|Year : 2019 | Volume
| Issue : 1 | Page : 3-11
Do noise stress impact to addiction?
Sundareswaran Lognathan1, Arbind Kumar Choudhary2, Kuppusamy Mahesh Kumar3
1 Department of Life Science, Ben-Gurion University of the Negev, Beersheva, Israel
2 Department of Physiology, Government Medical College, Shivpuri, Madhya Pradesh, India
3 Department of Physiology, Sri Ramachandra Medical College and Research Institute, Chennai, Tamil Nadu, India
|Date of Web Publication||18-Jan-2019|
Dr. Arbind Kumar Choudhary
Department of Physiology, Government Medical College, Shivpuri, Madhya Pradesh
Source of Support: None, Conflict of Interest: None
Numerous studies have illustrated the impact of stress on addiction, its development, relapse vulnerability, and the dopamine mechanism. However, various studies on noise exposures as a stressor had been done, which could alter the hypothalamic–pituitary–adrenal (HPA) axis. Noise exposure harmful effect and changes in the individual's health was at least consideration and were less noticed. This review elucidates the facts and consequences of noise exposure toward mesolimbic dopamine circuitry perceptible in addiction. Further, this review generates greater attention and awareness among people toward noise exposure influence on addiction and its relation with dopamine. The noise stress may act as a synergistic influence or augments effect on dopamine level in the synapse of an addicted or initial stage of addicted individual through the corticosterone through HPA axis. The combined effects of multiple stressors (physical, chemical, biological, social and mental etc.) have greater impact than simply the individual stressors. The elevated corticosterone level in noise exposure in turn inhibits the transporter involved in dopamine uptake and further enhance the dopamine level within the synapse of reward circuit may enhance the vulnerability of relapse in addiction. The significance of noise exposure as a stress and other mild stressors influence effect on addiction and psychiatric disorders need to be focused. Strict law-making measures need to be enforced to control and prevent the individual and combined effect of noise stress with other stressors on health.
Keywords: Addiction, corticosterone, dopamine, noise exposure
|How to cite this article:|
Lognathan S, Choudhary AK, Kumar KM. Do noise stress impact to addiction?. Indian J Health Sci Biomed Res 2019;12:3-11
| Introduction|| |
Humans and animals utilize sound as a mean of contact with their environment. Indirectly, sound has enabled the higher beings for their survival in evolution, besides serving a more direct purpose of communication and learning. Sound is a form of energy that is transmitted by pressure variations of which only a hearing apparatus can perceive. The human ear, an advanced hearing apparatus, perceives sound in the range of 20–20,000 Hz. However, when sound exceeds the physiological limits of a hearing apparatus, it becomes noise. Age is a cause for an individual's variability and sensitivity toward sound and frequencies. In addition, sound sources that include traffic, media, industries, loud music, and others have frequencies that tend to exceed the physiological hearing limit (≤90 dB) of the human ear. In spite of environmental noise that stresses the auditory system, it is considered neither hurtful nor noticeable if exposed for a short period of time. According to the National Institute for Occupational Safety and Health, humans are advised to avoid exposure to a noise level above 85 dB (A) for not >8 h. With rapid urbanization and ever-expanding population, exposure to excessive noise is unavoidable. Loud noise has been recognized as an occupational hazard and it not only results in auditory damage but also responsible for neurophysiological and mental side-effects in the longer term. Hence, this review aimed to explore the mechanisms, and in what manner exposure to noise stress may contribute to addiction and its behavior, and how it leads to negative health consequences.
| Sound and Noise|| |
The outcome of pressure changes in an air medium is called sound and it is produced by vibration or turbulence. Based on frequency ranges, sound can be classified broadly into three categories: (1) ≤200 Hz as low frequency, (2) 200–2000 Hz as medium frequency, and (3) >2000 Hz as high frequency. Conversely, the term “noise” indicates sound which is unpleasant, unwanted, dissenting, or interferes with the responses of required sound. There are two types of noise: (1) steady or continuous noise, that is, sudden or gradual onset and long, such as sounds from road, rail, air traffic, industries, and construction and (2) impulse or blast noise, that is, sudden onset and in brief pulses that usually exceed an intensity of 140 dB, such as sounds from firing a handgun, detonating a firecracker, and backfiring of a piston engine. The contrary effect of noise exposure on health varies with the organism morphology and physiology which was well defined., Further, it influences the organism vulnerability to harmful effects with other environmental stimuluses.
| Silent Effect of Noise Exposure|| |
Although many people are aware of possible adverse health effects of noise, these same individuals tend to ignore or even brush off its deleterious effects. Also in the modern life, there are many kinds of jobs and activities where the individuals cannot avoid excess and continuous noise. As a result, they may develop hearing loss, sleep disturbances, heart disease, and endocrine changes, especially of glucose metabolism., The deleterious effect of noise is due to reaction and excitations of the brain and it would occur even during the sleep-awake state. Remarkably during sleep, the auditory system remains alert to ambient noise despite a nonconscious perception of their presence, but this is also the danger part.,, Studies have observed that as compared to an awake state during sleep, there are greater cardiovascular responses to noise exposure and possibly more adverse effects., Furthermore, it is uncertain if the limbic regions are compromised by repeated noise exposure as there may be failure of innate protective mechanism in the middle ear (Rauschecker, 2011). The other potentially more health damaging complications can be a result of synergistic effects of noise with other stressors. Such additional stressors include psychological and unpredictable stress, heat stress, emotional stress, traumatic stress, and physical stress. Studies had already explained the greater and combined effects of multiple stressors other than the effect of individual stressor,, results in chronic sympathetic arousal or states of helplessness.
| Noise: a Psychological Stressor|| |
Noise is essentially a form of psychobiological stressor because of its effect on the central nervous system and also general well-being., Noise exerts its impact on hypothalamic–pituitary–adrenocortical (HPA) axis and the limbic system through the auditory system. The brain plays a central role in control and adaptation to stress, especially during the potentially threatening situation and also regulates the behavioral and physiological responses of an individual. Through stimulation of the reticular activating system (RAS), noise affects neural impulses from the RAS to the brain cortex, and this influences the perceptual, motor, and cognitive behavior as well as triggers the glandular, cardiovascular, and gastrointestinal changes. The circulating hormones also play a major role in modulation of stress and stressful experiences., The noise exposure activates the HPA and sympathetic–adrenal–medullary (SAM) axis leading to increased adrenal gland secretions such as cortisol and catecholamines [Figure 1]. As a result, noise increases the multi-RNA expressions of corticotrophin-releasing hormone in the brain limbic areas, especially the amygdala. This, in turn, causes the anterior pituitary gland to secrete adrenocortical tropic hormone and later from the adrenal gland.,,
|Figure 1: Noise exposure on hypothalamus–pituitary–adrenocortical and sympathetic–adrenal–medullary axis: The noise activates the hypothalamus–pituitary–adrenocortical and sympathetic–adrenal–medullary axis leading to the increased adrenal gland secretions such as cortisol (humans), corticosterone (rodents), and catecholamines|
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The catecholamines (norepinephrine and epinephrine) from the SAM axis affect both α- and β-adrenergic receptors, but especially the β2-adrenergic receptors. In addition described the alteration in catecholamine levels of discrete brain regions in rat after exposed to noise stress. The ability of the brain to distinguish and categorize different sound levels toward stress may well be explained by adaptive plasticity mediated through the HPA and SAM axis, where the functional and structural alterations were believed to be modulated by local neurotransmitters and endocrine hormones interaction. The acute stress response from noise augments the rate of respiration, heart rate, and blood pressure and a decrease in the gastrointestinal tract activity as part of the “fight or flight” response triggered by glucocorticoids., On the other hand, with chronic stress from continued noise exposure, the persistent activation of the SAM system sensitizes the cortex to the action of corticotropin-releasing hormone and also directly activates the cortex. In addition, chronic stress causes noticeable changes in the sympathetic neural and adrenocortical system associated with behavioral suppression. [Table 1] summarizes the various studies in relation to the HPA and SAM axis. Irrespective of numerous studies on noise exposure, its rapid adaptation and acclimatization toward or followed prolonged noise exposure is least convinced.
|Table 1: Noise stress and hypothalamus-pituitary-adrenocortical as well as sympathetic-adrenal-medullary axis|
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| Effects of Noise Stress on the Prefrontal Cortex and Limbic System|| |
Due to the extensive neural connections between the prefrontal cortex, basal ganglia and limbic systems noise stress may have a wider negative influence on cognition and emotion. Noise stress reported to cause impairment in cognitive function through dopaminergic mechanism mainly in the prefrontal cortex as evident in different studies [Table 2].
|Table 2: Studies on noise stress exposure with dopamine and catecholamines levels|
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The increased level of catecholamine following or during noise stress can weaken the cognitive function rapidly [Table 2] despite the homeostasis responses at the basal ganglia and amygdala. The prefrontal cortex can alter the reward circuit because of its control over dopamine release. Normally, the prefrontal cortex is resilient enough in maintaining an equilibrium of dopamine levels in the basal ganglia and limbic system. This is achieved by the prefrontal cortex through feedback information received from the limbic system. Noise stress on the amygdala and hippocampus in the limbic system may result in anxiety and emotional stress besides impaired memory and cognitive dysfunction. In individuals with noise addiction, the diminutive control over behavior by the prefrontal cortex becomes weaken with increasing addiction. Subsequently, the basal circuitry of dopamine regulation is further impaired by continuing noise stress exposure by trailing much of the prefrontal cortex inhibitory control on the addiction circuitry and augments it [Figure 2].
|Figure 2: Normally, the prefrontal cortex in the brain is strong enough in maintaining an equilibrium in dopamine level between the basal ganglia and limbic system involves emotional circuits. This can be achieved by continuously estimating the information from the above regions and then send back the corresponding potential response and inhibitory controller to these regions by the prefrontal cortex. In the individuals with addiction, the diminutive control over behavior by the prefrontal cortex becomes weaken with the severity. Subsequently, the basal circuitry on dopamine regulation may get further impaired through noise stress exposure by trailing much of the prefrontal cortex inhibitory control on the circuits in response to stimuli|
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| Noise Stress and Dopaminergic Pathway|| |
The multiphasic behavioral and endocrine changes associated with noise stress has wide individual variations. As a result, the varying dopaminergic, serotonergic, and noradrenergic responses allow the brain to counter and react by neuronal networks reorganization. The differences in individual cognition, attention, and motivated behavior are well correlated with dopamine changes. After chronic noise stress, the dopaminergic and serotonergic pathways are especially involved and often results in behavioral and motivational deficits in animals and human [Table 2]. Furthermore, noise stress can cause excess free radicals production and has the ability to change the brain neurotransmitters, neurochemical environment, neuronal responses, and microcircuitry networks.
| Noise Exposure and Addiction Vulnerability|| |
Stress induced by noise exposure is recognized by the limbic system through its neural connection with the auditory system. In addition, the adrenocorticotropin hormone and corticotropin-releasing factor (CRF) released from the hypothalamus as a result of noise stress have the ability to stimulate mesocorticolimbic dopaminergic system, and this is the main pathway responsible for addiction and reward circuitry. Dopamine release can be triggered by drugs as well as other stressors through the CRF pathway. In general, in acute stress, the body has the ability to maintain homeostasis through lowering of dopamine and its metabolites. While, in chronic noise stress, the dopamine levels exceed the physiological limit and this predisposes to addiction. Elevated cortisol can upsurge the secretion of dopamine in nucleus accumbens, and in turn, suppression of cortisol reduces the extracellular release of dopamine during response to stress and addictive substances. Hence, the cortisol induced by noise stressor may play a major role in dopamine alteration resulting in addiction and behavior. The differences in gender psychopathic traits personality could be due to alteration in cortisol production and women's whom are psychologically sensitive and also execute similar tendency like men to definite noise. It is also important to correlate traits such as dispositional coping strategies, personality factors and demographic variables (marital status, age, socioeconomic status, gender, and hereditary influences) with the combined effects of noise stress. In a synergistic fashion, noise stress may augment psychostimulants and other physiological behavioral effect on dopamine levels in the synapse. It is likely that there may be other additional factors that will increase the dopamine sensitivity and tolerance toward addiction. The elevated corticosterone levels with noise stress, in turn, inhibit the transporter involved in dopamine uptake,, and further enhance the dopamine levels within the synapse of reward circuit. This may be the reason for vulnerability to relapse with noise addiction [Figure 3].
|Figure 3: Noise stress and additional factor can activate the reward pathways through hypothalamus–pituitary–adrenocortical axis: Noise stress increases corticosterone level, augments dopamine release in synapse of reward circuit along with combined effect of additional factors (such as cocaine, smoke, amphetamine, sex, food, and drugs). The elevated corticosterone level in noise stress in turn inhibits the transporter involved in dopamine uptake|
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| Conclusion|| |
We conclude that corticosterone increased by noise exposure may contribute to the individual addiction, vulnerability, and relapse. The other stressors in day-to-day life such as psychological, personal, work related, cold, heat, chemical, and social isolation may also have influence in corticosterone, HPA axis. However, the consequence of noise stress on health is unavoidable. The combined effect of various stressors has greater deleterious affect than individual stressors. Further, more research should focus on the consequence of noise stress and other individual stressors persuade on addiction and psychiatric disorders. Strict law-making measures need to be enforced to control and prevent the individual and combined effect of noise stress on health.
The authors greatly acknowledge Research University Grant from Government Medical College, Shivpuri (MP), India.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2]