|Year : 2014 | Volume
| Issue : 1 | Page : 15-19
Evaluation of sound perception and its cardiovascular implications
Kenneth Akhabue Okojie1, Ahbor Dolly Awani Ighoroje2
1 Department of Physiology, University of Nigeria, Enugu State, Nigeria
2 University of Benin, Edo State, Nigeria
|Date of Web Publication||1-Jul-2014|
Kenneth Akhabue Okojie
Department of Physiology, University of Nigeria, Enugu State
Source of Support: None, Conflict of Interest: None
Background: Sound is a vibration from a particular machine, place or material which can be heard clearly whereas noise is mixed vibrations that will come to us from all directions. A sound can be clear and heard but noise will not be clear and cannot be heard. Noise is a known stress that affects various physiological responses of individual exposed to it and its pollution is increasingly being recognized as a physical factor in the environment that is injurious to many aspects of our health. Aim: To assess the effects of environmental noise on sound perception and cardiovascular system of those exposed to noise over a period of time. Materials and Methods: The study group included 50 subjects from a noisy environment (≥80 dB). This group was further divided into group Ia (those that have developed Noise Induced Hearing Impairment) and group Ib (those without Noise Induced Hearing Impairment). The control group consists of 50 subjects from a non-noisy environment (≤60 dB). An audio-visual scale which was marked between 0 and 10 cm and calibrated for differing sound levels was used as a tool for the determination of sound perception. Heart rate and blood pressure was measured using digital sphygmomanometer at rest and after exposure to noise at 60 dB, 90 dB, and 102 dB for 5 minutes each. All data were expressed as mean ± SEM. All the results were analyzed using one-way ANOVA. P ≤ 0.05 was considered as statistically significant. Results/Discussion: Noise exposure over a period of time produced a cardio-protective mechanism against arterial blood pressure in group Ia but produced a very significantly high arterial blood pressure in sub-group Ib and control subjects. There was also a very poor sound perception among those that have developed noise-induced hearing impairment unlike in sub-group Ib and control. Conclusion: Environmental noise is a possible contributing factor in the development of high arterial blood pressure and significantly affects individual's sound perception.
Keywords: Cardiovascular, noise, perception, sound
|How to cite this article:|
Okojie KA, Ighoroje AA. Evaluation of sound perception and its cardiovascular implications. Niger J Exp Clin Biosci 2014;2:15-9
| Introduction|| |
The term noise is commonly used to describe sounds that are disagreeable or unpleasant, produced by acoustic waves of random intensities and frequencies.  Noise is defined as unwanted sound and vibration or as an audible acoustic energy which adversely affects the physiology or psychological well-being of an individual.  Noise pollution is becoming increasingly more severe in industrialized countries and the cost of alleviating it in future is expected to be insurmountable.  Noise perception is the ability to perceive noise which varies greatly in individuals. Noise is typically characterized by the intensity, frequency and duration of sound. Sound is the result of pressure changes in air caused by vibration. Unwanted sound to some may be considered wanted to others as in the case of loud music.
Noise is a prominent feature of the environment including noise from transport, industry and neighbors. Community noise, neighborhood noise, domestic noise and workplace noise all constitute environmental noise. The dominant form of environmental noise in Nigeria is from transportation principally motor vehicles. Others are electro-acoustic noise from various sources like power generating sets, food processing machines, from live and recorded music, noise produced by aircraft, church, mosque and from domestic animals like dogs.
Hearing loss can be caused by a myriad of factors - exposure to occupational and/or environmental noise, ototoxic drugs and chemicals, physical trauma, infectious disease, developmental syndromes, and the aging process - all of which are further influenced by individual genetic susceptibility. Hearing loss is an "invisible" impairment. It often occurs gradually and insidiously over time. Because of this, hearing loss is frequently misinterpreted as inattentiveness, dementia, or simply "getting used to" sound. Often extensive and irreparable damage has been done to the auditory system before it is noticed. All of the current national estimates of the prevalence of hearing loss are based on self-report which can result in underestimation, particularly for mild and/or unilateral hearing losses. It is estimated that more than 30 million U.S. workers are exposed to potentially hazardous noise and an additional 9 million are exposed to ototoxic materials in their occupation.  Many more are similarly exposed through recreational or environmental sources.
Noise is implicated in various human illnesses and it is responsible for increased morbidity associated with modern life style. Immediate and serious attention must be given to the control of this mushrooming problem, since the overall loudness of environmental noise is rapidly increasing. Excessive noise pollution has been blamed not only for hearing impairment but also for hypertension, fatigue, heart trouble, disturbed serum lipid and reduced motor efficiency. 
Due to rapid industrialization, human beings are often time exposed to a wide variety of environmental noise from various sources. Adverse effects can be produced under several situations, by self exposing to the noisy environment. Environmental stress can be partially coped by using noise reduction devices, but effectiveness is still far away from producing a complete protection and devices are still problematic in various aspects. Consequently, limited effectiveness of speech communication and eventually hearing impairment or loss can be produced from environmental noise exposure. Therefore, the aim of this study was to assess noise exposure on sound perception and its possible effects on the cardiovascular system among market traders in Benin City.
| Research methodology|| |
A total of 50 subjects were recruited from the Evbareke Motor Spare Parts Market, New Benin Market, and University of Benin Generator House whose ambient noise level is ≥80 dB and between 17 and 60 years were selected using a cluster sampling technique. These study locations are all in Benin City, Edo State. Those selected would have spent a minimum of one year in that location and were in no way provided noise prevention aids. The subjects spend 7-10 hours daily and 6 days in a week in this location. A structural health and lifestyle questionnaire to elicit information from the subjects was utilized in this study and the information derived from the questionnaire formed the basis of selection of all subjects for either test or control groups. The exclusion criteria include: History of hypertension, head injury with unconsciousness, myocardial infarction, past ear trauma/infection, treatment with toxic drugs including streptomycin. The essence of these exclusion criteria was to minimize the influence of the many confounding factors in the development of hearing impairment.
A group of 50 consisting of staff of the University of Benin Teaching Hospital (UBTH) and students of the University of Benin (UNIBEN) served as the control group as the ambient noise level in these locations is ≤60 dB. All volunteers gave their informed consent.
Determination of Ambient Noise
The ambient noise was recorded by sound level meter (RDI-AR824 digital) in all the study locations. The sound level meter is a portable one which measures sound between 30 and 130 dB with resolution of 0.1 dB. Noise level was recorded after the sound level meter has been calibrated. The ambient noise level was determined at four different times of the day namely: 9 am, 12 noon, 3 pm, and 6 pm. The mean of these determinations was calculated. The aim of this determination is to ascertain if there is a peak period(s) for noise levels in these places.
Hearing Function Test
The pure tone audiometric values of all the subjects at different frequencies (rang 125-8000 Hz) was determined in collaboration with the technical staff of the Ear, Nose and Throat (ENT) sound laboratory in UBTH. A pure tone audiometry for both air conduction (AC) and bone conduction (BC) for both left and right ear was done in the clinic.
Determination of Sound Perception
An audio-visual scale which was marked between 0 and 10 and calibrated for differing sound levels was used as a tool for the determination of sound perception. The audio-visual scale was calibrated as follows: 0-3 (60 dB), 4-6 (90 dB), 7-10 (102 dB). Subjects were then randomly exposed to different sound levels and were told to indicate on the scale the point that corresponded with the loudness of the sound they were exposed to (0-10).
Measurement of Arterial Blood Pressure and Heart Rate
Blood pressure was measured in supine position by using digital sphygmomanometer. The systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate of all the subjects were recorded.
All data were expressed as mean ± SEM. All the results were analyzed using one-way ANOVA. P ≤ 0.05 was considered as statistically significant.
| Results|| |
All the subjects selected in this study were in the age range of 17-60 years. The experimental group Ia were those who were from a noisy environment of ambient noise level ≥80 dB and developed Noise-Induced Hearing Impairment (NIHI) while the experimental group Ib consist of subjects from environment with ambient noise level ≥80 dB but did not develop NIHI. [Table 1] shows the number of subjects in group Ia, group Ib, and control that use earphones
The SBP 5 minutes after arrival (at rest) in group Ia was significantly higher than that of group Ib and control (P ≤ 0.05). On subjects' exposure to noise at 60 dB, there was no remarkable difference from the SBP at rest of each of the groups. At 90dB, there was no remarkable increase in SBP of both groups Ia and Ib but there was a 17 mmHg increase in the control group when compared to SPB at rest. On further exposure to sound at 102dB, there was no significant increase in group Ia, but there was a significant increase of 20 mmHg and 37 mmHg in both group Ib and control when compared to their SBP at rest, respectively [Table 2].
The DBP 5 minutes after arrival (at rest) in group Ia was significantly higher than that of group Ib and control. On subjects' exposure to noise at 60dB, there was no remarkable effect on the DBP at rest of each of the groups. At 90 dB, there was a remarkable increase to 18 mmHg in DBP of control group but very minimal increase in groups Ia and Ib when compared to DBP at rest. On further exposure to noise at 102 dB, there was a significant increase in all groups. There was a 16 mmHg increase in group Ia, 11 mmHg in group Ib, and 29 mmHg in the control group when they were all compared to their DBP at rest respectively [Table 3].
HR at rest in all groups was the same. On subjects' exposure to sound at 60 dB, the differences were not significant from each other. At 90 dB, there was a remarkable increase in HR in both groups Ib and control and they were significantly higher than that of group Ia. On further exposure to sound at 102 dB, there was also a significant increase in all groups when compared to their HR at rest. The increase was as high as 8.7 bpm in group Ia, 19.5 bpm in group Ib, and 19 bpm in control when compared to HR at rest, respectively [Table 4].
Among the control group, 78% were able to perceive sound at 60 dB, 18% at 90dB, and 4% at 102 dB. This means that two (2) subjects in the control group that used earphones could not perceive sound at 60 and 90dB. In group Ia, none of the subjects could perceive noise at 60dB, 31.7% perceived sound at 90dB while 68.2% perceived sound at 102 dB. The subjects in this group Ia does not perceive sound within the normal range. So, they could only perceive sound from 90 dB and above which therefore shows that 100% of the subjects in this group have some degree of NIHI. In group Ib, 28.6% were able to perceive sound at 60 dB, 50% at 90dB and 21.4% at 102 dB. This result shows in this group Ib, 71.4% of the subjects have some very minor degree of NIHI though this was however not reflected in the hearing function test [Table 5].
| Discussion|| |
Noise pollution is increasingly being recognized as a physical factor in the environment that is injurious to many aspects of health.  Our result showed a significant increase in systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) in control and experimental groups Ia and Ib when exposed to sound. However, there was no significant increase in experimental group Ia SBP at rest when compared to 102 dB. This is in agreement with the work of many researchers that has shown that noise significantly increases blood pressure. ,,
Some studies observed a rise only in systolic BP , while we found a significant increase in both systolic and diastolic BP in response to sound. Babisch et al.  did not see any association between noise and blood pressure, whereas Elise et al.  observed an insignificant increase in blood pressure.
The possible mechanism for increase in blood pressure is not yet fully understood but the following mechanism could contribute: The catecholamines released from adrenal medulla as a result of activation of adrenergic system, the effect of suprarenal glands steroids, angiotensin and also the direct effect of noise on arterial wall tension influence the blood pressure and heart rate.  Stimulation by noise, through sympathetic nervous system, causes an elevation of blood pressure by an increase in total peripheral resistance and myocardial contractility.  Thus, repeated stimulation with noise could then accelerate the development of structural vascular changes in the peripheral resistant vessels and by this mechanism possibly create a permanent blood pressure elevation to hypertensive levels. 
Noise undoubtedly induces vasoconstriction of peripheral arteries. Exposure to noise over a period of time prevents individuals from the subsequent development of hypertension from noise as a stressor. The possible mechanism through which this is brought about could be due to unresponsiveness of the ear to low decibel of noise because when the sound level was increased to 102 dB there was an observable effect on the blood pressure. However, those with no previous exposure to noise had elevated blood pressure to hypertensive levels on exposure to sound at low decibel. This implies that, noise as a stressor in the development of hypertension acts through the auditory pathway.
Hearing loss due to noise exposure in an environment is extensively presented in the current literature. Many authors correlate noise, loss in auditory function perception and exposure to noise in relation to the environment. , Mechanism of ear impairment involved is repeated barotraumas which affect the middle ear leading to low frequencies impairment. Noise-induced hearing loss (NIHL) accrues progressively and often unnoticed until it has reached a certain degree. The main site of impairment is the outer hair cells of the cochlea, where the damage is irreversible.  Since NIHL is irreversible, the main form of treatment is prevention. Central transmission is not affected in those who have been exposed to environmental noise for several years though, there is a significant association between noise exposure and prevalence of NIHL, which is as a result of damage to peripheral cochlear organ.
Sound perception was very poor among groups Ia and Ib, with group Ia having worst results [Table 5]. This could be due to the fact that noise has already damaged their hair cells, so are unable to perceive noise of low decibel. However, 4% among the control group who persistently used plug-in earpiece could not perceive sound at low decibel except when the sound was increased to 102 dB. Though there were no audiometric finds indicating damage to their ear among these subjects in the control group, this was however shown in sound perception evaluation tool.
| Conclusion/Recommendations|| |
These results show that environmental noise causes disturbance of cardiovascular system of the exposed persons and the auditory system. So, effective actions should be taken to prevent or minimize the effects of environmental noise. Efforts should be made to control the noise at the source, control the transmission of noise and protect the exposed persons. There should be permanent arrangements for regular measurements of noise levels at different locations in cities and health education regarding noise control should be given serious attention.
| References|| |
|1.||Akhtar HN. Noise-induced hearing loss in traffic police constables. J Coll Physician 1996;6:265-8. |
|2.||Kryter KD. The effects of noise on man. New York: Academic Press; 1985. p. 389-93. |
|3.||Sangeeta S, Berendra Y, Hashmi SF, Muzammil M. Effects of workplace noise on blood pressure and heart rate. Biomed Res 2009;20:122-6. |
|4.||World Health Organization. Prevention of noise-induced hearing loss: Report of an informal consultation held at Geneva, 28-30 th Oct, 1997. |
|5.||Regecova V, Kellerova E. Effects of urban noise pollution on blood pressure and heart rate in preschool children. J Hypertens 1995;13:405-12. |
|6.||Mahmood R, Khan GJ, Alam S, Safi AJ, Salahuddin, Amin-ul-Haq. Effect of 90dB noise of 4000 Hertz on blood pressure in young adults. J Ayub Med Coll Abbottabad 2004;16:30-3. |
|7.||Mollar AR. Noise as a health hazard. In: Maxy Rossenau Public health and preventive medicine. 11 th ed. New York: Appleton Century Crofts; 1980. p. 790-9. |
|8.||Herbold M, Hense HW, Keil U. Effects of road traffic noise on prevalence of hypertension in men. Soz Praventivmed 1989;34:19-23. |
|9.||Evans GW, Lerchar P, Meis M, Ising H, Kofler WW. Community noise exposure and stress in children. J Acoust Soc Am 2001;109:1023-7. |
|10.||Germano G, Damiani S, Milito U, Giarrizzo C, San-tucci A. Noise stimulus in normal subjects: Time dependent blood pressure pattern assessment. Clin Cardiol 1991;14:321-5. |
|11.||Babisch W, Ising H, Gallacher JE, Sharp DS, Baker IA. Traffic noise and cardiovascular risk, first phase. Arch Environ Health 1993;48:401-5. |
|12.||van Kempen EE, Kruize H, Boshuizen HC, Ameling CB, Staatsen BA, de Hollander AE. The association between noise exposure and blood pressure and ischemic heart disease. Environ Health Prospect 2002;110:307-17. |
|13.||Andren L, Hanson L, Bjorkman M, Jonsson A. Noise as a contributing factor in the development of elevated arterial pressure. Acta Med Scand 1980;207:493-8. |
|14.||Andren L. Cardiovascular effects of noise. Acta Med Scand 1983;5(Suppl 657):1-45. |
|15.||Smookler HH, Goebel KH, Siegel MI, Clarke DE. Hypertensive effects of prolonged auditory, visual and motion stimulation. Fed Proc 1973;32:2105-10. |
|16.||Ibhazehiebo K, Ighoroje AD, Uche OK, Ogisi FO, Iyawe VI. Impact of noise on hearing amongst commercial motor bike riders in Benin City, Nigeria. J Biomed Sci 2008;7:30-6. |
|17.||Ighoroje AD, Marchie C, Nwobodo ED. Noise-induced as an occupational risk factor among Nigerian traders. Niger J Physiol Sci 2004;19:14-9. |
|18.||Bamiou D, Lutman ME. Interaction of NIHL and ageing: Epidemiological aspects. In: Luxon L, Prasher D, editors. Noise and its effects. Chichester, England: John Wiley; 2007. p. 64-84. |
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]