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|Year : 2010
: 12 | Issue : 48 | Page
|Effect of noise stress on autonomic function tests
Seema Goyal1, Vidushi Gupta2, Lily Walia2
1 Department of Physiology, Christian Medical College and Hospital, Ludhiana, India
2 Dayanand Medical College and Hospital, Ludhiana, India
Click here for correspondence address
|Date of Web Publication||30-Jun-2010|
The study was carried out in 200 male volunteers. They were divided into two groups. The study group was exposed to noise levels of more than 80 dB(A) for more than 8 hours a day for a period of 6 months, working in the steel and hammer industry, whereas the control group was working under normal conditions. The mean age of subjects was 33.33 + 0.867 years and the mean noise level to which they were exposed was 90.34 + 0.781 dB(A). Various autonomic function tests were carried out in both the groups and results were analyzed using Z test. Heart rate was recorded on cardiofax ECG machine and blood pressure (BP) was recorded using sphygmomanometer. The tests depicted significant increase in the mean resting heart rate and the heart rate response to standing (P=0.000), 30:15 ratio (P=0.002), the valsalva ratio (P=0.017), the % change in diastolic BP response to standing (P=0.000) and valsalva maneuver (P=0.000), the systolic BP and diastolic BP after cold pressor test (P=0.000) in study group as compared to the control group. The significant higher results in study group may be attributed to increased sympathetic activity. Thus, noise presents as a significant health hazard. It is recommended that maximum allowable duration of exposure should be reviewed and strictly followed.
Keywords: Autonomic functions, noise, sympathetic activity
|How to cite this article:|
Goyal S, Gupta V, Walia L. Effect of noise stress on autonomic function tests. Noise Health 2010;12:182-6
| Introduction|| |
Stress is an adaptive response, mediated by individual characteristics or psychological processes, i.e. a consequence of any external action, situation or event that places special physical and or psychological demands on a person.  In 1936, Seyle formulated a definition of stress as the non-specific result of any demands upon the body, be it a mental or somatic demand for survival or the accomplishment of our aims.
The three systems which are directly involved in the physiology of stress are nervous system, endocrine system and the immune system. The peripheral part of nervous system that is the autonomic system acts in co-ordination with the central part to maintain the homeostatic balance. It does so through its two branches: sympathetic and the parasympathetic which are activated by the hypothalamus. The sympathetic system is responsible for fight or flight response. Stressors can be in the form of infections, noise,  decreased oxygen supply, pain, under nutrition, heat, cold, trauma, prolonged exertion, anxiety, depression, anger, fear, radiation, obesity, old age, drugs and disease.
Noise is one of the most commonly encountered stressors in today's environment. Noise is defined as any audible acoustic energy that adversely affects the physiological or psychological well being of the people. 
In addition to its effect on hearing,  speech,  communication and architecture of sleep,  noise causes neuro-endocrine dysregulation.  There are neural connections between human auditory system and neural muscular glandular systems of the body. It is through these connections that sound causes autonomic responses with or without any conscious process.
Exposure to familiar noise such as occupational noise, but with levels above 90dB, causes release of nor-epinephrine, unfamiliar noise exposure causes release of adrenaline or epinephrine, whereas exposure to high intensity noise of level up to 120 dB causes increased release of cortisol. 
Noise presents as a significant cardiovascular risk factor causing increase in the total peripheral resistance and increase in the myocardial contractility and thus raising BP.  Thus, it is evident that noise causes changes in the autonomic cardiac and vascular regulation. There is a dearth of literature depicting the relationship between noise exposure and autonomic functions. Hence, this study was designed to evaluate effects of noise stress on the autonomic function tests.
| Materials and Methods|| |
The study was conducted in 200 male volunteers. They were divided into two groups: control group consisted of 100 healthy subjects of mean age group 34.89 th + 1.006 years working in an environment with noise levels <80 dB and study group consisted of 100 subjects of mean age group 33.33 th + 0.867 years working or living in noise levels >80 dB for more than 8 hours per day for a minimum period of 6 months in the steel and hammer industry. The tests were performed in the Department of Physiology at DMC and H.
Written informed consent was taken from all the volunteers before the test. Noise levels were measured with the help of hand held digital sound level meter (model 8928), ranging between 40-130 dB. With most sound level meters, the readings can be taken on either slow or fast response. The response rate is the time period over which the instrument averages the sound level before displaying it on the readout.
So, out of the given slow and fast responses, the slow response was taken which was displayed on the LCD screen. The instrument was used at the maximum holding and a single recording was taken. The A weighted filter was used. 
The assessment of autonomic functions was made by various noninvasive tests. Detailed history was taken from all the subjects to exclude any systemic or related diseases.
The subjects were subjected to a set of tests to evaluate autonomic functions. These tests were:
The heart rate in all these tests was calculated from R-R interval, using the formula of 1500/ R-R interval in millimeters R-R interval was obtained from continuous recording of ECG in lead II on cardio-fax machine. BP recording was done using standard sphygmomanometer. Before every test, the heart rate was allowed to come down to normal resting level.
- 30:15 ratio (heart rate response to immediate standing)
- Standing /lying ratio(heart rate response to lying down)
- Expiration / inspiration ratio
- Valsalva ratio
- B.P. response to standing
- B.P. response to valsalva maneuver
- B.P. response to cold pressor test
This test is based on the fact that on a change in posture from lying to standing position there occurs a transient fall in BP followed by baroreceptor response and consequent reflex tachycardia and peripheral vasoconstriction which is maximal at 15 th beat after standing. A relative overshoot bradycardia then occurs maximal at about 30 th beat.  It is a measure of the cardiac parasympathetic function.  For the test, the subject was made to lie on a couch quietly and ECG was recorded in lead II continuously on electrocardiogram for 30 seconds. The subject was then asked to stand up unaided within 3-4 seconds and remain motionless thereafter. The point when the patient started standing was marked on ECG. The ECG was recorded for 1minute from standing.
The R-R intervals were measured on ECG with a ruler. The 30:15 ratio was calculated by taking the ratio of longest R-R interval at beat 30 and shortest R-R interval at beat 15 after standing. A 30:15 ratio of 1.00 was taken as normal and value of <1.00 was considered abnormal. 
30:15 ratio = R-R interval at beta 30/R-R interval at beat 15
Normally, when a subject lies down from standing position, there is a brief initial rise followed by fall in heart rate. The initial brief rise is due to rapid decrease of vagal tone and latter fall is because of increase in vagal tone.  The heart rate response to lying down has been used as a simple test to assess cardiac parasympathetic activity. 
For the test, subject was made to stand quietly and then lie down without any support while a continuous ECG was recorded from 20 beats before to 60 beats after lying down. The point at which the subject started to lie down was marked. Recording of the R-R interval was made and the ratio was calculated as ratio of the longest R-R interval during 5 beats before lying down to shortest R-R interval during 10 beats after lying down.  Any abnormally low standing/lying ratio reflects parasympathetic damage. An S/L ratio of >1 was taken as normal. An standing/lying ratio of <1 was taken as abnormal. 
S/L ratio = longest R-R interval before lying down/shortest R-R interval during 10 beats after lying down
Expiration /inspiration ratio
This test is done to check the vagal supply of the respiratory system as well as the heart as there is complex interplay of reflexes that are involved in the heart rate variability with change in the pattern of respiration. Stretch receptors in chest probably serve as principal afferent for this reflex. The efferent pathway regulating beat-to-beat variation is vagal nerve. Loss of beat-to-beat variation in autonomic neuropathy is a result of vagal denervation of the heart, whereas sympathetic inhibition by administration of propranolol to normal subjects has no effect on beat-to-beat variation. 
During a period of deep breathing there is characteristic heart rate variability seen as an increase in heart rate with inspiration due to inhibition of cardiac vagal motor discharge. A decreased ratio reveals autonomic nervous dysfunction. 
For the test the subject was asked to breathe deeply at rate of six breaths per minute. A standard ECG recording was taken during deep inspiration and expiration. Variation in heart rate was calculated as the rate of longest R-R interval during expiration to shortest R-R interval during inspiration. A value of 1.20 or higher was taken as normal. 
Expiration/inspiration ratio =
longest R-R interval during expiration/shortest R-R interval during inspiration
The valsalva maneuver is a test to assess reflex process which is initiated in baroreceptors present in aortic arch and carotid sinus, the afferents travel via glossopharyngeal nerves and vagus nerves and the efferents come down through vagus. Thus, the ratio is a functional assessment of both the parasympathetic as well as the sympathetic divisions. 
For the test, the subject was made to perform valsalva maneuver for 15 seconds by blowing against closed glottis through a mouth piece attached to a manometer and maintained an expiratory pressure of 40 mm of Hg for 15 seconds. ECG was recorded during the maneuver (strain period, 15 seconds) and for 15 seconds after release of pressure. The ratio was calculated as the ratio of longest R-R interval after maneuver to shortest R-R interval during maneuver. Value >1.21 was taken as normal and value < 1.21 was considered abnormal. 
Valsalva ratio =
Longest R - R interval after manoeuvre/Shortest R - R interval during manoeuvre
Blood pressure response to standing
This is a test to check for the sympathetic nerve fiber activity. In healthy subjects, there is an immediate pooling of blood in the dependant parts resulting in fall in BP. Fall in BP in upright posture leads to tachycardia and hence an increase in cardiac output and peripheral vasoconstriction resulting in increase in BP via baroreflex mechanism.  The postural fall in BP is taken as the difference between systolic BP in lying position and then after standing.
For assessing the response, the subject was asked to stand from supine position within 3-4 seconds and to remain motionless. BP was recorded in 30-second interval. Difference between readings of systolic BP recorded in lying position and then after standing was calculated. Normal response was taken as <10mmHg fall in BP. A fall in BP >20-30mm Hg of systolic  and >20 mm Hg diastolic  is taken as abnormal.
Blood pressure response to valsalva maneuver
During valsalva maneuver, there are changes in the BP response. The increase in the BP in phase-1 is the result of increased intrathoracic pressure at the onset of straining, whereas the rapidly decreasing BP during phase-2 is caused by reduced venous return producing a fall in the cardiac output. In phase-3 release of intrathoracic pressure and consequent rise in preliminary venous capacitance produces momentary fall in cardiac output and a further decrease in BP. This is followed by rebound hypertension which is caused by increase in cardiac output occurring at a point where systemic vascular resistance is still raised in response to baroreflex produced by fall in BP during phase-2. When circulatory reflexes are damaged, as in autonomic neuropathy, there is a steady fall in BP during straining and slow return to normal BP after release and no change in heart rate during or after strain. 
The BP readings were taken at resting state for both systolic and diastolic BP and then after valsalva maneuver. The difference between the two readings was calculated and compared with that of the control group.
Cold pressor test
This test is done to assess the function of the sympathetic system.There is activation of sympathetic nervous system under the conditions of stress of either physiological or psychological origin. Cold pressor test consists of placing hand into cold water which acts as painful stimulus and is used to study autonomic responses to this stress in different individuals. The afferent fibers for this response are pain fibers (which are stimulated by placing hand in cold water) and efferent fibers are sympathetic fibers. Arterial pressure rises during first and second minute cold pressor test. 
For this test, subject's resting BP was recorded. The subject was then asked to immerse his dominant hand in cold water and temperature was maintained at 4-6°C throughout the procedure. BP was measured from other non-dominant arm at pain threshold time, which is defined as the time between immersion of hand and subjective feeling of pain. Then, the subject was allowed to remove his hand. Maximum increase in systolic and diastolic pressures was noted and then their difference was calculated.
Any condition where there is deficient sympathetic out-flow, a smaller rise in BP is expected. A rise of diastolic BP >15 mmHg was taken as normal and less than this was considered as abnormal.  Failure of systolic blood to rise by 16-20 mmHg and diastolic BP to rise by 12-15 mmHg was an indication of autonomic neuropathy. 
The results of autonomic tests were then compared with the control group Z test using the program SPSS 16.0.
| Results|| |
The volunteers in the study and control groups were comparable for age. Mean age of control group was 34.89+ 1.006 years and that of study group was 33.33th + 0.867 years. Control group was exposed to noise levels of 43 dB and study group to 90 dB [Table 1]. In this study, the mean resting heart rate was significantly more in study group as compared to control group [Table 2]. The 30:15 ratio, the valsalva ratio in study group was significantly higher as compared to control group. The standing/lying ratio in the study group was non-significantly lower than that of the control group. The expiration/inspiration ratio was the same for study group and control group. Mean percentage change in systolic BP from lying to standing posture was higher for study than that for control group but this increase was not significant, whereas the mean percentage change in the diastolic BP was significantly higher for study than that for control group.
The results of the valsalva test show that the mean percentage change in the diastolic BP was significantly higher for study group as compared to that of the control group [Table 2], whereas the mean percentage change in systolic BP was not significantly increased in the study group.
The mean percentage change in the systolic BP after CPT was significantly higher for study group as compared to control group. The mean percentage change in the diastolic BP was also significantly higher for study group as compared to that of the control group.
| Discussion|| |
The study results showed that noise, being one of the commonest hazards of the modern world, has an influence on the normal functioning of the cardiovascular, endocrinal, metabolic, gastrointestinal and neurological systems.
Noise as a stressor leads to increased release of the stress hormones including epinephrine, nor-epinephrine and corticosteroids.  These hormones have an effect on the functioning of the autonomic nervous system. The higher baseline heart rate recorded in the study group is due to noise induced sympathetic response which leads to increased release of nor-epinephrine. The significant increase in 30:15 ratio in the study group is attributed to vasoconstriction produced due to increased sympathetic activity which reduces the action of the baroreceptors and leads to stimulation of the vasomotor center causing tachycardia. 
The standing/lying ratio and the expiration/inspiration ratio both evaluate the parasympathetic division of the autonomic system and both these tests were non-significant in this study as the vagal tone is already decreased due to noise stress in the study group. So the relative change in the heart rate is same as that of the control group.
The valsalva ratio was significantly (P=0.000) more for the study group than that for the controls as it is established that during the phase of strain (phase 2 of maneuver), there is increased sympathetic discharge. In the study group, there is further sympathetic stimulation due to noise stress,  which leads to decrease in R-R interval (increase in heart rate) for the study group.
The significant (P=0.000) increase in diastolic BP on standing from supine position in study group as compared to that of the control may be attributed to the greater vascular response opposed to the cardiac response to standing induced sympathetic stimulation.  Similar results have been reported by other researchers  in noise-exposed individuals.
In the case of valsalva, the mean percentage change in diastolic BP was significantly higher for study group as compared to that of the control group (P=0.000). This may be due to development of vascular changes leading to changes in peripheral resistance. 
Also the mean percentage change in systolic BP was non-significantly higher (P=0.159) for the study group when compared with that of the control group. This can be due to the decreased baroreceptor's sensitivity index with increased circulating levels of nor ephinephrine. 
Cold pressor test assesses both sympathetic functions and somatic sensation of pain. It is used to study sympathetic autonomic response.  In the present study, the % change for SBP and DBP from resting to after CPT was significantly (P=0.000) increased in the study group as compared to that of the control group. This is because in addition to pain-induced sympathetic stimulation, there is an increased circulating level of nor-epinephrine in response to noise induced stress in study group. 
| Conclusions|| |
Thus, the results show that industrial noise causes increased sympathetic activity in noise-exposed workers, which may affect the cardiovascular system (CVS) by disturbing the autonomic nervous system regulation. So, efforts should be made to control the noise at the source. To control the transmission of noise and to protect the exposed persons, there should be permanent arrangements for regular measurements of noise levels at different locations in cities and factories, and education on noise control should be given importance.
| References|| |
|1.||Ellis BJ, Jackson JJ, Boyce WT. The stress response systems: Universality and adaptive individual differences. Dev Rev 2006;26:175-212. |
|2.||Sembulingum K, Sembuligam P, Namasivayam A. Effect of acute noise stress on acetyl-cholinesterase activity in discrete areas of rat brain. Indian J Med Sci 2003;59:487-92. |
|3.||Kryter KD, Poza F. Effects of noise on some autonomic system activities. J Acoust Soc Am 1980;67:2036-44. [PUBMED] [FULLTEXT] |
|4.||Berglund B, Harder K, Pries A. Annoyance perception of sound and information extraction. J Acoust Soc Am 1994;95:1501-9. |
|5.||Lazarus H. New methods for describing and assessing direct speech Communication under disturbing conditions. Environ Int 1990;16:373-92. |
|6.||Gitanjali B, Ananth R. Effect of acute exposure to loud occupational noise during day time on the nocturnal sleep architecture, heart rate and Cortisol secretion in healthy volunteers. J Occup Health 2003;45:146-52. [PUBMED] [FULLTEXT] |
|7.||Spreng M. Possible health effects of noise induced cortisol increase. Noise Health 2000;2:59-64. [PUBMED] |
|8.||Stephen SA, Matheson MP. Noise pollution: Non-auditory effects on health. Br Med Bull 2003;68:243-57. |
|9.||Ising H, Braun C. Acute and chronic endocrine effects of noise: Review of the research conducted at the Institute for water, soil and air hygiene. Noise Health 2000;2:7-24. [PUBMED] |
|10.||Kisku GC, Bhargava SK. Noise level of a medium scale thermal power plant. Indian J Occup Environ Med 2006;3:133-40. |
|11.||Ewing DJ, Clark BF. Diagnosis and management of diabetic autonomic neuropathy. Br Med J 1982;285:916-8. |
|12.||Ewing DJ, Campell IW, Murray A, Neilson JM, Clarkes BF. Immediate heart rate response to standing: Simple test for autonomic neuropathy in diabetes. Br Med J 1978;1:145-7. |
|13.||Jain AK. Manual of Practical physiology for MBBS. 1st ed. New Delhi: Arya Publications; 2003. p. 248-52. |
|14.||Bellavere F, Cardone C, Ferri M, Guarini L, Piccoli A, Fedele D. Standing to lying heart rate variation: A new simple test in the diagnosis of diabetic autonomic neuropathy. Diabet Med 1987;4:41-3. [PUBMED] |
|15.||Ewing DJ, Martyn CN, Young RJ, Clarke BF. The value of cardiovascular autonomic function tests: 10 year experience in diabetes. Diabetes Care 1985;8:491-8. [PUBMED] |
|16.||Ahuja VM, Kumar R. Basal autonomic functions in males and females. Indian J Physiol Pharmacol 1999;43:521-2. [PUBMED] |
|17.||Maiorano G, Di Bello V, Loiacono N, Altomare E. "Beat to beat" variation in diabetic patients. Boll Soc Ital Biol Sper 1981;57:266-71. [PUBMED] |
|18.||Sundkvist G. Autonomic nervous function in asymptomatic diabetic patients with signs of peripheral neuropathy. Diabetes Care 1981;9:529-34. |
|19.||Singhal S, Yadav B, Hashmi SF, Md. Muzammil. Effects of workplace noise on blood pressure and heart rate. Biomed Res 2009;20:122-6. |
|20.||Neumann C, Schmid H. Standardization of a computerized method for calculating autonomic function test responses in healthy subjects and patients with diabetes mellitus. Braz J Med Biol Res 1997;30:197-205. [PUBMED] |
|21.||Roy F. Diabetes autonomic neuropathy: Clinical testing of autonomic functions. Diabetes Care 2003;26:1553-79:1-5. Available from: http://www.highbeam.com/libraray/docfree.asp [last cited on 2003]. |
|22.||Wenner MM, Prettyman AV, Master RE, Fraquar WB. Preserved autonomic functions in amenorrheic athletes. J Appl Physiol 2006;101:590-7. |
|23.||Consensus statement on the definition of orthostatic hypotension, pure autonomic failure and multiple system atrophy: The Consensus Committee of the American Autonomic Society and the American Academy of Neurology. Neurology 1996;46:1470. |
|24.||Naronha JL, Bhandarkar SD, Shenoy PN, Retnam VJ. Autonomic neuropathy in diabetes mellitus. J Postgrad Med 1981;27:1-6. |
|25.||Victor RG, Leimback WN Jr. Seals DR, Waillin BG, Mark AL. Effects of the cold pressor test on muscle sympathetic nerve activitiy in humans. Hypertension 1987;9:429-36. |
|26.||Babisch W. Stress hormones in the research on cardiovascular effects of noise. Noise Health 2003;5:1-11. [PUBMED] |
|27.||Davos CH, Davies LC, Piepoli M. The effect of baroreceptor activity on cardiovascular regulation. Hellenic J Cardiol 2002;43:145-55. |
|28.||Lucini D, Norbiato G, Clerici M, Pagani M. Hemodynamic and autonomic adjustments to real life stress conditions in humans. Hypertension 2002;39:184-8. [PUBMED] [FULLTEXT] |
|29.||Mahmood R, Khan GJ, Alam S, Safi AJ, Salaudiin, Amin-Ul-Haq. Effect of 90 decibel noise of 4000 hertz on blood pressure in young adults. J Ayub Med Coll Abbottabad 2004;16:64-9. |
|30.||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. |
|31.||Wirch JL, Wolfe LA, Weiss-gerber T, Davin GA. Cold pressor test protocol to evaluate cardiac autonomic function. Appl Physiol Nutr Metab 2006;31:235-43. |
Department of Physiology, Christian Medical College and Hospital, Ludhiana
Source of Support: None, Conflict of Interest: None
[Table 1], [Table 2]
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