochlear synaptopathy is confirmed in human subjects, the conventional belief that noise would be safe if it does not cause a threshold shift

Severity of cochlear damage after noise exposure varies among individuals. Genetic factors would account for the different susceptibility up to 50% [22]. In animal study, genetic deficits leading to ARHL predispose the inner ear to NIHL [23]. Single Nucleotide Polymorphism (SNP) is the most common site of genomic

(HSP) gene in the inner ear is associated with the sensitivity of NIHL [24, 25]. ISO 1999:2013 model assesses the risk of NIHL with age, gender in addition to intensity of exposed noise and exposure time in years [26]. The prevalence of NIHL is higher in male than in female and racial difference exists with lower prevalence in darker pigmentation [27]. Increasing age, smoking, poor diet, lack of exercise, comorbidity such as diabetes, cardiovascular disease may increase risk of NIHL

[28]. Sufficient nutrition helps to preserve high frequency hearing [29].

The prevalence of hearing loss among noise-exposed workers is various across industries and occupations. Noise exposure is common in industries of mining, construction, manufacturing, forestry, utilities, repair and maintenance, and transportation sectors [2]. Sixty-one percent of the mining workers, 51% of the construction workers, and 47% of the manufacturing workers are exposed to noise [1]. Among workers of the above industry sectors, 20 ~ 25% have a material hearing impairment [30]. In Korea, NIHL was most common in the workers of manufactur-

Audiometric evidence of NIHL is characteristic notch or bulge between 3 kHz and 6 kHz, mostly worst at 4 kHz, with preserved hearing at 8 kHz and lower frequencies [31]. Notch deepens and widens with continued noise exposure, eventually involving lower frequencies. Hearing aggravates in the first 10–15 years of noise exposure, and then process slows down [17]. The maximum hearing loss from NIHL has been accepted not to exceed 75 dB at higher frequencies and 40 dB at lower frequencies [32]. However, it could reach 80 dB or worse in 2.6% of construction industry engineers [33]. Notch could be observed in 19.9% of persons without history of loud noise exposure, so audiometric notch does not necessarily

Unlike NIHL, the ARHL accelerates over time. Hearing loss in ARHL starts at 8 kHz or higher frequencies and expands to lower frequencies. When NIHL and ARHL coexist, the notch widens and looks like a bulge [34]. As the combined ARHL progresses with advanced age, noise notch may be rarely observed [35]. Sometimes medicolegal opinion is sought about which factor contributes more on the etiology of hearing loss between noise and age. It is impossible to distinguish the allocation

Hearing in noise may be compromised probably due to cochlear synaptopathy. To quantify damage from noise exposure, speech recognition in quiet and noise is

recycling gene and heat shock protein

**16**

**1.5 Diagnosis**

mean NIHL [3].

of each factor in aged persons.

*Prevalence of noise-induced hearing loss (D1) according to Korean standard industrial classification. A total of 12,822 cases were diagnosed as NIHL in 2018 in Korea. Among them, NIHL was most commonly reported in manufacturing sector with 9,455 cases, followed by construction, mining, transportation, and business facility management and business support services sectors. http://www.kosha.or.kr/kosha/data/healthExamination.do.*

also recommended [21]. Otoacoustic emission (OAE) can be used as an earlier test before PTA deficit is evident [36]. But recent studies showed that OAE was not more sensitive than PTA in assessing hearing loss caused by long-term exposure to noise [37]. Possibility of middle ear acoustic reflex as a diagnosis of cochlear synaptopathy was also suggested [38].

#### **1.6 Asymmetric NIHL**

Noise-induced hearing loss is typically bilateral because noise affects both ears symmetrically. However, it could be asymmetric. Prevalence of asymmetric hearing gap larger than 15 dB in general population is 1% while those of NIHL were reported as 4.7–36% [35]. Left ear was more affected, especially in male [39, 40]. Lateral difference was most prominent in 3–6 kHz [41]. The firefighters and public safety workers may no longer be able to carry their duties because asymmetric hearing disturbs to distinguish sound direction and causes work-related risk [42].

There are two theories about mechanism of lateral asymmetry. One is head shadowing effect that makes noise level affecting each ear unequal [43]. Another is that left ear is more susceptible to noise damage for physiological reasons. It involves a less sensitive acoustic reflex in left side and a stronger protective auditory efferent system of the right olivocochlear bundle [44, 45].

MRI scan should be performed to rule out vestibular schwannoma in asymmetric hearing loss. Medicolegal decision of asymmetric NIHL is quite unconvincing. According to Robinson's criteria, if there is no evidence of NIHL in the better ear, patients can be declined compensation [45]. Whereas, Fernandes et al. insisted that comment should be made on the causation as being noise-induced, if there is no other cause to explain the asymmetry [46].

#### **1.7 Tinnitus and hyperacusis**

The prevalence of tinnitus among noise-exposed workers is 24%, which is much higher than that of the general population [47]. Tinnitus is bilateral in majority of

workers exposed to noise, however, some of them complains of unilateral symptom, more commonly in left ear [48]. Tinnitus degrades quality of life in workers and distracts military personnel during military operation [49]. Although association of noise and hyperacusis have rarely been studied, pop and rock musicians were at high risk for the development of hyperacusis [50].

#### **1.8 Noise and dizziness**

Besides hearing loss, noise can induce vestibular dysfunction through the damage to sacculocolic reflex pathway or damage to vestibular hair cell [51, 52]. The relationship between NIHL and abnormal vestibular evoked myogenic potentials (VEMPs) was reported in human study [53]. Noise exposure reduced the stereocilia bundle density of the vestibular end organ and reduces the firing rate of the anterior semicircular canal (ASCC) without significant change of the vestibular-ocular reflex, suggesting possibility of "hidden vestibular loss" [52]. Abnormal electronystagmography (ENoG) was more common in the asymmetrical NIHL group than in symmetrical NIHL [54].

#### **1.9 Prevention**

Noise regulation is the best option to prevent NIHL. Current noise regulations are based on the intensity of chronic continuous noise rather than impulsive acoustic trauma. Degree of exposure is calculated as registered in individual reporting or hearing protection programs [30]. Noise of intensity below 80 dB (A) (weighted decibel relative to human ear) reduces the risk of NIHL [55]. Daily permissible exposure limit (PEL) and exchange rate should be set to run hearing conservation program. Many countries legislate PEL at 85 dB(A) for an 8-hour workday. Some countries loosely permit up to 90 dB(A). Exchange rate defines the 3–5 dB increase in noise intensity with which exposure time should be halved to protect hearing. Exchange rate of 5 dB appears to be more accurate than 3 dB [56]. For example, 4 hours of exposure to 90 dB(A) is as hazardous as 8 hours of exposure to 85 dB(A). Number of workplaces of which noise exceeds PEL of 85 dB(A) for an 8-hour workday has been decreasing in Korea. It reduced from 20.2% of total workplaces in 2014 to 15.3% in 2018 (**Figure 3**). For impulse noise, 140 dB is generally set as the upper limit [57].

Hearing protection devices (HPDs), including earmuffs and earplug, are secondary level personal protection. Most workplace noise can be attenuated to a safe level by reducing noise by 5–10 dB, and this goal can be achieved when if HPDs are worn properly and continuously [30]. However, many workers do not wear HPDs for enough time and the effect is cut in half if workers remove HPDs for only 30 minutes of an 8-hour workday [58]. Therefore, it is efficient, when selecting HPDs, to focus on consistency of use than noise reduction rate of HPDs [59]. Individual fit-test system for earplugs is more feasible for field use and could effectively prevent hearing deterioration [60]. Earmuffs can reduce noise more consistently than earplug, and 3D print earmuffs made from light materials such as acrylonitrile butadiene styrene/clay nanocomposites was helpful in reducing weight of earmuffs and would probably increase comfort [61]. Hearing conservation program in elementary school are potentially effective way to know the risks of noise exposure early in life, leading to behavioral changes such as noise reduction and HPDs [62].

It is important to reduce the "know-do" gap between knowledge accumulated to prevent NIHL and actual implementation at workplace. This requires frequent

**19**

*Occupational Hearing Loss*

*DOI: http://dx.doi.org/10.5772/intechopen.97109*

communication meetings for noise control, assigning staff to provide daily program support, noise hazard identification, selection of HPDs, and providing inexpensive

*Korean workplaces of which noise exceeded permissible exposure limit (2014 to 2018). Percentage of Korean workplaces of which noise exceeded permissible exposure limit was 21% until 2010 but is gradually decreasing. In the second half of 2018, it was 15.3% showing the lowest rate for the past 5 years. https://www.moel.go. kr/info/publict/publictDataView.do;jsessionid=adRh47EovBcKL142qoR3sKQStfieMxcEVFYSD2N*

*Xqjie0s2D438avLaPebxaainR.moel\_was\_outside\_servlet\_www1?bbs\_seq=20200200123.*

We suggest that hearing conservation program should include administrative or engineering controls to reduce sound levels. Workplace noise should be monitored using either a wearable sound level meter or a dosimeter to determine if noise exposure level is at or above 85 dB(A). If the workplace noise exceeds an 85 dB(A) for an 8-hour workday, exposed employees should be enrolled in a hearing conservation program (HCP) and audiometric test should be conducted annually by audiologist to check if the standard threshold shift occurs. Employees enrolled in HCP should be offered HPDs and take mandatory training program annually about effects of noise on hearing, purpose and value of HPDs and hearing test. Managers or supervisors must attend training sessions and should keep the record of all hearing tests,

There is no practical medication to prevent NIHL from chronic noise exposure.

Most drugs have been studied either on an experimental level or on an animal

The noise exposure increases the immune and inflammatory factors in the cochlea. Steroids are the only approved medicine in treating sudden hearing loss. Animal study showed that steroids before and after the exposure to acoustic trauma were effective through control of the inflammatory response [63, 64]. It is estimated that intratympanic steroid injection would be effective in protecting outer hair cell efferent terminal synapse, and intraperitoneal steroid injection would be effective in protecting organ of Corti and stria vascularis [65]. In human studies, combined systemic & intratympanic steroid administration was more effective than systemic steroid only [66]. Long-term administration of steroid is inadequate

sound level meters or sound measuring apps [30].

noise surveys, and training records.

**1.10 Pharmacotherapy**

due to its possible side effects.

study basis.

**Figure 3.**

#### **Figure 3.**

*Hearing Loss - From Multidisciplinary Teamwork to Public Health*

high risk for the development of hyperacusis [50].

**1.8 Noise and dizziness**

symmetrical NIHL [54].

**1.9 Prevention**

upper limit [57].

and HPDs [62].

workers exposed to noise, however, some of them complains of unilateral symptom, more commonly in left ear [48]. Tinnitus degrades quality of life in workers and distracts military personnel during military operation [49]. Although association of noise and hyperacusis have rarely been studied, pop and rock musicians were at

Besides hearing loss, noise can induce vestibular dysfunction through the damage to sacculocolic reflex pathway or damage to vestibular hair cell [51, 52]. The relationship between NIHL and abnormal vestibular evoked myogenic potentials (VEMPs) was reported in human study [53]. Noise exposure reduced the stereocilia bundle density of the vestibular end organ and reduces the firing rate of the anterior semicircular canal (ASCC) without significant change of the vestibular-ocular reflex, suggesting possibility of "hidden vestibular loss" [52]. Abnormal electronystagmography (ENoG) was more common in the asymmetrical NIHL group than in

Noise regulation is the best option to prevent NIHL. Current noise regulations are based on the intensity of chronic continuous noise rather than impulsive acoustic trauma. Degree of exposure is calculated as registered in individual reporting or hearing protection programs [30]. Noise of intensity below 80 dB (A) (weighted decibel relative to human ear) reduces the risk of NIHL [55]. Daily permissible exposure limit (PEL) and exchange rate should be set to run hearing conservation program. Many countries legislate PEL at 85 dB(A) for an 8-hour workday. Some countries loosely permit up to 90 dB(A). Exchange rate defines the 3–5 dB increase in noise intensity with which exposure time should be halved to protect hearing. Exchange rate of 5 dB appears to be more accurate than 3 dB [56]. For example, 4 hours of exposure to 90 dB(A) is as hazardous as 8 hours of exposure to 85 dB(A). Number of workplaces of which noise exceeds PEL of 85 dB(A) for an 8-hour workday has been decreasing in Korea. It reduced from 20.2% of total workplaces in 2014 to 15.3% in 2018 (**Figure 3**). For impulse noise, 140 dB is generally set as the

Hearing protection devices (HPDs), including earmuffs and earplug, are secondary level personal protection. Most workplace noise can be attenuated to a safe level by reducing noise by 5–10 dB, and this goal can be achieved when if HPDs are worn properly and continuously [30]. However, many workers do not wear HPDs for enough time and the effect is cut in half if workers remove HPDs for only 30 minutes of an 8-hour workday [58]. Therefore, it is efficient, when selecting HPDs, to focus on consistency of use than noise reduction rate of HPDs [59]. Individual fit-test system for earplugs is more feasible for field use and could effectively prevent hearing deterioration [60]. Earmuffs can reduce noise more consistently than earplug, and 3D print earmuffs made from light materials such as acrylonitrile butadiene styrene/clay nanocomposites was helpful in reducing weight of earmuffs and would probably increase comfort [61]. Hearing conservation program in elementary school are potentially effective way to know the risks of noise exposure early in life, leading to behavioral changes such as noise reduction

It is important to reduce the "know-do" gap between knowledge accumulated to prevent NIHL and actual implementation at workplace. This requires frequent

**18**

*Korean workplaces of which noise exceeded permissible exposure limit (2014 to 2018). Percentage of Korean workplaces of which noise exceeded permissible exposure limit was 21% until 2010 but is gradually decreasing. In the second half of 2018, it was 15.3% showing the lowest rate for the past 5 years. https://www.moel.go. kr/info/publict/publictDataView.do;jsessionid=adRh47EovBcKL142qoR3sKQStfieMxcEVFYSD2N Xqjie0s2D438avLaPebxaainR.moel\_was\_outside\_servlet\_www1?bbs\_seq=20200200123.*

communication meetings for noise control, assigning staff to provide daily program support, noise hazard identification, selection of HPDs, and providing inexpensive sound level meters or sound measuring apps [30].

We suggest that hearing conservation program should include administrative or engineering controls to reduce sound levels. Workplace noise should be monitored using either a wearable sound level meter or a dosimeter to determine if noise exposure level is at or above 85 dB(A). If the workplace noise exceeds an 85 dB(A) for an 8-hour workday, exposed employees should be enrolled in a hearing conservation program (HCP) and audiometric test should be conducted annually by audiologist to check if the standard threshold shift occurs. Employees enrolled in HCP should be offered HPDs and take mandatory training program annually about effects of noise on hearing, purpose and value of HPDs and hearing test. Managers or supervisors must attend training sessions and should keep the record of all hearing tests, noise surveys, and training records.

#### **1.10 Pharmacotherapy**

There is no practical medication to prevent NIHL from chronic noise exposure. Most drugs have been studied either on an experimental level or on an animal study basis.

The noise exposure increases the immune and inflammatory factors in the cochlea. Steroids are the only approved medicine in treating sudden hearing loss. Animal study showed that steroids before and after the exposure to acoustic trauma were effective through control of the inflammatory response [63, 64]. It is estimated that intratympanic steroid injection would be effective in protecting outer hair cell efferent terminal synapse, and intraperitoneal steroid injection would be effective in protecting organ of Corti and stria vascularis [65]. In human studies, combined systemic & intratympanic steroid administration was more effective than systemic steroid only [66]. Long-term administration of steroid is inadequate due to its possible side effects.

Free oxygen radicals and oxidant stress are important pathological mechanisms of NIHL. N-acetylcysteine (NAC) is an antioxidant and is known to reduce noiseinduced ototoxicity in animal study. There was no significant differences of overall hearing loss in military population between NAC group and placebo group [67].

Neurotropin-3 (NT3) and Brain derived neurotrophic factor (BDNF) are known to be important factors in the generation and maintenance of cochlear hair cell ribbon synapse [68, 69]. Animal study demonstrated a reduction in synaptopathy and a restoration of hearing immediately after strong noise exposure [70] but human data is lacking.

#### **1.11 Conclusion**

Noise-induced hearing loss is drawing more attention than ever before. Besides hearing loss, noise can also compromise the vestibular function. Recently, evidence on noise-induced cochlear synaptopathy is accumulating. Exposure to noise in short duration or less intense noise may result in functional hearing loss without threshold change on audiogram. So far, prevention is the best option, but we expect that continuous research on NIHL will open up the possibility for treating drug ototoxicity and ARHL as well.

#### **2. Chemical induced hearing loss**

#### **2.1 Introduction**

Chemicals such as organic solvents, metals and asphyxiants are known for their neurotoxic effects on both the central and peripheral nervous systems. These agents could injure the sensory cells and peripheral nerve endings of the cochlea [71].

Over the past 3 decades, several studies investigated the relationship between occupational exposure to chemical substances and hearing loss for humans [72]. According to the score combining human and animal data, lead (and its inorganic salts) as an only inorganic substance and the organic chemicals including toluene, styrene, and trichloroethylene were ranked as "ototoxic". Other candidate substances classified as "possibly ototoxic" are nitriles (acrylonitrile, 3-butenenitrile), carbohydrates (n-hexane, p-xylene, and ethylbenzene), hydrogen cyanide, carbon monoxide, carbon disulfide, and mercury, germanium, and tin. Recently, a classification criteria on ototoxic substances was delivered by the Nordic Expert Group (NEG). The NEG chose a quantitative approach, meticulously comparing the "no observed" or "lowest observed" effect levels with occupational exposure limits from various countries. This information can be useful for the management of toxic substances and prevention of hearing loss (**Table 1**) [73].

Until now, regarding regulatory problem, the interaction with noise has not been investigated in a satisfactory way. Although it is very difficult to combine all of the data to arrive at solid conclusions, this does not exclude the possibility of other chemical substances can worsen hearing losses due to noise.

#### **2.2 Organic solvents induced hearing loss**

In workplace, one of the most common kinds of exposure is solvents mixture. The most prevalent exposures seem to happen in industries where workers have contacts with paints, thinners, lacquers and printing inks [74]. In Korea, organic solvents have the second highest excess rate among harmful factors in workplaces.

**21**

*Occupational Hearing Loss*

hearing loss.

**Table 1.**

*DOI: http://dx.doi.org/10.5772/intechopen.97109*

exposure

OELs.

*OEL: occupational exposure limits.*

existing OELs.

The exceeded rate of the occupational exposure limit maintained a similar level of 0.4 to 0.7% for the last five years from 2014 to 2018 (**Figure 4**). Although the ototoxic effects of organic solvents have been widely studied, there is no consensus about the correlation between the solvents exposure level and the resultant

**Classification Criteria Ototoxic substances**

toluene, styrene, carbon monoxide, carbon disulfide,

p-xylene, ethylbenzene, and

lead and mercury

hydrogen cyanide

Other substance

the existing OELs. There are also robust animal data supporting an effect on hearing resulting from

indicate an auditory effect below or near the

*Classification and the criteria of ototoxic substances based on occupational exposure limits.*

indicate an auditory effect well above the existing

Category 1 Human data indicate auditory effects below or near

Category 2 Human data are lacking, whereas animal data

Category 3 Human data are poor or lacking. Animal data

In occupational condition, the ototoxicity of organic solvents is more difficult to prove. Because the workplace concentration of chemicals is much lower than that used in animal studies, and the workers are usually exposed to a mixture of solvents with widely varying compositions and concentrations, it is difficult to assess the effect of a single substance. Furthermore, in industrial settings, exposure to chemicals often coexists with an elevated level of noise, which makes it difficult to distinguish the

Recently, Hormozi et al. reported dose–response relationship between organic solvents mixture exposure and risk of hearing loss from a meta-analysis [72]. The results showed a statistically significant dose–response relationship between the occupational exposure level (Exposure Index, EI), duration of exposure or number

Long-term exposure to organic solvents has been shown to cause irreversible hearing impairment damaging the cochlear hair cells as the first target [75]. The mechanism of acute injury would be the direct action of solvents on the cells of the organ of Corti, resulting in disorganization of their membranous structures, whereas chronic ototoxic effects may be explained by the formation of chemically

The ototoxicity mechanisms with strong evidence were described in **Table 3**. These solvents adversely affect both peripheral and central auditory system. For example, toluene may enhance inhibitory synaptic responses as CNS depressants, also can inhibit the middle-ear acoustic reflex (cholinergic efferent system). This would make inner ear more susceptible to co-exposure even to a noise intensity

Śliwinska-Kowalska (2007) summarized a risk/odds ratio of organic solventinduced hearing loss, compared to non-exposed population, as followings. 1) No excess risk was found for workers exposed to solvent mixture when: the exposure history was short (up to 4 years), or the exposure level was very low (current exposure ranged from few to 18 ppm for toluene, to few ppm for xylene and other

solvent effect from the noise-induced hearing loss [22].

**2.3 Mechanism of organic solvent ototoxicity**

and biologically reactive intermediates [76].

below permissible limit value [77].

of solvents and the risk of developing hearing loss (**Table 2**).

#### **Table 1.**

*Hearing Loss - From Multidisciplinary Teamwork to Public Health*

human data is lacking.

ototoxicity and ARHL as well.

**2. Chemical induced hearing loss**

**1.11 Conclusion**

**2.1 Introduction**

(**Table 1**) [73].

Free oxygen radicals and oxidant stress are important pathological mechanisms of NIHL. N-acetylcysteine (NAC) is an antioxidant and is known to reduce noiseinduced ototoxicity in animal study. There was no significant differences of overall hearing loss in military population between NAC group and placebo group [67]. Neurotropin-3 (NT3) and Brain derived neurotrophic factor (BDNF) are known to be important factors in the generation and maintenance of cochlear hair cell ribbon synapse [68, 69]. Animal study demonstrated a reduction in synaptopathy and a restoration of hearing immediately after strong noise exposure [70] but

Noise-induced hearing loss is drawing more attention than ever before. Besides hearing loss, noise can also compromise the vestibular function. Recently, evidence on noise-induced cochlear synaptopathy is accumulating. Exposure to noise in short duration or less intense noise may result in functional hearing loss without threshold change on audiogram. So far, prevention is the best option, but we expect that continuous research on NIHL will open up the possibility for treating drug

Chemicals such as organic solvents, metals and asphyxiants are known for their neurotoxic effects on both the central and peripheral nervous systems. These agents could injure the sensory cells and peripheral nerve endings of the cochlea [71].

Over the past 3 decades, several studies investigated the relationship between

occupational exposure to chemical substances and hearing loss for humans [72]. According to the score combining human and animal data, lead (and its inorganic salts) as an only inorganic substance and the organic chemicals including toluene, styrene, and trichloroethylene were ranked as "ototoxic". Other candidate substances classified as "possibly ototoxic" are nitriles (acrylonitrile, 3-butenenitrile), carbohydrates (n-hexane, p-xylene, and ethylbenzene), hydrogen cyanide, carbon monoxide, carbon disulfide, and mercury, germanium, and tin. Recently, a classification criteria on ototoxic substances was delivered by the Nordic Expert Group (NEG). The NEG chose a quantitative approach, meticulously comparing the "no observed" or "lowest observed" effect levels with occupational exposure limits from various countries. This information can be useful for the management of toxic substances and prevention of hearing loss

Until now, regarding regulatory problem, the interaction with noise has not been investigated in a satisfactory way. Although it is very difficult to combine all of the data to arrive at solid conclusions, this does not exclude the possibility of other

In workplace, one of the most common kinds of exposure is solvents mixture. The most prevalent exposures seem to happen in industries where workers have contacts with paints, thinners, lacquers and printing inks [74]. In Korea, organic solvents have the second highest excess rate among harmful factors in workplaces.

chemical substances can worsen hearing losses due to noise.

**2.2 Organic solvents induced hearing loss**

**20**

*Classification and the criteria of ototoxic substances based on occupational exposure limits.*

The exceeded rate of the occupational exposure limit maintained a similar level of 0.4 to 0.7% for the last five years from 2014 to 2018 (**Figure 4**). Although the ototoxic effects of organic solvents have been widely studied, there is no consensus about the correlation between the solvents exposure level and the resultant hearing loss.

In occupational condition, the ototoxicity of organic solvents is more difficult to prove. Because the workplace concentration of chemicals is much lower than that used in animal studies, and the workers are usually exposed to a mixture of solvents with widely varying compositions and concentrations, it is difficult to assess the effect of a single substance. Furthermore, in industrial settings, exposure to chemicals often coexists with an elevated level of noise, which makes it difficult to distinguish the solvent effect from the noise-induced hearing loss [22].

Recently, Hormozi et al. reported dose–response relationship between organic solvents mixture exposure and risk of hearing loss from a meta-analysis [72]. The results showed a statistically significant dose–response relationship between the occupational exposure level (Exposure Index, EI), duration of exposure or number of solvents and the risk of developing hearing loss (**Table 2**).

#### **2.3 Mechanism of organic solvent ototoxicity**

Long-term exposure to organic solvents has been shown to cause irreversible hearing impairment damaging the cochlear hair cells as the first target [75]. The mechanism of acute injury would be the direct action of solvents on the cells of the organ of Corti, resulting in disorganization of their membranous structures, whereas chronic ototoxic effects may be explained by the formation of chemically and biologically reactive intermediates [76].

The ototoxicity mechanisms with strong evidence were described in **Table 3**. These solvents adversely affect both peripheral and central auditory system. For example, toluene may enhance inhibitory synaptic responses as CNS depressants, also can inhibit the middle-ear acoustic reflex (cholinergic efferent system). This would make inner ear more susceptible to co-exposure even to a noise intensity below permissible limit value [77].

Śliwinska-Kowalska (2007) summarized a risk/odds ratio of organic solventinduced hearing loss, compared to non-exposed population, as followings. 1) No excess risk was found for workers exposed to solvent mixture when: the exposure history was short (up to 4 years), or the exposure level was very low (current exposure ranged from few to 18 ppm for toluene, to few ppm for xylene and other

#### **Figure 4.**

*Korean workplaces of which organic solvents exceeded permissible exposure limit (2014 to 2018). https://www. moel.go.kr/info/publict/publictDataView.do;jsessionid=adRh47EovBcKL142qoR3sKQStfieMxcEVFYSD2 NXqjie0s2D438avLaPebxaainR.moel\_was\_outside\_servlet\_www1?bbs\_seq=20200200123.*

*\*Hearing loss: average hearing threshold greater than 25 dB in at least one ear (250–8000 Hz). †Reference group: not exposed to either noise or solvents mixture.*

*‡EI: the sum of the mean time-weighted exposures to each solvent was divided by its occupational exposure limit (American Conference of Governmental Industrial Hygienists threshold limit value, ACGIH TLV).*

*Cited from THE RISK OF HEARING LOSS ASSOCIATED WITH OCCUPATIONAL EXPOSURE TO ORGANIC SOLVENTS MIXTURE WITH AND WITHOUT CONCURRENT NOISE EXPOSURE: A SYSTEMATIC REVIEW AND META-ANALYSIS. International Journal of Occupational Medicine and Environmental Health 2017;30(4):521–535 https://doi.org/10.13075/ijomeh.1896.01024.*

#### **Table 2.**

*Dose–response relationship between organic solvents mixture exposure and risk of hearing loss\* .*

solvents, and the exposure index was <1). 2) Excess risk was found for workers exposed to solvent mixture when: the exposure level was moderate (toluene exposure ranged from 25 to 70 ppm, xylene exposure 25–40 ppm, and exposure index from 0.3–1.53), or the workers were exposed to high solvent concentrations and noise (the mean lifetime exposure to xylene was 696 ppm, to toluene 203 ppm, and the mean exposure index was 6.3) [72]. Risk/odds ratios of hearing loss due

**23**

each other.

**Table 3.**

Target: Outer hair

sensory hair cell, spiral ganglion cells, auditory nerve

pathways

**Mechanism Points to consider**

1.Prolonged exposure causes irreversible hearing impairment.

middle-ear acoustic reflex, which partially explain the synergistic effects of co-exposure to noise and aromatic solvents.

Permanent hearing damage may occur due to combined exposure

Presumed to be a sequelae of thyroid disease caused by halogenated hydrocarbons.

Hearing loss tends to occur only at high level

of exposure.

with noise.

2.Affect the

1.In case of acute effect, direct action on the cells of the organ of

flow

 massive efflux and tunnel accumulation.

Corti. 2.In case of chronic effect, formation of intermediates such as reactive oxygen

species. 3.Cause K+

dysfunction. 4.Outer hair cell toxicity

1.Induce loss of inner ear hair cells and spiral ganglion cells. 2.In the case of acrylonitrile, the risk of oxidative damage to the inner ear is increased due to damage to the cellular antioxidant defense mechanisms.

due to K+

In the case of polychlorinated biphenyls (PCB), it is assumed to have a direct effect on outer hair cells.

Unknown, but dose dependent hearing loss

**Chemicals Targets and**

Aromatic solvents Target: Central

to exposure to organic solvent mixture were ranged 1.4 to 5.0, while the ratio of

Previous experiments on ototraumatic substances in animals have confirmed the synergistic adverse effects of combined exposure to noise and solvents on hearing [79, 80]. In the case of combined exposure to noise and organic solvents, depending on the parameters and characteristics associated to the noise (such as intensity and impulsiveness) and solvent (such as concentration), they might interactively affect

From the animal studies, the increase in auditory brainstem response (ABR) latencies after exposure by inhalation of more than two solvents observed an additive effect rather than a synergistic or antagonistic interaction. Results of these studies imply that the mechanism of ototoxicity for these solvents may be similar.

populations co-exposed to noise and solvents were 1.7 to 8.25 [78].

*Summary for impacts and mechanisms of ototoxic chemicals in workplace exposure.*

**2.4 Interactive effects of organic solvents and noise**

#### *Occupational Hearing Loss DOI: http://dx.doi.org/10.5772/intechopen.97109*

*Hearing Loss - From Multidisciplinary Teamwork to Public Health*

solvents, and the exposure index was <1). 2) Excess risk was found for workers exposed to solvent mixture when: the exposure level was moderate (toluene exposure ranged from 25 to 70 ppm, xylene exposure 25–40 ppm, and exposure index from 0.3–1.53), or the workers were exposed to high solvent concentrations and noise (the mean lifetime exposure to xylene was 696 ppm, to toluene 203 ppm, and the mean exposure index was 6.3) [72]. Risk/odds ratios of hearing loss due

*‡EI: the sum of the mean time-weighted exposures to each solvent was divided by its occupational exposure limit*

*Cited from THE RISK OF HEARING LOSS ASSOCIATED WITH OCCUPATIONAL EXPOSURE TO ORGANIC SOLVENTS MIXTURE WITH AND WITHOUT CONCURRENT NOISE EXPOSURE: A SYSTEMATIC REVIEW AND META-ANALYSIS. International Journal of Occupational Medicine and Environmental Health*

*.*

*Korean workplaces of which organic solvents exceeded permissible exposure limit (2014 to 2018). https://www. moel.go.kr/info/publict/publictDataView.do;jsessionid=adRh47EovBcKL142qoR3sKQStfieMxcEVFYSD2*

**Variable Reports (n) OR (95% CI)† p** Duration of exposure 0.001

Exposure index (EI)‡ 0.049

Solvents 0.045

*NXqjie0s2D438avLaPebxaainR.moel\_was\_outside\_servlet\_www1?bbs\_seq=20200200123.*

< 5 years 4 1.01 (0.92–1.10) 5–10 years 3 1.57 (1.27–1.93) > 10 years 7 3.36 (2.36–4.79)

< 0.5 3 1.37 (0.75–2.48) 0.5–0.99 3 3.25 (1.88–5.62) ≥ 1 7 4.51 (3.46–5.90)

2–5 7 1.62 (1.07–2.44) 6–8 4 4.22 (2.72–6.56) *\*Hearing loss: average hearing threshold greater than 25 dB in at least one ear (250–8000 Hz).*

*(American Conference of Governmental Industrial Hygienists threshold limit value, ACGIH TLV).*

*Dose–response relationship between organic solvents mixture exposure and risk of hearing loss\**

*†Reference group: not exposed to either noise or solvents mixture.*

*2017;30(4):521–535 https://doi.org/10.13075/ijomeh.1896.01024.*

**22**

**Table 2.**

**Figure 4.**

#### **Table 3.**

*Summary for impacts and mechanisms of ototoxic chemicals in workplace exposure.*

to exposure to organic solvent mixture were ranged 1.4 to 5.0, while the ratio of populations co-exposed to noise and solvents were 1.7 to 8.25 [78].

#### **2.4 Interactive effects of organic solvents and noise**

Previous experiments on ototraumatic substances in animals have confirmed the synergistic adverse effects of combined exposure to noise and solvents on hearing [79, 80]. In the case of combined exposure to noise and organic solvents, depending on the parameters and characteristics associated to the noise (such as intensity and impulsiveness) and solvent (such as concentration), they might interactively affect each other.

From the animal studies, the increase in auditory brainstem response (ABR) latencies after exposure by inhalation of more than two solvents observed an additive effect rather than a synergistic or antagonistic interaction. Results of these studies imply that the mechanism of ototoxicity for these solvents may be similar.

However, rats simultaneously exposed to both toluene and noise induced a more severe hearing loss than the summated hearing loss obtained from an equivalent exposure level to each agent alone [77].

From the human studies, exposure to a mixture of solvents may damage the inner ear to a much greater extent than noise exposure. The relative risk for hearing loss in workers exposed to solvents was greater (RR = 9.6) in comparison to workers exposed only to noise (RR = 4.2). Hearing loss associated with styrene significantly increased in high frequency (8–16 kHz) and mid-audiometric frequency of 2 kHz [22]. Sliwinska-Kowalska et al. (2003) found a positive linear relationship between average working life exposure to styrene concentrations and hearing thresholds at 6 and 8 kHz. The possible synergism of combined exposure to solvents and noise on hearing has not been consistently identified in human studies. Some researchers have failed to find a synergistic effect between these agents on hearing [22].

Although it is difficult to derive a dose–response relationship between the solvent concentration and the hearing outcome, the risk of hearing loss increase with the longer duration of employment and accompanying noise in workers exposed to organic solvent [72].

#### **2.5 Diagnostic tool for ototoxic substances**

Although there is no consensus on the lowest OELs for solvents in relation to their effect on the auditory organ, the current standards for solvent-exposed populations seem to be inadequate. Since organic solvents have detrimental effects both on the peripheral and central parts of the auditory pathway, pure-tone audiogram might be insufficient to monitor their ototoxicity [78].

From previous studies, researchers have found some useful tests for the evidence of adverse effects on the central auditory system in workers exposed to mixture of solvents: 1) dichotic listening: useful tool in the assessment of solventexposed workers, particularly in those who have had intermediate levels of exposure; 2) electrophysiological techniques (ABR): increase of the absolute latencies and inter-peak latencies (IPL) between waves of the ABR (I-III IPL; I-V IPL; III-V IPL) or prolonged P300 (a long latency auditory evoked potential); 3) otoacoustic emissions (OAEs): gradual deterioration of hearing threshold before audiometric change; 4) comprehensive battery of behavioral central auditory function assessment procedures: solvent-exposed participants presented with poorer results adjusted for age and hearing thresholds in comparison to non-exposed subjects [77]. These tests can be conjugated to evaluate possible adverse effects of solvents on the auditory system.

#### **2.6 Recommendations**

So far, the robust evidence confirms that the effects of ototoxic substances on auditory function can be aggravated by noise, which is supported by data from epidemiologic studies on human workers.

In real world, the exposure to solvent mixtures is various in terms of levels and composition. Numerous study groups reported an association between low to moderate exposure to solvent mixtures and hearing disorders. However, occupational legislation does not take environmental chemicals hazardous to hearing into consideration. Thus, there may be numerous workers with unmet needs concerning hearing conservation.

Here we are going to make some necessary suggestions for occupational health professionals and the workforce. Health care provider should be aware of the risks related to ototoxic substances. Employers and workers should be advised

**25**

**Author details**

Joong-Keun Kwon1

and Jiho Lee2

The authors declare no conflict of interest.

\*Address all correspondence to<EMAIL_ADDRESS>
provided the original work is properly cited.

College of Medicine, Ulsan, Republic of Korea

\*

1 Department of Otolaryngology, Ulsan University Hospital, Ulsan University,

I would like to thank the members of the Department of Occupational and Environmental Medicine, Ulsan University Hospital. A Ram Kim, Daeyun Kim, Sunghee Lee, Jisoo Kim, and Hanjoon Kim, also Jinhee Bang, member of Environmental health center have contributed directly or indirectly to this chapter. We have shared information and ideas. Moreover, they have made suggestions and

2 Department of Occupational and Environmental Medicine, Ulsan University Hospital, Ulsan University, College of Medicine, Ulsan, Republic of Korea

© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

*Occupational Hearing Loss*

well-designed studies.

exposure levels.

**Thanks**

comments.

**Conflict of interest**

*DOI: http://dx.doi.org/10.5772/intechopen.97109*

accordingly. Risk management measures aimed at reducing exposure to noise and ototoxic substances, especially co-existence of them, should be encouraged. In occupational health-screening activities, ototoxicity should be included. Appropriate diagnostic tools should be developed for early detections of chemically induced hearing impairment. Suitable scientific investigations into ototoxic properties of substance and combined effects with noise should be encouraged by

Occupational noise exposure has been well-known as the most deleterious factor to hearing loss, however, the impact of chemical-induced hearing loss on workers should not be underestimated [81]. Industry-based initiatives should include the identification of populations at risk and the delivery of tailored hearing conservation program accordingly to noise and chemical-exposed workers regarding their

#### *Occupational Hearing Loss DOI: http://dx.doi.org/10.5772/intechopen.97109*

accordingly. Risk management measures aimed at reducing exposure to noise and ototoxic substances, especially co-existence of them, should be encouraged. In occupational health-screening activities, ototoxicity should be included. Appropriate diagnostic tools should be developed for early detections of chemically induced hearing impairment. Suitable scientific investigations into ototoxic properties of substance and combined effects with noise should be encouraged by well-designed studies.

Occupational noise exposure has been well-known as the most deleterious factor to hearing loss, however, the impact of chemical-induced hearing loss on workers should not be underestimated [81]. Industry-based initiatives should include the identification of populations at risk and the delivery of tailored hearing conservation program accordingly to noise and chemical-exposed workers regarding their exposure levels.

### **Conflict of interest**

The authors declare no conflict of interest.

### **Thanks**

*Hearing Loss - From Multidisciplinary Teamwork to Public Health*

exposure level to each agent alone [77].

**2.5 Diagnostic tool for ototoxic substances**

might be insufficient to monitor their ototoxicity [78].

organic solvent [72].

on the auditory system.

**2.6 Recommendations**

hearing conservation.

epidemiologic studies on human workers.

However, rats simultaneously exposed to both toluene and noise induced a more severe hearing loss than the summated hearing loss obtained from an equivalent

From the human studies, exposure to a mixture of solvents may damage the inner ear to a much greater extent than noise exposure. The relative risk for hearing loss in workers exposed to solvents was greater (RR = 9.6) in comparison to workers exposed only to noise (RR = 4.2). Hearing loss associated with styrene significantly increased in high frequency (8–16 kHz) and mid-audiometric frequency of 2 kHz [22]. Sliwinska-Kowalska et al. (2003) found a positive linear relationship between average working life exposure to styrene concentrations and hearing thresholds at 6 and 8 kHz. The possible synergism of combined exposure to solvents and noise on hearing has not been consistently identified in human studies. Some researchers

have failed to find a synergistic effect between these agents on hearing [22].

Although it is difficult to derive a dose–response relationship between the solvent concentration and the hearing outcome, the risk of hearing loss increase with the longer duration of employment and accompanying noise in workers exposed to

Although there is no consensus on the lowest OELs for solvents in relation to their effect on the auditory organ, the current standards for solvent-exposed populations seem to be inadequate. Since organic solvents have detrimental effects both on the peripheral and central parts of the auditory pathway, pure-tone audiogram

From previous studies, researchers have found some useful tests for the evidence of adverse effects on the central auditory system in workers exposed to mixture of solvents: 1) dichotic listening: useful tool in the assessment of solventexposed workers, particularly in those who have had intermediate levels of exposure; 2) electrophysiological techniques (ABR): increase of the absolute latencies and inter-peak latencies (IPL) between waves of the ABR (I-III IPL; I-V IPL; III-V IPL) or prolonged P300 (a long latency auditory evoked potential); 3) otoacoustic emissions (OAEs): gradual deterioration of hearing threshold before audiometric change; 4) comprehensive battery of behavioral central auditory function assessment procedures: solvent-exposed participants presented with poorer results adjusted for age and hearing thresholds in comparison to non-exposed subjects [77]. These tests can be conjugated to evaluate possible adverse effects of solvents

So far, the robust evidence confirms that the effects of ototoxic substances on auditory function can be aggravated by noise, which is supported by data from

In real world, the exposure to solvent mixtures is various in terms of levels and composition. Numerous study groups reported an association between low to moderate exposure to solvent mixtures and hearing disorders. However, occupational legislation does not take environmental chemicals hazardous to hearing into consideration. Thus, there may be numerous workers with unmet needs concerning

Here we are going to make some necessary suggestions for occupational health

professionals and the workforce. Health care provider should be aware of the risks related to ototoxic substances. Employers and workers should be advised

**24**

I would like to thank the members of the Department of Occupational and Environmental Medicine, Ulsan University Hospital. A Ram Kim, Daeyun Kim, Sunghee Lee, Jisoo Kim, and Hanjoon Kim, also Jinhee Bang, member of Environmental health center have contributed directly or indirectly to this chapter. We have shared information and ideas. Moreover, they have made suggestions and comments.

### **Author details**

Joong-Keun Kwon1 and Jiho Lee2 \*

1 Department of Otolaryngology, Ulsan University Hospital, Ulsan University, College of Medicine, Ulsan, Republic of Korea

2 Department of Occupational and Environmental Medicine, Ulsan University Hospital, Ulsan University, College of Medicine, Ulsan, Republic of Korea

\*Address all correspondence to<EMAIL_ADDRESS>
© 2021 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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**27**

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#### *Occupational Hearing Loss DOI: http://dx.doi.org/10.5772/intechopen.97109*

differences between temporary and permanent threshold shift. Hear Res. 2000;139(1-2):13-30.

[18] Parsons TD, Sterling P. Synaptic Ribbon: Conveyor Belt or Safety Belt? Neuron. 2003;37(3):379-382.

[19] Shi L, Chang Y, Li X, Aiken S, Liu L, Wang J. Cochlear Synaptopathy and Noise-Induced Hidden Hearing Loss. Neural Plast. 2016;2016:6143164.

[20] Furman AC, Kujawa SG, Liberman MC. Noise-induced cochlear neuropathy is selective for fibers with low spontaneous rates. J Neurophysiol. 2013;110(3):577-586.

[21] Kujawa SG, Liberman MC. Adding insult to injury: cochlear nerve degeneration after "temporary" noise-induced hearing loss. J Neurosci. 2009;29(45):14077-14085.

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[24] Lim HH, Jenkins OH, Myers MW, Miller JM, Altschuler RA. Detection of HSP 72 synthesis after acoustic overstimulation in rat cochlea. Hear Res. 1993;69(1-2):146-150.

[25] Yoshida N, Kristiansen A, Liberman MC. Heat stress and protection from permanent acoustic injury in mice. J Neurosci. 1999;19(22):10116-10124.

[26] Nageris BI, Raveh E, Zilberberg M, Attias J. Asymmetry in noise-induced hearing loss: relevance of acoustic reflex and left or right handedness. Otology &

neurotology: official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology. 2007;28(4):434-437.

[27] Themann C, Suter A, Stephenson M. National Research Agenda for the Prevention of Occupational Hearing Loss—Part 1. Seminars in Hearing. 2013;34:145-207.

[28] Daniel E. Noise and hearing loss: a review. J Sch Health. 2007;77(5):225-231.

[29] Spankovich C, Le Prell CG. Associations between dietary quality, noise, and hearing: data from the National Health and Nutrition Examination Survey, 1999-2002. Int J Audiol. 2014;53(11):796-809.

[30] Themann CL, Masterson EA. Occupational noise exposure: A review of its effects, epidemiology, and impact with recommendations for reducing its burden. J Acoust Soc Am. 2019;146(5):3879.

[31] Dobie RA. Hearing conservation in industry. West J Med. 1982;137(6):499-505.

[32] Kirchner DB, Evenson E, Dobie RA, Rabinowitz P, Crawford J, Kopke R, et al. Occupational noise-induced hearing loss: ACOEM Task Force on Occupational Hearing Loss. J Occup Environ Med. 2012;54(1):106-108.

[33] Hong O. Hearing loss among operating engineers in American construction industry. Int Arch Occup Environ Health. 2005;78(7):565-574.

[34] Dobie RA. Estimating noiseinduced permanent threshold shift from audiometric shape: the ISO-1999 model. Ear Hear. 2005;26(6):630-635.

[35] Le TN, Straatman LV, Lea J, Westerberg B. Current insights in

**26**

*Hearing Loss - From Multidisciplinary Teamwork to Public Health*

of Noise-Induced Hearing Loss in the United States. J Speech Lang Hear Res.

[9] Suvorov G, Denisov E, Antipin V, Kharitonov V, Starck J, Pyykkö I, et al. Effects of peak levels and number of impulses to hearing among forge hammering workers. Appl Occup Environ Hyg. 2001;16(8):816-822.

[10] Ward WD, Santi PA, Duvall AJ, 3rd, Turner CW. Total energy and critical intensity concepts in noise damage. Ann

Otol Rhinol Laryngol. 1981;90

[11] Kujawa SG, Liberman MC. Acceleration of age-related hearing loss by early noise exposure: evidence of a misspent youth. J Neurosci.

[12] Hawkins JE, Schacht J. Sketches of otohistory. Part 10: noise-induced hearing loss. Audiol Neurootol.

Rodriguez GP, Yanke RB. Relationship between outer ear resonance and permanent noise-induced hearing loss. Am J Otolaryngol. 1994;15(1):37-40.

[15] Yamashita D, Jiang HY, Schacht J, Miller JM. Delayed production of free radicals following noise exposure. Brain

Harris KC, Hu BH. The role of oxidative stress in noise-induced hearing loss. Ear

(6 Pt 1):584-590.

2006;26(7):2115-2123.

2005;10(6):305-309.

[13] Pierson LL, Gerhardt KJ,

[14] Kurabi A, Keithley EM, Housley GD, Ryan AF, Wong AC. Cellular mechanisms of noise-induced hearing loss. Hear Res. 2017;349:129-137.

Res. 2004;1019(1-2):201-209.

Hear. 2006;27(1):1-19.

[16] Henderson D, Bielefeld EC,

[17] Nordmann AS, Bohne BA, Harding GW. Histopathological

2017;60(1):182-189.

[1] Kerns E, Masterson EA, Themann CL, Calvert GM. Cardiovascular conditions, hearing difficulty, and occupational noise exposure within US industries and occupations. Am J Ind Med.

[2] Nelson DI, Nelson RY, Concha-Barrientos M, Fingerhut M. The global burden of occupational noiseinduced hearing loss. Am J Ind Med.

[3] Carroll YI, Eichwald J, Scinicariello F, Hoffman HJ, Deitchman S, Radke MS, et al. Vital Signs: Noise-Induced Hearing Loss Among Adults - United States 2011-2012. MMWR Morb Mortal Wkly

2018;61(6):477-491.

**References**

2005;48(6):446-458.

Rep. 2017;66(5):139-144.

2019;62(10):826-837.

[6] Girard SA, Leroux T,

Prev. 2015;21(e1):e88–e92.

[4] Lawson SM, Masterson EA, Azman AS. Prevalence of hearing loss among noise-exposed workers within the Mining and Oil and Gas Extraction sectors, 2006-2015. Am J Ind Med.

[5] Livingston G, Sommerlad A, Orgeta V, Costafreda SG, Huntley J, Ames D, et al. Dementia prevention, intervention, and care. Lancet. 2017;390(10113):2673-2734.

Courteau M, Picard M, Turcotte F, Richer O. Occupational noise exposure and noise-induced hearing loss are associated with work-related injuries leading to admission to hospital. Inj

[7] Kramer SE, Kapteyn TS, Houtgast T. Occupational performance: comparing normally-hearing and hearing-impaired

employees using the Amsterdam Checklist for Hearing and Work. Int J

Audiol. 2006;45(9):503-512.

[8] Neitzel RL, Swinburn TK,

Hammer MS, Eisenberg D. Economic Impact of Hearing Loss and Reduction noise-induced hearing loss: a literature review of the underlying mechanism, pathophysiology, asymmetry, and management options. J Otolaryngol Head Neck Surg. 2017;46(1):41.

[36] Job A, Raynal M, Kossowski M, Studler M, Ghernaouti C, Baffioni-Venturi A, et al. Otoacoustic detection of risk of early hearing loss in ears with normal audiograms: a 3-year follow-up study. Hear Res. 2009;251(1-2):10-16.

[37] Seixas NS, Neitzel R, Stover B, Sheppard L, Feeney P, Mills D, et al. 10-Year prospective study of noise exposure and hearing damage among construction workers. Occup Environ Med. 2012;69(9):643-650.

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[40] Pirilä T. Left-right asymmetry in the human response to experimental noise exposure. I. Interaural correlation of the temporary threshold shift at 4 kHz frequency. Acta Otolaryngol. 1991;111(4):677-683.

[41] Chung DY, Willson GN, Gannon RP. Lateral differences in susceptibility to noise damage. Audiology. 1983;22(2):199-205.

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otoacoustic emissions. Hearing research. 1993;68(2):143-151.

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*Hearing Loss - From Multidisciplinary Teamwork to Public Health*

otoacoustic emissions. Hearing research.

Normal development and ear effect for contralateral acoustic reflex in children six to twelve years old. Dev Med Child

[45] Masterson L, Howard J, Liu ZW, Phillips J. Asymmetrical Hearing Loss in Cases of Industrial Noise Exposure: A Systematic Review of the Literature. Otol Neurotol. 2016;37(8):998-1005.

[46] Fernandes SV, Fernandes CM. Medicolegal significance of

Otol. 2010;124(10):1051-1055.

711-718.

[47] Shargorodsky J, Curhan GC, Farwell WR. Prevalence and

characteristics of tinnitus among US adults. Am J Med. 2010;123(8):

[48] Flores LS, Teixeira AR, Rosito LP, Seimetz BM, Dall'Igna C. Pitch and Loudness from Tinnitus in Individuals

with Noise-induced Hearing Loss. Int Arch Otorhinolaryngol.

[49] Yankaskas K. Prelude: noiseinduced tinnitus and hearing loss in the

military. Hear Res. 2013;295:3-8.

[50] Di Stadio A, Dipietro L, Ricci G, Della Volpe A, Minni A, Greco A, et al. Hearing Loss, Tinnitus, Hyperacusis, and Diplacusis in Professional Musicians: A Systematic Review. Int J Environ Res Public Health. 2018;15(10).

[51] Wang YP, Hsu WC, Young YH. Vestibular evoked myogenic potentials in acute acoustic trauma. Otology & neurotology: official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology.

2006;27(7):956-961.

2016;20(3):248-253.

asymmetrical hearing loss in cases of industrial noise exposure. J Laryngol

[44] Johnson DW, Sherman RE.

Neurol. 1979;21(5):572-581.

1993;68(2):143-151.

noise-induced hearing loss: a literature review of the underlying mechanism, pathophysiology, asymmetry, and management options. J Otolaryngol Head Neck Surg. 2017;46(1):41.

[36] Job A, Raynal M, Kossowski M,

Baffioni-Venturi A, et al. Otoacoustic detection of risk of early hearing loss in ears with normal audiograms: a 3-year follow-up study. Hear Res.

[37] Seixas NS, Neitzel R, Stover B, Sheppard L, Feeney P, Mills D, et al. 10-Year prospective study of noise exposure and hearing damage among construction workers. Occup Environ

Studler M, Ghernaouti C,

2009;251(1-2):10-16.

Med. 2012;69(9):643-650.

1995;109(4):291-295.

1991;111(4):677-683.

1983;22(2):199-205.

2008;5(3):210-215.

[38] Valero MD, Hancock KE,

Liberman MC. The middle ear muscle reflex in the diagnosis of cochlear neuropathy. Hear Res. 2016;332:29-38.

[39] Cox HJ, Ford GR. Hearing loss associated with weapons noise exposure: when to investigate an asymmetrical loss. J Laryngol Otol.

[40] Pirilä T. Left-right asymmetry in the human response to experimental noise exposure. I. Interaural correlation of the temporary threshold shift at 4 kHz frequency. Acta Otolaryngol.

[41] Chung DY, Willson GN, Gannon RP. Lateral differences in susceptibility to noise damage. Audiology.

[42] Hong O, Samo D, Hulea R, Eakin B. Perception and attitudes of firefighters on noise exposure and hearing loss. J Occup Environ Hyg.

[43] McFadden D. A speculation about the parallel ear asymmetries and sex differences in hearing sensitivity and

**28**