@2024 Afarand., IRAN

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ISSN: 2252-0805    The Horizon of Medical Sciences 2016;22(2):117-123

Background
… [1-11] Several studies have confirmed the role of sound pollution and vibration as a risk factor for cardiovascular diseases [12, 13].
Previous Studies
Sound pollution can cause confusion, increase in heart rate, increase in blood pressure, damages of myocardia and heart valves, and risk factors which increase cardiovascular diseases such as viscosity, lipid and blood sugar [14-17]. … [18-25]
Aim(s)
The aim of this study was to investigate the effects of short-term and long-term exposure to the sound pollution on some cardiac electrophysiological and biochemical parameters in the Wistar rats.
Research type
This is an experimental study.
Research society, place and time
Wistar male rats (200 to 250 gr) were studied.
Sampling method and number
60 rats were studied.
Used devices&materials
After one week that rats became accustomed to the new situation, they randomly divided into the experimental groups in one of which the rats had short-term exposure (one day exposure) to sound pollution and in the other one the rats had long-term exposure to the sound pollution (abbreviated as short-term group and long-term group). Short-term groups included four different groups i.e. a control group and three experimental group of 4, 8 and 12 hours of exposure to sound (each group consisted of 5 mice). And for investigating the short-term exposure to sound pollution the rats in these groups once entered the sound room and were exposed to 100 dB sound intensity. Control group animals were kept in the animal room and were not exposed to the sound. The rats in control group entered the sound room (without exposure to the sound) every day for 8 hours to experience the condition of sound room. Long-term groups were, also, included four different groups namely a control group and three experimental groups of 4, 8 and 12 hours exposure to sound (each group included 10 rats). These animals were transferred to the sound room every day for 4, 8 and 12 hours and were exposed to 100 dB sound intensity. Animals in the control group were in the animal room during a 30-day trial, and were not exposed to the sound. The sound pollution in form of white noise with the intensity of 100 dB and the frequency of 250-350 Hz was created by a Dictaphone stereo (Sony; Japan). To control the intensity and frequency of sound, an audiometer machine (PCE instruments; England) was used. The start and end time of exposure was controlled by a timer. Heart`s electrical activity was recorded using electrocardiography (Nexus Lifecare; India) and subcutaneous electrodes which were designed to record ECG in rats. Time parameters included RR interval, PQ interval, QT interval, QTC corrected interval (using Bazett`s formula: QT Interval/√ (RR interval)), PR segment, QRS complex; and voltage parameters including P wave height, QRS complex height, and the T wave height. Finally, the number of heart beats per minute was calculated from the RR interval on ECG. In long-term group, after recording the electrocardiogram, the mice were dissected and a drop of blood from their dorsal aorta was used for measuring creatine phosphokinase (isoenzyme MB) and troponin. The level of creatine phosphokinase and cardiac troponin 1 enzymes was determined qualitatively by rapid one-step immunochromatographic kits (ALUXBIO Co., LTD; China). The collected data were analyzed by SPSS 21 software (IBM; Chicago; USA) applying statistical methods including one-way ANOVA and Tukey`s post-hoc test considering the significance level of 0.05 for investigating between-group differences.
Findings by Text
Short-term exposure to sound pollution had only significant effect on the time interval between two R waves (RR-interval) (p<0.05). That is to say, the RR interval had a significant decrease in a group which was exposed to sound pollution four hours compared to control group (p=0.021). However, there was no significant difference between groups exposed to 8 and 12 hours of sound pollution on one hand and control group on the other hand (Table 1). Short-term exposure to sound pollution had no significant effect on ECG voltage parameters (results have not been shown). Long-term exposure to sound pollution had significant effect on RR, QT and QTc intervals (p<0.05) i.e. the QT, RR and QTc intervals in the group which exposed to 12 hours of pollution (p=0.023, p=0.045 and p=0.041, respectively) and the group which exposed to eight hours of sound pollution (p=0.032, p= 0.046 and p=0.044, respectively) were significantly less than control group. However, in the group exposed to 4 hours of sound pollution, the parameters did not have any significant difference with control group. Long-term exposure to sound pollution did not have any significant effect in different groups in PR interval, QRS and PR segment (p>0.05; Table 1). Long-term exposure to the sound pollution had only significant effect on the QRS complex voltage (p<0.05) and QRS complex voltage in two experimental groups exposed to 12 hours (p= 0.02) and 8 hours (p=0.031) of sound pollution increased significantly compared to control group. However, no significant difference was observed in the group exposed to four hours of sound pollution compared to control group. Long-term exposure to sound pollution did not have any significant effect on P and T wave voltages in the different groups (p>0.05; Table 2). Short-term exposure to sound pollution had significant effect on the heart rate (p<0.05) and heart rate in the group which is exposed to four hours of exposure to sound pollution was significantly increased compared to control group (p = 0.028) while no significant difference was observed between the groups exposed to 8 and 12 hours of sound pollution and control group (Diagram 1). Long-term exposure to sound pollution, also, had significant effect on the heart rate (p<0.05) and the heart rate in the groups exposed to eight (p = 0.031) and 12 hours (p = 0.013) of sound pollution was significantly increased compared to control group while in the group which was exposed to sound pollution four hours no significant difference was observed compared to control group (p>0.05; Diagram 1). The results of the test for determining the effect of long-term exposure to sound pollution on the level of creatine phosphokinase (CPK) and cardiac troponin I (Tn I) were negative in all groups.
Main comparison to the similar studies
Short and long term exposures to sound pollution with the intensity of 100 dB changed some of the time parameters of ECG in male Wistar rats. And short-term four-hour exposure to the sound pollution reduced the interval of RR wave. However, long-term exposure to pollution (8 and 12 hours) significantly reduced QT and QTc waves, as well as a significant decrease in RR intervals. Long-term exposure to sound pollution, also, significantly increased QRS complex voltage. And this change was not seen in short-term exposure. Moreover, short and long term exposures to sound pollution significantly increased heart rate in the rats, while in the short-term exposure only four-hour exposure caused an increase in heart rate and in the daily long-term exposure, 8 and 12 hours exposure to sound pollution increased the heart rate. Sound pollution as an environmental stressor to activate the hormonal axis of hypothalamus-pituitary-adrenal cortex and the nervous axis of hypothalamus- sympathetic nervous system-the center of adrenal gland increases the level of cortisol, vasopressin and catecholamine including epinephrine and norepinephrine in the blood and creates a series of hemodynamic, structural and functional changes in the cardiovascular system [7, 14, 26, 27]. An increase in QRS complex voltage which was observed in this study, mechanically could mean more severe contraction of the ventricles or an increase in the cardinal muscle mass called hypertrophy [28]. … [29] The result of immunochromotographic tests for creatine phosphokinase and troponin I was negative in all groups indicating lack of severe damage in cardiac muscle. Many studies have shown that the sounds over 130 dB can cause serious damages to myocardial cells and even cause the heart attack [30, 31].
Suggestions
In a human study, the effect of different sound pollution which people are faced with at their work or life on the function of cardiovascular system should be examined.
Limitations
Of the limitations of this study, the difficulty in determining the specific and standard definition of sound pollution can be mentioned.
Conclusions
Short-term exposure to 100dB sound pollution can reduce RR wave interval in the Wistar rats. However, long-term exposure to the sound pollution, in addition to a reduction in RR wave interval, significantly reduces QT and QTc waves and significantly increases QRS complex voltage. In addition, short-term and long-term exposures to sound pollution can significantly increase the heart rate in rats. In general, continuous exposure to sound pollution can increase heart rate and cardiac function through changing the hemodynamic condition.
Acknowledgments
Deputy of Research and Technology of Sabzevar Univeristy of Medical Sciences is appreciated.
Conflict of interest
Non-declared
Ethical Permissions
All tests were in accordance with the instruction in the care and use of laboratory animals (National Institute of Health, Publication No. 23-80, revised 1996). In addition, all the methods were approved by Ethics Committee of Sabzevar University of Medical Sciences.
Funding Sources
This project has been sponsored by Deputy of Research and Technology of Sabzevar University of Medical Sciences.

TABLES and CHARTS

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