Exposure to hazardous sounds is a common cause of hearing loss in adults. The sources of sound that commonly lead to noise-induced hearing loss (NIHL) include occupational noise (as in factory workers, army men), environmental noise (as in traffic police), music (as in professional musicians & habitual music listeners), and firecrackers.
• Learn the effects of hazardous noise on the structure and function of the human auditory system.
• Understand the signs and symptoms of noise-induced auditory damage, the definition of hazardous noise, ways to identify the auditory damage, and the methods to assess individual susceptibility for noise-induced damage of the auditory system.
Before we dwell into the details of auditory effects of noise, it is necessary to understand the definition of “a hazardous noise”. Simply stated, it is a noise that results in any kind of health hazard/s. History reveals that one of the unexpected byproducts of the industrial revolution was the increased prevalence of hearing loss. The occupational noise that the persons were exposed to was causing permanent hearing loss. To minimize this health hazard, measures were taken to understand the relationship between exposure levels and their effect on hearing. Eventually, National Institute for Occupational Safety and Health (NIOSH) defined the damage risk criteria (DRC) for persons with occupational noise exposure in terms of sound intensity and duration of exposure. According to NIOSH, DRC is 85 dB A (decibels measured using A weighted network of sound level meter) for 8 hours. This is the combination of noise exposure level and duration that no worker exposure shall equal or exceed. If exposure exceeds DRC, the person is at risk of developing permanent hearing loss. This hearing loss, however, will not happen in a day or two, but will take several years of such exposure. There is also a systematic trade-off of permissible exposure duration with an increase in exposure intensity, the specific details of which can be found in Publication No. 98–126, (June 1998) of NIOSH. In any case, no exposure to either continuous, varying, intermittent, or impulsive noise shall exceed 140 dBA. These standards of permissible noise exposure are based on data from several large-scale demographic studies of hearing loss in industrial workers (Baughn, 1973; Burns & Robinson, 1978).
Exposures beyond the DRC are likely to result in noise-induced auditory damage. It can either be one exposure to loud impulse noise of intensity 130dBA and above or routine exposure to continuous noise having intensity 85dBA and above. Although the auditory damage caused by both types of exposures can be referred to as noise-induced damage, the one caused by one-time exposure to very loud impulse noise is specifically referred to as “Acoustic trauma.” In an acoustic trauma, in addition to permanent damage to the inner ear, one may find rupture to the eardrum and dislocation of the ossicular chain in the middle ear. Whereas exposure to continuous occupational noise over the years results in damage of only the inner ear. The subsequent sections of this chapter primarily deal with this second type of occupational noise exposure, which is more prevalent.
Pathophysiology of noise-induced hearing loss (NIHL) has been extensively studied. The primary pathological basis of NIHL is the mechanical stress to cochlear structures. The cochlea is the hearing organ of the inner ear and houses the organ of Corti, within which are thousands of specialized sensory cells. Figure 8.1 shows the different parts of the ear highlighting the cochlea and sensory cells of the cochlea. These cells mediate between mechanical forces in the middle ear and electrical impulses of the cochlear nerve (Eighth cranial nerve). The noise exposure induces mechanical forces that drive the basilar membrane of the inner ear to vibrate. Excessive movement of the basilar membrane due to overexposure to noise causes structural changes in the sensory cells and supporting cells of the cochlea, in turn compromising cochlear function. Although overexposure to noise affects both peripheral and central auditory systems, the cochlea suffers the maximum damage. Also, it doesn’t cause significant changes in either the outer or the middle ear. Within the cochlea, outer hair cells are specifically damaged. Outer hair cells of the inner ear are necessary to hear the sounds below 70dBSPL, and through their nonlinear properties, they expand the dynamic range of hearing. In other words, in the absence of outer hair cells, one can have hearing loss up to 70dB and issues with loudness tolerance.
Individuals with NIHL have demonstrated disruption of stereocillia of outer hair cells of the cochlea, swollen nuclei of hair cells, abnormal mitochondria, cytoplasmic vesiculation, and vacuolization (Kim et al., 2014; Spoendlin, 1985). Metabolic damage is attributed to the formation of free radicals and glutamate excitotoxicity, leading to cell death (Yamane et al., 1995). Noise exposure can also increase free calcium (Ca2+) in outer hair cells (Fridberger et al., 1998), which in turn can trigger apoptotic and necrotic cell death pathways (Orrenius et al., 2003). Apart from these direct effects on the auditory system, noise exposure also causes psychological as well as physiological stress. The hypothalamus-pituitary-adrenal activity, which can modulate auditory sensitivity, is activated by noise-induced stress (Canlon et al., 2007), thereby can contribute to a reduction in hearing sensitivity.
The damage caused by hazardous noise may result in hearing loss, tinnitus (ringing sensation in the ear), blocking sensation in the ear and dizziness. Among these symptoms, hearing loss and tinnitus are more prevalent (Masterson et al., 2016). NIHL can either be temporary or permanent and is always of sensorineural type. If temporary (technical term is temporary threshold shift — TTS), hearing loss will be sudden in onset, mild in degree, and recover within a few hours or a couple of days (Humes & Durch, 2005). On the contrary, permanent hearing loss (typically referred to as occupational NIHL) will be gradual in its onset, can be severe in degree, and is irreversible. It takes several years of noise exposure for the NIHL to occur. NIHL is typically bilateral (occurs in both ears) and symmetrical between the two ears.
In these individuals, hearing sensitivity is assessed using pure tone audiometry. An audiologist tests their ear-specific hearing sensitivity in an acoustically insulated double room suite. The hearing thresholds at octave frequencies will be tracked in the air conduction (using headphones/insert phones) and bone conduction (using bone vibrator) modalities. A classical NIHL case shows a notch at 4 kHz in the pure tone audiogram (Boiler’s notch). Hearing thresholds at frequencies between 3 kHz and 6 kHz will be at least 15dB poorer than the lower frequencies and that at 8 kHz (as depicted in Figure 8.2). If the exposure continues, hearing loss at 4 kHz increases, and there would be gradual involvement of the lower frequencies (depicted in curves 2, 3 & 4 of Figure 8.2). However, hearing loss at low-frequencies limits to about 40dB, while the hearing loss at high frequencies goes up to 70dBHL, even in extreme cases. If noise exposure is discontinued, there won’t be a substantial further progression of hearing loss.
It is not necessary that every NIHL shows a 4 kHz notch in the audiogram. In instances of exposure to impulse noise, one may show a notch at 6 kHz instead of 4 kHz. If one only tests for hearing at octave frequencies in the pure tone audiometry (0.25, 0.5, 1, 2, 4 & 8 kHz), the notch in the audiogram will be missed out in such cases. Therefore, it is recommended that hearing thresholds be estimated at 3 kHz and 6 kHz also in those with a history of noise exposure. This ensures identifying NIHL with higher accuracy. Similarly, it is not necessary that every 4 kHz notch is indicative of only the NIHL. Some of the other causative factors of hearing loss, such as ototoxic drugs and acoustic neuroma, may also manifest with a 4 kHz notch in the audiogram. Therefore, obtaining the case history on noise exposure also becomes crucial in the accurate diagnosis of NIHL.
It is important to note that, with continuous noise exposure, there would be progressive covert damage to outer hair cells of the inner ear much before it is reflected as hearing loss. If the damage can be detected at this stage and subsequent noise exposure can be minimized, the occurrence of hearing loss can be prevented. Thankfully, it is possible to detect such covert damages using otoacoustic emission (OAEs) test. OAEs are low intensity sounds (below 30dBSPL) emitted by normal functioning outer hair cells. They can be evoked by an external stimulus and are recorded using a sensitive microphone placed in the ear canal. The test takes only a minute for each ear and is an objective test (doesn’t need the active participation of the patient/subject). The mere presence of OAEs with good amplitude indicates that the outer hair cells are functioning normally: OAEs with reduced amplitude or absent OAEs suggest abnormal functioning of outer hair cells. Therefore, absence or weak OAEs can serve as an early indicator of noise induced damage to the inner ear and in turn help prevent of NIHL. Therefore, it is advised that persons exposed to hazardous noise regularly monitor the status of their inner ear functioning by undergoing OAE test.
There are four types of OAEs. Among them, transient evoked OAEs (TEOAEs) and distortion product OAEs (DPOAEs) are more used for the early detection of noise-induced damage to the auditory system, owing to their technical ease of recording and specificity rate. Both TEOAEs and DPOAEs give frequency-specific information i.e., one can assess the functioning of outer hair cells at each octave/mid-octave frequency similar to that in a pure tone audiogram. Considering that noise maximally impacts the 3 kHz to 6 kHz region, OAEs will show deterioration in this region first and eventually show a reduction in the other frequencies. However, deterioration in OAEs will occur a few years earlier to any such evidence in pure tone audiogram. TEOAEs and DPOAEs are generated by the outer hair cells, but the generation mechanisms are quite different between the two OAEs. It is unanimously accepted that TEOAEs are more sensitive to noise-induced auditory damage and can detect it earlier than DPOAEs.
Apart from damage to the inner ear, studies have shown evidences of deviant neural functioning in the auditory system due to noise exposure. Hair cells of the inner ear are innervated by the afferent and efferent fibers of the eighth cranial nerve (Spoendlin, 1985). The afferent fibers carry information from hair cells to the auditory cortex. Acoustic overstimulation compromises the structural and functional integrity of nerve innervations to hair cells. It results in degenerative changes in the synaptic junctions and the nerve fibers secondary to hair cell damage: swollen afferent dendrites have been found beneath the inner hair cells (B. Canlon, 1988; Goulios & Robertson, 1983). Such changes are likely to occur within 24–48 hours of overexposure to noise (Liberman & Mulroy, 1982) and are linked to the excessive release of glutamate (Puel et al., 1998), which is the principal neurotransmitter in the inner hair cells.
The changes in synaptic junctions and the nerve fibers have been technically termed “Cochlear Synaptopathy.” The functional consequences of cochlear synaptopathy are found in the form of deviations in some of the suprathreshold measures of hearing and are typically subclinical in nature. Persons with cochlear synaptopathy will show normal hearing in pure tone audiometry, yet will have reduced central auditory processing abilities. They will have good speech perception abilities in a quiet environment but show poorer abilities when the same speech is presented in the presence of noise. The condition is referred to as “Hidden hearing loss” by one group of researchers. It is important to note that most daily listening environments are noisy, due to which persons with cochlear synaptopathy are likely to face challenges in understanding speech despite having normal hearing sensitivity. Kumar et al. (2012) found poorer temporal auditory processing and speech in noise perception abilities in normal hearing train drivers, exposed to occupational engine noise of more than 80dBA compared to their control counterparts. The evidences of cochlear synaptopathy have also been found in terms of deviant latency and amplitude of auditory brainstem responses (Pushpalatha & Konadath, 2016). A take-home message would be that the functional impairments in the case of cochlear synaptopathy are subtle, yet they can compromise the individual’s quality of life. Even though pure tone audiometry will surely miss cochlear synaptopathy, it can be identified with special audiological tests. Effects similar to occupational noise exposure have been found in individuals who regularly use personal music systems. Kumar and Deepashree (2016) found that large proportions of young adults listened to their personal music systems at levels higher than the safety limits prescribed by regulatory bodies. They also found that those who listened at levels higher than 80dBLAeq showed reduced hearing sensitivity at extended high frequencies, reduced TEOAE amplitudes, reduced auditory processing abilities, and poor speech in noise perception.
Further, a few animal studies have investigated the effects of noise exposure levels below the DRC on auditory functioning (Noreña et al., 2006; Zhou & Merzenich, 2012). These studies have used noise levels that are lower than 80dB, which typically should not result in hearing loss. The findings reveal that even exposure levels below DRC have effects on central auditory processing, in spite of hearing being unaffected. Specifically, they have evidenced structural and functional changes in the auditory cortex. Maruthy et al. (2018) found that humans exposed to below-DRC levels of occupational noise tend to have poor stream segregation abilities than their control counterparts. This hints at the possible speech perception difficulty they may have in the presence of background noise. In summary, these evidences support that even the noise levels below DRC are deleterious to the auditory system. The DRC, when derived, was primarily based on the effects of noise exposure on pure tone hearing thresholds. The then scientific evidences were limited to hearing sensitivity. However, the current scientific evidences show that several subclinical structural and functional deviations occur much before the reduction in hearing sensitivity. These deviations can affect the persons’ speech understanding in challenging listening environments, ability to appreciate music, and in general, their quality of life. It is time that we revisit the DRC on account of the current scientific evidences.
Scientific attempts have also been made to understand whether noise exposure at young age accelerates age-related hearing loss. One exposed to hazardous noise at a young age is likely to develop age-related hearing loss at an earlier age and develop a higher degree of hearing loss at an equivalent age than their counterparts who are not exposed to noise. While animal studies reveal that TTS at young age accelerated age-related hearing loss (Kujawa & Liberman, 2006), human studies offer only weak support for such a relationship (Gates et al., 2000).
Researchers have observed that, despite the nature of noise exposure being constant, there is a large variability in the resultant degree of NIHL: ranging from 10 to 70dB. This large variability is true for temporary as well as permanent threshold shifts. Several factors have been tested to verify whether they serve as predictors of susceptibility. They include TTS, age, gender, eye color, ototoxic drugs, middle ear muscle reflex, efferent auditory functioning, and genetic predisposition (Henderson et al., 1993). Most of these factors are poor predictors of susceptibility, except ototoxic drugs and middle-ear muscle reflex. Some ototoxic drugs such as aminoglycoside antibiotics and antineoplastic agents can interact significantly with noise resulting in greater hearing loss than could be caused by either agent alone. That is, if a person exposed to occupational noise consumes ototoxic drugs, he is likely to be more susceptible to inner ear damage, in turn to develop the NIHL. Ototoxic drugs as well as noise exposure results in increase of free radicals around the sensory cells, leading to cell death. Similarly, those with elevated acoustic reflex thresholds or absent acoustic reflexes are found to be more susceptible for NIHL than ones with normal acoustic reflexes. Studies in mice have revealed genes that underlie susceptibility to NIHL. However, their generalization in human cohort is debatable.
Tinnitus refers to a ringing sensation in the ear in the absence of any such external sound source. Persistent tinnitus is a sign of deviant functioning in the auditory system. Abnormality anywhere in the auditory system can result in tinnitus, and noise-induced damage to the auditory system is no exception. Nearly one-fourth of persons exposed to occupational noise report significant tinnitus, and the prevalence is alarmingly high in military persons. The majority of persons with NIHL present with bilateral tinnitus, and the severity of tinnitus may vary with the degree of NIHL. The tinnitus either in isolation or along with NIHL can negatively impact the quality of life of the affected person.
Noise has harmful effects on the human auditory system. The exposure levels above the DRC can lead to permanent hearing loss by damaging the cochlea. However, if the noise exposure is inevitable, the damage can be minimized either by cutting down the noise at the source or by using hearing protective devices. The DRC holds true even for music exposure. The audiological tests such as otoacoustic emissions can determine the individual susceptibility to develop NIHL as well as detect the damage to the ear early. The persons exposed to noise in their routine shall consult Audiologists to understand the risk and monitor their hearing status.
Robert Lacey once stated, “Of all the varieties of modern pollution, noise is the most insidious.” The 21st century is witnessing, among other things, wars, burning of fossil fuels, increasing presence of vehicles, and industrialization resulting in the loss of natural quiet. Insights from epidemiological studies show that exposure to traffic noise (from aircraft, road vehicles, and trains) is associated with increased cardiovascular morbidity and mortality.1
Although medical and scientific efforts have focussed primarily on the diagnosis, treatment, and prevention of traditional cardiovascular risk factors (e.g., diabetes, smoking, arterial hypertension, hyperlipidaemia), recent studies indicate that the risk factors in the physical environment may also facilitate the development of cardiovascular disease.2 Epidemiological and observational studies done by Munzel et al. demonstrated that persistent noise can trigger elevated levels of stress hormone (epinephrine) and this is supported by the Noise reaction model introduced by Babisch. During normal metabolic processes, the cells in our bodies produce unstable compounds known as free radicals and also antioxidants that neutralize these free radicals, hence maintaining the equilibrium. However, owing to certain factors such as diet, lifestyle, and the environment, the body’s immune response gets triggered causing an imbalance and inflammation which ultimately leads to oxidative stress. These vascular changes have been found to contribute directly or indirectly to the initiation and progression of cardiovascular disease.2, 3
With industrialization and globalization, the importance of new environmental factors such as noise pollution and its impact on the cardiovascular system is becoming increasingly evident.
• Understand the mechanism of cardiovascular system
• Review the molecular levels changes in the human body due to noise
• Discuss the implementation of safety measures
In 1972, Saphiro and Baland were the first to record the intensity of noise and noise pollution and describe it as the “third pollution” after air pollution and water pollution.2, 3 As the intensity of sound moves northwards on the decibel scale, its ill effects on human health result in more severe and chronic health issues such as headaches, irritability, nervousness, fatigue owing to hypertension, increased heart rate, atherosclerosis, and cardiovascular disease.
Blood in the human body flows in a continuous movement through the capillaries that permeate every tissue and cell. The vital role of the cardiovascular system in our body is to maintain homeostasis, which depends on this controlled movement of blood.4 Numerous control mechanisms help to regulate and integrate the diverse functions and various parts of the cardiovascular system to supply blood to specific parts of the body according to need. These mechanisms ensure a constant internal environment surrounding each body cell regardless of their differing demands for nutrients or production of waste products.5, 6
The arterial system is regulated by three mechanisms: the autonomic nervous system, kidneys (Renin angiotensin – aldosterone), and endocrine system (catecholamines, kinin, serotonin, histamine).The autonomic nervous system is a part of the nervous system that controls involuntary actions such as heartbeat, blood flow, breathing, and digestion. This system consist of two divisions– sympathetic and parasympathetic –that work in unison to maintain balance.6 The autonomic nervous system functions by receiving information from the environment and other parts of the body. The sympathetic and parasympathetic divisions tend to have opposing actions in which one system (sympathetic) stimulates a response while the other (parasympathetic) inhibits it.
Sympathetic efferent nerves are present throughout the atria (especially in the SA node) and ventricles, including the conduction system of the heart. Sympathetic stimulation of the heart increases heart rate and conduction velocity whereas parasympathetic stimulation of the heart has the opposite effect.7, 8
In the blood vessels, sympathetic activation constricts arteries and arterioles, which increases vascular resistance and decreases distal blood flow. When this occurs throughout the body, the increased vascular resistance causes arterial pressure to increase. The overall effect of sympathetic activation is to increase cardiac output, systemic vascular resistance of both arteries and veins, and arterial blood pressure. Enhanced sympathetic activity is particularly important during exercise and emotional stress.9
Noise is a nonspecific stressor that activates the autonomous nervous system and endocrine signalling. Such chronic stress can cause high cholesterol, high blood glucose, high blood pressure, increased blood viscosity, and activation of blood coagulation – leading to cardiovascular risk factors.
Blood vessels are lined with endothelial cells that produce powerful vasoconstricting and vasodilating substances such as the radical nitric oxide (NO.). Nitric oxide is a free radical which causes relaxation of the inner muscles of the blood vessels causing them to widen and increase circulation.
Stress induced by noise can also increase the permeability of the endothelium to inflammatory cells such as macrophages, leading to endothelial dysfunction and prothrombotic and inflammatory pathways. If stress persists for a prolonged period, it leads to a build-up of cholesterol and immune cells below the endothelium, which leads to plaque formation and, eventually, accumulation of smooth cells and lipids. Hence, acute noise stress can cause a physical disruption of the plaque, leading to cardiovascular events.10
Two enzymes play an important role in the induction of vascular function disorders –nicotinamide adenosine dinucleotide phosphate oxidase (NADPH oxidase) and nitric oxide synthase (NOS).The molecular effect of enzymes like NADPH oxidase and NOS due to noise, results in decreased bioavailability of the radical nitric oxide produced in the body, leading to deterioration of the endothelial function.10, 11
Babisch, who proposed the noise reaction model, described two pathways – direct and indirect –for determining the adverse effects of noise on health. The nonauditory or indirect pathway, with an exposure of low-level noise ranging from 50–60 dB in the form of conversations, interferes with communication, concentration, daily activities, and sleep, resulting in annoyance, mental stress, and subsequent sympathetic and endocrine activation (Figure 9.1).11
It was this pathway that Babisch suspected to be the central player for noise-induced cardiovascular effects. He hypothesized that if the exposure is persistent and chronic, noise contributes to pathophysiological changes that are characterized by increased stress hormone levels, high blood pressure, and accelerated heart rate.11
As a consequence, the body generates its own cardiovascular risk factors, including high cholesterol and glucose levels, increased blood viscosity, and activation of blood coagulation. If stress persists for years, cardiovascular diseases such as hypertension, coronary heart disease, heart failure, arrhythmia, and stroke can begin to manifest, along with mental stress or related disorders such as depression and anxiety, which are themselves known to negatively affect cardiovascular health.12
Hence, it has been proven that occupational noise exposure can produce adverse effects on the cardiovascular system including hypertension, ischemic heart disease (IHD), and stroke.
Blood pressure, or systemic arterial pressure, refers to the pressure measured within large arteries in the systemic circulation. This splits into systolic blood pressure and diastolic blood pressure. Systolic pressure refers to the maximum pressure within the large arteries when the heart muscle contracts to propel blood through the body. Diastolic pressure describes the lowest pressure within the large arteries when the heart muscle relaxes between beats.
The principal mechanism regulating arterial pressure within the blood vessels in the body is the baroreceptor reflex. Most studies have shown that long-term exposure to occupational noise significantly raised systolic blood pressure (SBP) and diastolic blood pressure (DBP) and increased the prevalence of hypertension.11
A study done on a subsample of HYENA (Hypertension and Exposure to Noise near Airports) data (n = 149) showed a non-dipping effect of diastolic blood pressure at night, which has been previously identified as an independent risk factor for cardiovascular disease with a more pronounced dose-response relation for men and affecting the middle-age group.12
Similarly, a meta-analysis of 24 studies by van Kempen and Babisch revealed that road traffic noise is associated with an elevated risk of the occurrence of high blood pressure starting at 45 dB and per increase of 5 dB. However, this analysis was restricted to cross-sectional studies.13
Hyperlipidaemia, or high cholesterol, is a condition where there is high fat content in the blood. This is one of the most common risk factors for atherosclerosis.
Noise is found to be an environmental stressor that is believed to activate the endocrine system. Hence, elevated stress hormones in the body may stimulate an increase in blood lipids causing atherosclerosis which in turn leads to coronary heart disease, degenerative changes in the myocardium, and atherosclerotic changes in arterial blood vessels.14
One historical cohort study included male workers in high-level (n=154) and low-level (n=146) noise exposure groups and found a significant relationship between noise exposure and triglyceride concentrations in the two groups. Workers exposed to noise greater than 90 dB without ear protection appear to have increased triglyceride levels.14
The negative association between noise and endothelial function are seen more in patients with established coronary artery disease and can also cause altered heart rate. Some evidence shows that occupational exposure to noise may lead to increased heart rate in workers.15 Data from the large, population-based Gutenberg Health Study (n= 15010 persons resident in Mainz and the Mainz–Bingen region) showed that the stress reaction to various sources of noise during the day and while sleeping at night is associated dose-dependently with an increased risk of atrial fibrillation.16
Increased cardiovascular risk was also confirmed in studies such as the Netherlands Cohort Study on Diet and Cancer, and Stockholm Heart Epidemiology Program which has acknowledged noise as one such potential agent along with air pollutants.
Beelen et al. investigated several cardiovascular diseases mortality end points in the Netherlands Cohort Study on Diet and Cancer using modelled noise levels.17 For the highest noise exposure category (>65 dB L DEN) they found increased relative risk (adjusted) for all cardiovascular diseases (1.25, 95% CI 1.01-1.53%) and heart failure. The study found, in addition, that the risk of ischemic heart disease and dysrhythmia were also elevated, but neither of the latter effects was statistically significant.
Selander et al. confirmed an increased risk for acute myocardial infarction morbidity in the Stockholm Heart Epidemiology Program.18
Noise has been found to trigger a stress response in the limbic system of the brain consisting of the amygdala, a region of the brainstem. This response from the brain is perceived as danger and sends a distress signal to the hypothalamus, a gland in the brain which controls the hormone system. The reaction triggers a release of cortisol (a stress hormone) which results in increased heart rate and blood pressure, a rapid release of energy in the bloodstream, reduced metabolism with a decrease in salivary and gastrointestinal activity, and activation of some immune functions.18
Sleep is an essential function during which the mind and body are recharged and is of vital importance for human development, optimal health, and overall well-being.
Sleep restriction has been found to be associated with decreased insulin production, inadequate pancreatic insulin secretion, changes in appetite regulating hormones, increased sympathetic tone, and venous endothelial dysfunction.
When individuals fail to obtain adequate duration or quality of sleep, they may experience reduced performance, measurable changes to different organic systems, especially to cardiovascular system, and increased risk of accidents and death.19
Noise is found to have ill effects on the human body and its consequence range from headache and anxiety to insomnia, obesity, diabetes, hypertension, atherosclerosis, and cardiovascular disease. It is also associated with oxidative stress, vascular dysfunction, mental stress, and metabolic abnormalities resulting in increased susceptibility to cardiovascular events.19
Measures should be taken to minimize noise by employing protective measures such as imposing standardized safety and health policies with regard to urban planning and industries.
Policies should work to bring noise exposure levels in line with the new guidelines developed by the World Health Organization, which lowered the recommendations for mean daily noise sound pressure levels to 45 dB for aircraft noise, 53 dB for road traffic noise, and 54 dB for railway noise, with even stricter limits for night-time hours to reduce the burden of disease from noise.
Along with this, the state and local governments should work towards providing adequate laws to prevent noise pollution near residential areas. Rolling noise in the form of the sound generated by the interaction of tires and road surface is the dominant noise source. This can be counteracted with the installation of quiet road surfaces, promotion of low-noise tires, and speed reductions in densely populated areas. Another strategy applied in some countries is the introduction of driving bans for trucks during the core night-time hours.
Public should also be made aware of the fact that loud sounds can be reduced by the use of barriers such as trees and fences, and by insulating buildings.20 With these measured small steps, the overall ill effects of noise can be reversed over time.
• Prolonged exposure to excessive noise is now considered a health hazard.
• Occupational noise exposure can produce adverse effects on the cardiovascular system including hypertension, ischemic heart disease, and stroke.
• Noise is also associated with oxidative stress, vascular dysfunction, mental stress, and metabolic abnormalities
• Measures should be taken to minimize noise by implementing protective measures such as imposing standardized safety and health policies.
Noise is unwanted sound but omnipresent in the modern world. Persistent loud noise in the environment leads to a deleterious effect on the nervous system and negatively impacts our health (1). Neurocognitive functions are the mental processes that helps us to receive, choose, store, modify, generate and recover information that are being absorbed from the external and internal sources. It includes functions such as attention, language, memory, concentration, and learning that enable us to adapt to the environment and function to an optimal level are most commonly affected by noise.
1. Understand how sound is processed and perceived by the brain.
2. Summarize the deleterious effect of noise.
2.1. Identify the effect on cognition due to disturbance caused by noise.
2.2. Explain how noise can serve as a barrier to communication.
3. Describe the impact of noise on the developing foetus during pregnancy.
4. Comprehend the effect of environmental noise on children and their school performance.
5. Compare the impact of road, aircraft, and railway noise exposure on children.
6. Predict how noise is affecting the aging population.
1. Auditory Cortex – part of the brain that processes auditory information.
2. Cranial Nerve – group of nerves that arises from the brain to provide motor and sensory information to the head and neck.
4. Lateral lemniscus – tract of axons in the brainstem that carries information about sound from the auditory nerve to various brainstem nuclei and ultimately the contralateral inferior colliculus of the midbrain.
5. Brain Stem – The area at the base of the brain that connects the uppermost portion of the brain with the spinal cord.
6. Inferior Colliculi – A paired structure in the midbrain, which serves as an important relay point for auditory information as it travels from the inner ear to the auditory cortex.
7. Medial Geniculate Nucleus – principal relay nucleus for the auditory system between the inferior colliculus and auditory cortex.
8. Thalamus – located above the brain stem that relays sensory impulses from receptors in various parts of the body to the cerebral cortex
9. Neurodegenerative Disorder – it encompasses a wide range of incurable and debilitating conditions resulting from progressive damage to neurons or cells of the nervous system.
10. Somatic – relating to the body, distinct from the mind.
11. Psychosomatic – physical illness caused due to mental conditions such as stress, anxiety, depression etc.
12. Hippocampus – brain area primarily responsible for learning and memory.
13. Slow-wave Sleep – deepest phase of sleep considered responsible for memory consolidation.
14. Positron Emission Tomography (PET) – Neuroimaging techniques that uses a radioactive drug to study the metabolic and biochemical function of tissues and organs
15. Rapid Eye Movement (REM) – phase of sleep characterized by rapid movement of the eye, low muscle tone and vivid dreams.
16. fMRI – It is a non-invasive neuroimaging technique that measures brain activity by detecting changes associated with blood flow.
17. Parietal Lobe – One of the four lobes, that processes sensory information being received from external stimuli, primarily related to touch, taste, and temperature.
18. Oxidative Stress – it is an imbalance between free radicals and antioxidants in the body as a result of which the oxygen free radicals attack biological molecules such as lipids, proteins, and DNA
19. tau and β-amyloid (Aβ) – These are protein fragments, that gets accumulated in the brain causing damage and destruction of synapses that mediate memory and cognition.
20. Phosphorylation – A biochemical process that involves the addition of phosphate to an organic compound.
The auditory cortex in the temporal lobes is primarily responsible for auditory perception in the brain. The eighth cranial nerve (the auditory nerve) from the cochlea carries the auditory information, through the superior olivary complex and lateral lemniscus of the brain stem. The information then passes through the inferior colliculi involved in sound localization, then to the medial geniculate nucleus of the thalamus, where interaction between attentional processes and auditory information takes place. Finally, the information reaches the primary auditory cortex of the temporal lobes (refer to Figure 10.1). The primary auditory region receives bilateral input – ipsilateral and contralateral inputs. The right ear transmits auditory information to the left cerebral cortex and vice versa (2). The primary auditory area is spatially organized, which means that different auditory frequencies are progressively anatomically represented. High frequencies are received and analysed in the anterior-medial portions and low frequencies in the posterior-lateral regions of the superior temporal lobe.
Language is primarily processed in the left temporal lobe, whereas the right temporal lobe is involved in the identification and recognition of nonverbal environmental acoustics (e.g., wind, rain, animal noises, prosodic-melodic nuances, understanding emotional meanings of sounds and music) (2). It has long been known that, under most circumstances, cognitive processing is easily disturbed by environmental noise and non-task compatible distractors. This effect is believed to be due to competition for attentional resources between the distractor and the target stimuli.
The ability to sort out and focus on meaningful auditory messages from a complex background of sounds is referred to as the cocktail party effect (3). The cocktail party phenomenon is an example of selective attention, which first occurs in the superior olivary nucleus. Selective attention enhances activity in one part of the sensory cortex and reduces it in other parts (2).
Noise is unpleasant and unwanted indistinguishable sound. It can have an adverse effect on the various cognitive and neuropsychological functioning either directly or concomitantly. For instance, noise directly impairs attention and concentration. Moreover, noise can affect the quality of sleep that indirectly has a negative impact on attention and concentration. Noise is considered as a noxious stimulus and modern transportation and products of the latest technology emit extensive noise pollution of varying intensities all round the clock, causing annoyance, disrupting sleep, concentration and, other cognitive and biological functions (1). Noise is believed to affect physical health, specifically hypertension, heart disease and the release of stress hormone.
The impact of noise pollution on the cognitive and brain functioning of humans has often been ignored. Noise is considered as a risk factor for cognitive impairment and neurodegenerative disorder. It is considered that noise can affect health in either of the two ways. Firstly, noise can have a negative effect on health by causing annoyance in both adults and children. Annoyance is the feeling of uneasiness that does not encompass the number of negative reactions associated with noise, including, anger, exhaustion, helplessness, distraction. An inability to control the noise can escalate these affect, causing stress response and result in somatic and psychosomatic health issues. Low frequency (between 10 Hz to 200 Hz) noise along with vibrations are found to cause greater annoyance (1). The second way, noise can affect health is by disruption of sleep, resulting in poor quality of life and cognitive impairment.
Noise can interfere with cognitive processing and cause problems in both occupational and non-occupational environments. It can cause workplace accidents in roles requiring high levels of cognitive functioning as they need to maintain efficient performance while being exposed to high-intensity noise. Research evidence has shown that noise can lead to cognitive impairment and oxidative stress in the brain and has also been observed to negatively trigger the central nervous system causing stress, anxiety and memory defects. Attention is one of the primary cognitive functions on which other cognitive functions rely and can be significantly affected by noise. Furthermore, attention is responsible for various other activities such as motor movements, emotional responses and perceptual functions. Due to lack of adequate information processing, the attentional system controls human behaviour based on spatial and time-related characteristics, due to which strategic responses are not efficient, subsequently, degrading performance. Noise can also affect working memory performance but not performance speed. Other cognitive functions that are affected by exposure to noise are reaction time, memory, intelligence and concentration, to name a few. These affected cognitive functions can lead to increased error and accidents, resulting in reduced performance and productivity. Performance deficit can lead to both health and economic repercussion (1). However, certain research studies have demonstrated that noise can improve performance in sleep-deprived workers by enhancing arousal. Relevant literature has conflicting reviews on the effect of noise on cognitive performance. One review study conducted by Gawron (1982), on the effect of noise on cognitive performance, revealed that out of 58 studies, 29 studies reported having a negative impact on cognitive performance, whereas 22 has no effect and 7 has a positive effect. It has been found that loud noise at 100 dBA in comparison to 70 dBA elevates central visual stimuli processing but degrades peripheral stimulus processing. Parameters such as the characteristic of noise, exposure time, type of task, gender, age and sensitivity to noise collectively affect the cognitive performance of an individual (4).
Our hearing mechanism remains active even during sleep, therefore noise can be perceived subconsciously in sleep. The quality and quantity of sleep have a large impact on our day-to-day functioning. Lack of uninterrupted sleep is detrimental to our mental as well as physical health. Sleep disturbances resulting from noise can be primarily in the initiation of sleep, recurrent awakenings and difficulty in maintaining sleep, waking up earlier than usual and diminished REM sleep. These disturbances are considered to have the most deleterious effect on our cognitive function. One of the key roles of sleep on our cognition is the consolidation of various types of memory as well as insightful, abstract thinking. Neuroimaging studies have revealed that the hippocampus responsible for memory formation, remains active during a learning task, subsequently becomes reactivated during sleep, particularly slow-wave sleep. It was examined with Positron Emission Tomography (PET) by measuring cerebral blood flow to the hippocampal areas (5). Therefore, many researchers concluded that the recently encoded memories are activated and replayed again during sleep, hence, mediating memory processing. According to Stickgold (2009), slow-wave sleep stabilizes recently encoded memory and REM sleep integrates the memory into the larger neuronal networks. It has been suggested, in terms of exposure to noise during sleep that, continuous noise tends to interrupt REM sleep whereas intermittent noise exposure disrupts slow-wave sleep (6).
The importance of sleep in neuropsychological functioning has been demonstrated in several research studies. In one study by Van Dongen and colleagues (2003) subjects were restricted to 4, 6 or 8 hours of sleep time for 14 days. They were then assessed for attention, concentration and working memory several times during the day. It was found that the performance of the subjects obtaining 4 and 6 hours of bed-time deteriorated steadily, and after 14 days their performance was comparable to those who are sleep-deprived for 24 to 48 hours (7). A similar study showed that, in addition to attention, concentration and working memory, sleep-deprived subjects are found to have impairment in executive functions, verbal fluency, creative thinking and planning. Deficit in cognitive functioning was also observed in real-life circumstances requiring a high level of performance, e.g., medical interns. One study using functional magnetic resonance imaging (fMRI) has demonstrated that the areas of the brain that are activated in sleep-deprived subjects during the performance of an arithmetic task are far less than the areas activated in those with the rested condition while performing similar task. However, in the case of verbal memory, in a sleep-deprived state, additional brain areas including the parietal lobe get activated during the task performance, even though the overall performance remains comparatively poor (8). It indicates the compensatory role of the newly activated brain area. Therefore, sufficient evidence implicates that sleep disturbance is highly associated with poor cognitive functioning and noise pollution is one of the primary hindrances to quality sleep.
Understanding normal speech is obstructed by noise pollution resulting in a number of personal and behavioural difficulties. It involves concentration, fatigability, ambiguity, poor self-confidence, anger, irritation and misunderstanding, lack of working capacity, strained interpersonal relationships and stress reaction. Subsequently, it may result in increased chances of accident, impaired classroom learning, leading to poor academic performance (1). Noise pollution also affects task performance at school and at work, resulting in an increased error and reducing motivation. Domains that are most adversely affected by noise are reading, problem-solving and memory. Experimental research has primarily identified two domains of memory post noise exposure, namely, recall of subject content and recall of incidental details (1). It has been found that in a noisy home environment, children’s cognitive and language development is decreased.
In contemporary times, pregnant women are exposed to sound and noise, which could have an influence on the developing foetus, thereafter affecting the cognitive function of the new born (9). The central nervous system goes through structural and functional growth, during early mammalian life and hence, is more vulnerable to environmental stimuli such as noise. Hippocampus is an important structure of the brain responsible for memory formation and learning novel tasks. Another, primary structure of the brain includes the inferior colliculi which processes auditory information and relays it to the auditory cortex. It is believed that noise is transmitted via the inferior colliculi to areas of the hippocampus, influencing its function. Therefore, it can cause oxidative stress, which is highly implicated in cognitive impairment.
Conducting studies on human subjects to understand the effect of high decibel sound on the developing foetus during pregnancy has its limitation (9). Hence, animal studies are considered for the same. Cheng and colleagues (2011) conducted a study on mice to understand noise-induced cognitive impairment and its underlying mechanism. The study revealed that pre-natal exposure to noise can cause a reduction in the formation of new neurons in areas of the brain called the hippocampus, which is responsible for memory and learning, and the inferior colliculus which acts as a relay station in the auditory pathway. Thus, resulting in cognitive impairment (10). A similar study showed growth impairment, reduced neurogenesis in the hippocampus, and impaired spatial learning ability in pups due to noise exposure during pregnancy. Hippocampus is also regarded as a key structure for spatial learning and memory. In an experiment, conducted on one-day-old chicks, it was found that exposure to noise at 110dB, resulted in impaired spatial behaviour like spatial learning, memory and orientation (9).
Children are considered as the most vulnerable group to the deleterious effects of noise, as childhood is the most crucial developmental age for cognitive development. Furthermore, children are less equipped to manage and exercise control over noise and the damage caused due to noise exposure can likely be irreversible. Each year 45,000 healthy life years are lost due to cognitive impairment in children aged 7–19 years, as computed by the World Health Organization in western European countries (11). Mechanisms by which cognitive functions are affected in children includes communication problem, stress, annoyance, frustration and sleep disruption, as children have less developed coping strategies than adults. Research studies have consistently revealed that environmental noise can affect cognitive performance of children. Children residing in deprived social conditions experience a higher level of noise and perform worse on tests assessing cognitive functions than do children not socially deprived. And it has been found that healthy normal children with fragmented sleep showed lower performance on neuro-behavioural functioning and behavioural problems (12).
Studies have also revealed that children exposed to noise during school hours experience impairment in cognitive performance including central processing, reading comprehension and memory (13). Impairment has been found in sustained and visual attention (13). Similarly, reports collected from school teachers have revealed that children exposed to noise struggle concentrating in contrast to children studying in a quieter school environment. Auditory discrimination and speech perception is also found to be retarded in children experiencing chronic environmental noise, moreover, they also have a high demand for processing due to poor memory. Eventually, they tend to have poor reading ability and performance in school. Numerous pathways have been believed to be associated between noise exposure and impairment in children’s cognitive functioning, namely; teacher and pupil frustration, learned helplessness, impaired attention, increased arousal, indiscriminate filtering out of the noise (14).
The first naturalistic study that was ever carried out in the ’70s was by Cohen, Glass, and Singer, (1973) to investigate the effects of chronic noise exposure on primary school children living in a four 32-floor apartment buildings next to a busy road. The findings revealed that children living on the lower floors had greater impairment in comparison to children living on the higher floors in auditory discrimination and reading level. As children living on the lower floor are more exposed to road traffic noise than those living on the upper floors in the building (15).
Several studies have shown that chronic rail, aircraft or road traffic noise exposure leads to a damaging effect on children’s learning outcomes and cognitive performance. One such naturalistic field study by Hygge and colleagues (1996) (16) was carried out in Munich in the 1990s when the currently existing Munich airport was closed down and shifted to another location. In this longitudinal study, the effect of exposure to noise on children with a mean age of 10.8 years was investigated. Data collection was done at both the old and new airport sites on three occasions: first, before the old airport is shut down and the new airport is opened and two subsequently. Results of the first data analysis revealed that long-term episodic memory and reading comprehension are affected in children at the old airport site. The longitudinal results showed that after three sessions of testing, improvement was shown in children at the old airport in the domain of long-term memory, indicating that the effect caused is reversible. Children at the new airport were manifesting deficits in long-term memory and reading comprehension, supporting strong evidence for a causal link between noise pollution and cognitive deficits.
One of the largest multi-centre studies comparing the effect of road traffic and aircraft noise on the cognitive performance of children was conducted by Stansfeld and colleagues (2005) in the Netherlands, Spain and the UK. The result revealed no significant association between chronic road traffic or aircraft noise exposure on cognitive performance except reading comprehension (17). Therefore, the results of this study along, with other findings indicate that noise has a negative impact on reading comprehension or could be justified by other mechanisms such as learned helplessness, attention difficulty and frustration in both teacher and pupil. Children adapt to noise by filtering out unwanted noise and this filter may then be applied to situations devoid of any noise, leading to inattention and subsequent learning deficit.
Intervention studies have shown that reducing the noise level by either insulation or closure of airports is connected to the alleviation of cognitive functions, suggesting that noise reduction can reverse the negative impact caused by noise on cognition. One comparative study was carried out by Bronzaft and McCarthy (1975), to understand the effect of railway noise on children in comparison to children who are not exposed to any kind of environmental noise in a school. The findings reveal a significant difference in reading scores between the two groups of children. Further, the noise-exposed children’s mean reading age was 3–4 months behind that of the children not subjected to noise (18).
The aging process has been found to be driven by environmental exposure such as noise pollution and is considered as one of the risk factors for dementia in the aging population. There is a large intersection of cardiovascular disease risk factors with cognitive decline and dementia. However, the degree to which noise pollution exposure directly affects cognitive decline, resulting in dementia is poorly comprehended. Dementia and cognitive deterioration are the primary health concern of the geriatric population, with a consequent increase in economic and social burden for the caretakers. The accumulation of tau and β-amyloid (Aβ), which are a type of protein, is considered to be the underlying cause of most nonvascular dementia and cognitive impairment. Animal studies have revealed that the high-level exposure of noise for long-term influences tau pathology and increased production of Aβ, and evocation of aberrant auditory input in the brain, resulting in abnormal changes in the cortex and the hippocampus (10). Oxidative stress in the brain due to noise exposure is also been suggested by most studies (19). It is not known whether there is a relevant period of noise exposure exists for late-life cognitive decline, however, exposures extending over decades or the entire life span are believed to affect these outcomes (19).
One long-term study by Nubaum et al., 2020, investigated the association of noise pollution with neurocognitive test performance and brain atrophy in older adults between 55 to 85 years of age. It was found that noise pollution has a damaging effect on higher neurocognitive functions such as vocabulary, verbal fluency and short-term/working memory, with local atrophy of the fronto-parietal network (20). A similar study conducted by Tzivian (2016), found a negative correlation between noise pollution and the scores of neuropsychological tests measuring verbal fluency, immediate and delayed recall tests, problem-solving and processing speed (21). Additionally, air pollution was found to be strongly associated with mild cognitive impairment, an earlier stage of dementia, for highly noise-exposed subjects, but not with participants who are not exposed to noise.
It has been hypothesized that chronic noise exposure affects the central nervous system in two proposed ways. First, sleep disturbance due to noise decreases vigilance in the daytime and increases oxidative stress in the brain mediating phosphorylation of tau protein, considered one of the earliest changes in the brain in Alzheimer’s disease. Secondly, noise induces a series of signalling through the release of the stress hormone, causing changes in the auditory system, cortex and hippocampus. It is regarded as one of the significant neurochemical changes in Alzheimer’s disease.
The impact of noise on our neuropsychological functioning is tremendous.
• Noise can have a detrimental effect on cognitive functioning across the lifespan. It can affect our cognitive functioning by disrupting sleep, causing annoyance, inattention and decreasing concentration.
• Noise can also indirectly affect productivity at work by reducing the quality of life.
• Exposure to noise during pregnancy can have a negative effect on the developing embryo leading to growth impairment in the brain structures.
• Children are the most vulnerable group of the population affected by noise exposure, as they are not able to exercise control over noise, unlike adults.
• Noise can also have a massive impact on the development of various late-life neurological conditions including Mild Cognitive Impairment and dementia.
• Noise can not only cause annoyance but it also affects our brain in many ways. Noise is inevitable in our daily life, and it is almost next to impossible to live in a completely noise free environment. However, being aware of the negative consequences of prolonged noise exposure on our neuropsychological functioning can help us make informed decision in modifying our living conditions to limit our exposure to noise and provide awareness to others as well.
Noise is one of the fastest growing environmental stressors with well-established direct and indirect effects on the human body. Low frequency noises (<100 Hz) have the potential to harm the human body, including the Endocrine and Immune system. Noise between 70–120 dB has the capacity to stimulate the release of the stress hormones apart from affecting the cardiovascular system like the increased heart rate and the blood pressure. Chronic noise exposure, with sustained physiological arousal, and the continuous effort to cope with this puts an individual at the risk of developing diseases because of the change in the hormonal milieu in the body.1
• To understand the basic concepts of endocrine and immune systems and their inter-relationship.
• To know the important effects of noise and music on these systems and their association with disease causation and overall well-being.
• Key Terms
• Endocrine system: It is a messenger system in the human body, consisting of many organs called as glands. These glands produce substances/mediators called as hormones, which travel in the blood-stream to different tissues and have many important functions in the body.
• Receptors: These are chemical structures present on the target cells to which a specific hormone binds and exerts it’s effect.
• Immune system: It is a complex network of cells, tissues and organs that help the body fight against infections and other diseases. It consists of different cells and organs.
• Cytokines: These are small proteins which are produced mainly by immune cells. They have an important function in maintaining the immunity of the body apart from some other functions.
• Auto-immune diseases: A condition in which the body’s immune system attacks its own healthy cells, causing a disease
In simple terms, the endocrine system is the communication network in the body. It consists of a series of organs called glands, which are located throughout the body, and these help in regulating the important functions. Hypothalamus and pituitary in the brain, thyroid and parathyroid in the neck, pancreas, adrenal and gonads in the abdomen are some of the endocrine glands in our body. These glands release the chemical messengers called the hormones, in response to various stimuli, into the blood stream. The messengers travel through the blood to reach the different target organs and attach to the specific receptor sites like the lock and key system. Only the organs which have the specific receptors will respond to the particular hormone released in the blood stream.
The hypothalamus is an important gland in the brain. It plays a crucial role in producing the hormones that controls the functioning of the pituitary, the master endocrine gland of our body. Pituitary is a tiny gland, weighing about 500mg, but is the main regulator of the secretion of hormones from all the other endocrine glands in the body (thyroid, adrenal, testis and ovary). Few of the most important hormones such as cortisol and catecholamines (epinephrine and norepinephrine), which regulate the immune system and respond to stress, are secreted from adrenal gland.
The hypothalamic pituitary adrenal (HPA) axis is one of the most important neuroendocrine links. The hypothalamus releases the corticotrophin releasing factor (CRF). When this CRF binds to the CRF-receptor in the pituitary, a hormone called adrenocorticotrophic hormone (ACTH) is released. The ACTH binds to receptors in the adrenal cortex (outer part of gland) and releases cortisol (steroid hormone). The classical effects of cortisol are increasing blood glucose concentration and blood pressure, inhibiting growth and reproduction and regulating the immune system. Once a certain blood concentration is achieved, cortisol exerts negative feedback to the hypothalamus and the production of hormones seizes.
Similarly, another system called the sympathetic adrenal medullary (SAM) axis is present. It is also known as the fight-or-flight system and is mediated by catecholamines, which are secreted by the adrenal medulla (inner part of gland). Catecholamines activate numerous beneficial responses like increased blood flow to muscles, heart and lungs while inhibiting processes like digestion. This system is very important for a human being to fight against any immediate threat.
The thyroid is another important gland, which is situated in the neck. It is also regulated by hypothalamus (through TRH – thyrotrophin releasing hormone) and pituitary gland (through TSH – thyroid stimulating hormone). The thyroid gland produces hormones called T3 and T4, which circulate to various parts of the body and are responsible for many important functions in the body like regulating body metabolism, maintaining body temperature, heart and bone health, menstrual cycles, brain development, etc.
The parathyroid glands are present in the neck behind the thyroid gland and are necessary for maintaining the calcium levels in the body. The ovary and testis are the glands present in females and males respectively, which play an important role in sexual development and reproduction.
Every day, the human body is exposed to several disease causing micro-organisms. The ability of the body to protect itself from these pathogens is called immunity. This task is handled by the immune system.
The immune system is comprised of billions of cells that travel through the bloodstream. The most important of these are the white blood cells, specifically lymphocytes (B and T cells) and phagocytes. The B cells develop in the bone marrow, get activated on contact with foreign particles or pathogens (disease causing agents) and produce antibodies. While the T cells also originate in the bone marrow, they develop in a gland known as the thymus. They further differentiate into helper cells, cytotoxic cells and regulatory cells.
There are two types of immunity: Natural and Acquired. Acquired immunity is gained over the lifetime. It is specific to particular pathogen and mediated by antibodies or lymphocytes. The antibody mediated reaction is called the humoral immune response. The cellular immune response is initiated by the helper T cells, which release cytokines. Cytokines are small protein molecules that are the mediators of the inflammatory response. They initiate a call to action and attract other immune cells to take part in the reaction. The cytotoxic T cells release toxins and promote death of pathogens or unwanted cells, while the regulatory T cells control this immune response.
The brain responds to stress by sending a distress signal to the hypothalamus. The hypothalamus activates the SAM system by stimulating the release of catecholamines from the adrenal glands. As the initial surge of the catecholamines subsides, the hypothalamus activates the second component, the HPA system resulting in the release of the stress hormone called the Cortisol. Individuals under stress tend to have disturbed, fragmented sleep that leads to further increase in cortisol levels.3
Noise Stress Model 4
Henry and Stephen proposed the link between the noise and the stress and how the hormones play a role in this. This was based on the psycho-physiological stress model. There are three types of reaction that will be elicited in response to the exposure of the noise at different intensities.
Exposure to the loud habituated or non-habituated noise >90dB (A) stimulates the sympatho – adrenal system and release the adrenaline and noradrenaline from the sympathetic synapses. Whereas the extremely intense noise or above the threshold of pain will stimulate the release of cortisol by the activation of HPA system.
Acute and chronic endocrine effects of noise on animals and humans has been studied and was found that the acute noise exposure causes the increase in the levels of catecholamines; while extremely intense acute noise equivalent to threshold of pain, caused an increase in release of cortisol.4
A recent study showed that the suppression of the cellular and humoral response to noise stress was related to neuroendocrine changes. In this study they found that mice exposed to 4 weeks of 90 dB (A) white noise had a significant increase in cortisol and epinephrine along with a significant reduction in splenic lymphoproliferation, CD4 T cells and serum IgG levels.5
The influence of the neuroendocrine system on the immune system is bi-directional. Not only does the neuroendocrine system affect the immune function, but the immune responses also have profound effects on the neuroendocrine system. The link between the two systems is due to the sharing of receptors and mediators. Hormone receptors have been found on immune cells while cytokine receptors have been found in both endocrine glands and nervous system.
Stress is known to influence the immune system via activation of the HPA axis and secretion of cortisol. Similarly, cytokines released by an immune response have effects on the hypothalamic control of hormones like ACTH and growth hormone.6
Chronic low levels of stress keeps the HPA axis activated and also causes resistance to the negative feedback signals leading to over-production of stress hormones.
The effect of stress on diabetes is multifactorial. However, the main culprit is the excess secretion of cortisol. Cortisol increases the blood glucose levels by converting the protein to glycogen and also by stimulating the catecholamine induced breakdown of this glycogen to glucose. It also induces the resistance to the action of insulin in different tissues like muscle and fat tissues, thereby increasing the blood glucose levels. High levels of cortisol can also result in the increase of body fat tissue and weight, which are risk factors for diabetes. Stress induced poor sleep affects glucose metabolism by reducing glucose tolerance and insulin sensitivity. In adults, there is a well-established relationship between stress and poor diabetic control.
Thyroid hormones are the regulators of body metabolism. Stress causes down-regulation of thyroid function by cortisol-induced inhibition of the secretion of TSH from the pituitary gland thereby leading to reduced production of thyroid hormones causing hypothyroidism.
Stress induced immunological disturbances can lead to production of thyroid receptor antibodies, causing autoimmune thyroid disorders such as Graves Disease (over active thyroid) and Hashimoto’s disease.
Exposure to stress can lead to impairment of reproductive functions while prolonged exposure can cause infertility. Reproductive functions are regulated by the hypothalamic pituitary gonadal (HPG) axis which functions like the HPA axis. Cortisol can suppress this pathway leading to reduced circulating levels of testosterone and estrogen. Decreased levels of testosterone in males lead to reduced sperm count and motility. In females, reduced estrogen can cause anovulation, amenorrhea and other menstrual irregularities.
Besides these, excess production of the Cortisol secondary to stress can cause failure to thrive and psychosocial dwarfism in children. It is also implicated for the cause of obesity (over-weight) in children.7
A chronically stressed individual is more prone to develop infections, especially viral infections. Individuals exposed to stress showed an increase in the rates of infection (74–90%) and also the reactivation of infections such as HIV and Herpes, which have remained dormant in the B cells, is more common with increased stress. The occurrence of common cold also increases (27–47%). This is due to the stress induced dysregulation of the humoral and cellular immune response to pathogens, which cause suppression of the host’s resistance to infection. Stress is known to alter the antibody production and T cell response to antiviral vaccinations resulting in suppressed immune responses.
Wound healing is a process that occurs during recovery from an injury or surgery. Inflammation is a pre-requisite for this process. Cellular immunity, through inflammatory cytokines and chemokines, plays an important role in the regulation of wound healing. Stress disrupts the production of these pro-inflammatory cytokines causing significant delay in the healing process.
An increased level of IL-6, a pro-inflammatory cytokine was seen in chronically stressed individuals. IL-6 is associated with premature ageing of cells, increasing the risk of several age-related diseases like cardiovascular (heart) disease, arthritis, osteoporosis and frailty. It is also associated with higher mortality.
Chronic stress, by increasing inflammation and altering the protective immune responses, increased the susceptibility to certain types of cancer. Increased levels of catecholamines have been associated with occurrence of cancer and metastasis (spread of cancer to other organs). Besides, several inflammatory mediators are involved in tumour growth and progression.
Noise related sleep disturbances was shown to increase risk of auto-immune disorders like rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and systemic sclerosis (SS), by suppressing the activity of regulatory T cells and production of cytokines. An increased level of IL-17 was associated with RA, SLE and inflammatory bowel disease (IBD). Increased activity of addictive habits like smoking have an indirect risk of certain autoimmune diseases like RA, SLE, SS, Grave’s disease and primary biliary cirrhosis.
The therapeutic use of music is well-documented. Numerous studies have found that listening to pleasant music has a calming effect on the body. Happiness trifecta is a term used to define the positive emotions and mood the body experiences and this is driven by certain hormones like dopamine, serotonin and oxytocin. Music has a strong correlation to elevate these hormones causing the feeling of happiness and relaxation.
The music reduces the stress levels in the body. It is known to reduce the levels of cortisol and catecholamines. This leads to decreased incidence of cardio-vascular diseases. There is some evidence that classical music has a beneficial effect on the thyroid hormones. Besides, music also improves the immunity of a person and reduces the occurrence of infections and some of the auto-immune diseases. 11
Stress is a part of life. The body responds to environmental noise similar to other non-specific physical stressors by activation of the HPA and SAM systems, apart from changes in other organs of endocrine system.
• The deleterious effects of exposure to noise on the endocrine and immune systems are mediated mainly by increased levels of cortisol. This, in long term, can result in increased occurrence of diseases like diabetes, hypertension, heart diseases, etc.
• Exposure of noise can affect the other endocrine glands and cause thyroid dysfunction, reproductive problems in both males and females.
Music on the other hand is shown to have some beneficial effects on the endocrine and immune systems of the body by reducing stress levels and its associated complications.
It is documented in many text books that human beings have the ability to hear sounds with the frequencies ranging from 16 to 20,000 Hz and that sound is inaudible below 16 Hz.1 But the fact is hearing sensation does not suddenly cease at 16 Hz and ear responds to sounds with much lower cut off of 1.5 Hz. Since hearing sensitivity decreases with frequency, humans perceive infrasound when sufficient sound pressure level exists as necessary stimulus. Infrasonic sound therefore refers to sound wave with a frequency varying from 0.01–16 Hz. Watnabe and Moller (1990)2 have demonstrated that at high stimulus levels, humans can hear sound as low as that of 4 Hz. Till this was published people thought that the hearing of human ear starts at 20 Hz. But the stimulus pressure level required for the ear to feel the hearing sensation has to be more by 28 dB compared to pressure level at 20 Hz.
Table12.1 gives threshold levels of hearing from 4 to 200 Hz by healthy human beings. Sounds between 16 Hz and 500Hz are classified as “Low frequency noise” and it is common to combine together the “infrasound and Low frequency” noise (ILFN) due to the unique characteristics of this particular frequency range in interaction with human body. This chapter will deal mostly with the effects of sound in this ILFN range.
Sources of infrasound in nature which include infrasonic sound sometimes results from severe weather, surf, lee waves (mountain size waves), avalanches, earthquakes, volcanoes, bolides (a large meteor when explodes), waterfalls, calving of icebergs, aurorae (caused by charged particles from sun entering into earth’s magnetic field and stimulating particles in the earth’s atmosphere), meteors and lightning. etc., are known to lie between 0.1 to 1.0 Hz. Human activities also produce infrasound, like running by sports persons, sonic booms, explosions, machinery such as diesel engines, wind turbines and specially designed industrial vibration tables etc. which generally goes up in the range up to 500 Hz. A number of species of animal kingdom such as whales, elephants, hippopotamuses, rhinoceroses, giraffes, okapis, peacocks, and alligators are known to use infrasound to communicate over long distances. They use sounds in the infrasonic and low frequency range for their habitation and survival. For example, baleen whales can produce sounds of 10–31 Hz, which potentially travel hundreds of kilometers in underwater.
• To understand the origin of natural and manmade infrasound and ILFN
• To understand the generation, transmission and attenuation of infra sound.
• To understand the basis for infrasound-human body interaction through the cellular model based on tensegrity structure.
• To understand how infrasonic waves interact with the human body.
• To understand the symptoms and pathology of vibroacoustic disease.
Sound waves at low frequencies suffer less attenuation while travelling in any media and therefore will travel farther. Low frequency sound easily passes through barriers like walls, headphones etc. with less reflection and less attenuation unlike it happens at high frequencies of sound. The low frequency sounds bend over the wall and return to the ground due to large wavelength. The wavelengths of sound frequencies audible to the human ear (10 Hz–20 kHz) are thus between approximately 34 m and 17 mm. To design a barrier to protect the body from this sound, one has to design it to a thickness 8.5 m which is not practical to realize. It is a very difficult to protect by closing a door or building a wall or wearing an ear plug against infrasound waves. These waves easily penetrate all obstacles to almost full strength. Special sound absorbing ear defenders can offer some protection to one’s hearing.
Infrasounds, though out of easily perceivable audible range for humans, are used for communication in many animals in nature. Whales, giraffes, peacocks, rhinos, hippopotamuses, elephants, tigers and alligators are some of the animals known to us that use infrasounds for communication. The purr of felines is reported to cover a range of 20–50 Hz, and the roar of a tiger itself has an incredibly low frequency of only 18 Hz! Researchers have found a tiger roars at 18 HZ frequency producing a sound that can make its prey to go disoriented making it is easy to paralyze the victim with fear.3 Natural infrasounds can also work as a navigational aid in case of many migratory birds.
It is a known that 7HZ infrasound has the capacity to create theta wave in the brain which is known to be associated with meditation and harmony. This 7HZ musical products are known to take human beings into a kind of musical trance. Infrasound is also known as sound of fear. Scientists discovered that low frequencies in infrasound can effect humans and animals in several ways causing discomfort, dizziness, blurred vision (by vibrating eyeballs), hyperventilation and fear possibly leading to panic attacks.
The traditional model of the biological cell presumes it to be an elastic cortex surrounded by a viscous cytoplasm which holds an elastic nucleus at the center. For the past 30 years, the Ingber lab at Harvard medical school4 has been showing that this balloon model of the cell is grossly inappropriate. Instead, a cellular model based on tensegrity architecture has been proposed and has been successfully explaining many cellular and tissue behaviors, both during normal metabolic activity and in disease alike. The new cellular model is important in understanding the type of pathology developed by ILFN-exposed organisms because only the tensegrity model appropriately explains how mechanical signals are transduced over cells and tissues. In this model of tensegrity (tension integrity) model, there are some structural components in tension and some structural components in compression and together they form a cellular structure to handle mechanical loads.
Infrasonic sounds are produced in human body as vital sign in the 1–16HZ frequency range caused by the mechanical movement of the heart and can be recorded non-invasively with simple instruments. Ballistocardiography (BCG) is a known technique for graphically studying the repetitive motions of the human body caused due to ejection of blood into the blood vessels with each heartbeat. Similarly other techniques, such as seismocardiogram (SCG), are used to understand abnormalities of heart related aliments combined with machine bearing algorithms.
Phenomenon of resonance occurs when an excitation frequency of an external vibratory force coincides with natural frequency of human body. At resonance, the human body absorbs the energy with high efficiency and experiences high vibration amplitude causing discomfort and/or damage to the human body. The damage could be at cellular level or tissue level or even an organ level.
The natural frequencies of a healthy average human body is given in Table 12.2 below.
Human body has some rigid hard structures like head, spine and some flexible tissue filled structures like thoracic cavity and heart. The natural frequencies of these parts vary according to their stiffness and distributed mass. The natural frequencies of other parts such as pelvic cavity, abdomen etc. remain in between.
If a human body is exposed for a longer period of such ILFN of varying frequency, the body will go into resonant vibration problems, which may slowly lead to urinary, digestive, nervous and cardiovascular system diseases culminating into serious physiological disorders.
Thus, the sensation we feel inside the body is not necessarily through the ears but because of the resonance effect in the body. The natural frequency of a big building is in the range of fraction of 1 Hz to 3 Hz, which is close to that of the body’s. This explains why infrasounds commonly present, annoy/affect people living in big buildings. The feeling of unpleasantness or uneasiness that some people experience in some older churches is found to be due to the harmonics of sound created in giant organ pipes at the infrasound frequencies. The long-term effect of infrasound waves on human beings who live close to such sources of sound include headache, laziness, dizziness, nausea, irritability etc. If the intensity level is high these problems may precipitate into respiratory impairment and aural pain. The frequencies associates with these problem is given in Table 12.3.
Excessive exposure to ILFN can cause Vibro-Acoustic disease (commonly known as VAD),6 a systemic pathology characterized by the abnormal proliferation of collagen and elastin fibers without the presence of any inflammation. It has also been found in people exposed to natural/environmental ILFN in Industries like sheet metal fabrication, ship building industry, aircraft industry, etc. Simultaneously, other populations occupationally exposed to ILFN were also studied like helicopter and military pilots.7 It was found that the fundamental agent of disease to which aircraft personnel were exposed was ILFN.7 All aircraft technicians presented abnormal pericardial and/or cardiac valve thickening.8
In 1993, during a scientific meeting, the term ‘‘vibroacoustic’’ was proposed for this pathological entity and ‘‘vibroacoustic syndrome’’ became the new name for the ailment seen in aircraft technicians and now, also in aircraft and helicopter pilots.9
Additional neurological disorders were found in ILFN-exposed populations, such as the existence of the palmo-mental reflex, usually only seen in primates, newborns, and the elderly (balance disturbances and facial dyskinesia induced by auditory stimuli).10 The first human pericardial fragments were studied in VAD patients who needed cardiac bypass surgery for other reasons. Abnormal amounts of collagen as well as the neo-formation of an extra layer of tissue was shown to be the cause underlying the pericardial thickening, supplying anatomical confirmation of the autopsy and echo-imaging observations.11
Other ILFN-exposed professionals were also studied, such as civil aviation pilots and cabin crewmembers, confirming echocardiography results of aircraft technicians and military pilots.
More neurological pathology was found: VAD patients were found to be unable to hyperventilate when in the presence of excessive CO2 .12
Mechanically induced cellular death was found in the pericardia of VAD patients and it was hypothesized that this situation could be related to the large incidence of auto-immune disorders in these patients.7
All bronchoscopic examinations of VAD patients showed lesions that, upon analysis, proved the existence of abnormal amounts of collagen and neo-formation of vascular beds. Disrupted collagen fibers were seen and correlated with a positive testing of anti-nuclear antibodies, providing a deeper understanding of auto-immune processes.12
• Animal studies showed that the respiratory tract could be considered a primary target for ILFN: abnormal amount of fibrosis/collagen was ubiquitous in trachea, lungs and pleura; damaged (sheared) tracheal and bronchial cilia; fused actin-based microvilli of tracheal and bronchial brush cells. The atypical cases of pleural effusion were partially explained by morpho functional impairment of pleural microvilli13 as well as of pleuralphagocytic capabilities.
• Wistar rats were chosen as animal models to investigate the effects of ILFN exposure on the respiratory tract, to explain the atypical cases of pleural effusion, of unknown etiology.
• The genotoxicity of ILFN was proved in both human and animal models and was confirmed by teratogenic features in mice.14
Further rat studies suggested that fusion of cochlear cilia (actin-based structures) may supply a biomechanical explanation for noise intolerance or annoyance.7
(The below data in Table 12.4 is based on research conducted on 140 individuals working in an aeronautical industry. ILFN exposure time (years) refers to the amount of time it took for 70 individuals (50%) to develop the corresponding sign or symptom12).
|Stage I-Mild (1–4 years)||Light mood swings, indigestion and heartburn, mouth/throat infections, bronchitis|
|Stage II-Moderate (4–10 years)||Chest pain, definite mood swings, back pain, fatigue, fungal, viral and parasitic skin infections, inflammation of stomach lining, pain
and blood in urine, conjunctivitis, allergies
|Stage III–Severe (4–10 years)||Psychiatric disturbances, haemorrhages of nasal, digestive and conjunctive mucosa, varicose veins and haemorrhoids, duodenal
ulcers, spastic colitis, decrease in visual acuity, headaches, severe joint pain, intense muscular pain, neurological disturbances
Aural Pain: This is known to occur when displacements of the middle-ear system undergoes beyond its comfortable limits. It is researched that persons with hearing ability and hearing loss and with normal middle ears experience aural pain at similar intensity levels of about 165 dB at 2HZ.13
i. Pericardial thickening— In human beings affected by VAD, it was found that there is pericardial thickening, without any pericarditis or inflammation.
ii. Actin-based structures—
• Brush cell (BC) microvilli and cochlear cilia: it was found that among rats exposed to ILFN, clustering of the microvilli occurred, and on prolonged exposure, fusing of the microvilli occurred.
• It was also found that the cochlear stereo cilia are also fused among themselves and to the upper tectorial membrane.
• The appearance of respiratory tract epithelium is such that they appear clipped, sheared or shaggy.
Hearing impairment is the only pathology that can develop due to excessive noise exposure. Therefore, occupational physicians rarely see VAD symptoms as caused by excessive noise exposure. In fact, given the multitude of symptoms associated with VAD, often physicians regard the patient as a malingerer or hypochondriac. This is also collaborated by the fact that routine medical tests (e.g.: blood chemistry analysis, Electrocardiography (ECG) and electroencephalography (EEG)) do not confirm the existence of any pathology. The reason for this is that most of the medical diagnostic tests are based on biochemical, and not biomechanical pathways. In the case of occupational exposure to ILFN, workers can develop some disabilities which call for early retirement. Usually, ILFN environments are associated with machinery that, in an ever-changing technological environment, often becomes obsolete within a few years’ time. Hence, the VAD developed by many individuals cannot be proven since many of the ILFN sources no more exist to correlate easily.
A specific characteristic of VAD is pericardial thickening with no diastolic dysfunction. Therefore, to identify this, an echocardiogram would be a preferred means to evaluate thickening of pericardium and cardiac valves. However, this will only suffice for an informal diagnosis due to the limitations of echo-imaging procedures. A legal or forensic proof for the presence of VAD can only be provided by more invasive procedures like bronchoscopic examination and other complementary tests such as brainstem auditory evoked potentials, brain MRI, PCO2 rebreathing test, cognitive evoked potentials, blood coagulation factors and a thorough neurological examination.
Given below are some key symptoms of VAD as expressed by patients, which can aid in its diagnosis:
• People may complain of being extremely sensitive to noise, and not being able to stand any type of noise. Loud noises cause much mental disturbance, making them uneasy when exposed to any sound.
• Patients may also report prolonged fatigue and waking up tired despite enough hours of sleep
• Patients may also experience shortness of breath in public spaces such as malls or restaurants and have a strong feeling that they cannot breathe and must get out of there
• Patients may also experience heart palpitations for prolonged periods as well as with high intensity
• They may also report having a cough, though they don’t smoke. The patient may also report having a hoarse throat and constantly irritated throat with over-the-counter-medication being of no use.
Or if the patient enters with one of the following diagnoses:
• Late-onset epilepsy
• Auto-immune disease, particularly systemic lupus erythematous and vitiligo
• Balance disorders
• Recommendation for cardiac bypass surgery
• Respiratory tract tumor, especially if a non-smoker
It is to be stated that there are no proper standards or recommendations from national and international agencies for protection of humans from infrasound. The main reason for this state of affairs is the difficulty in the measurement of sound wave intensities at infrasonic frequencies. World Health Organization (WHO) has also recognized that the general assessment measures for environmental noise are deficient for evaluation of noises with large low frequency components.17
There are four causative factors of human disease and illness. They are biological, chemical, physical and psycho-social. The infrasound or low frequency noise come under the physical causes of disease. For this reason WHO classifies it as inanimate mechanical force as the damage is done by a physical force.
Infrasound is clearly audible up to a lower cut off frequency of 1.5 Hz but the threshold of hearing is comparatively high at infrasonic frequencies. Infrasounds and low frequency noise form important sources of disease and ill-health among individuals. Due to mechano-vibratory effects, it can cause multiple pathologies like thickening of pericardium, changes in the microvilli structure of respiratory epithelium etc. on the human body.
• Sources of infrasound include low-frequency natural occurrences, low-speed machinery sources like wind turbines, diesel engines etc. and these sources become causative factors of ill health only when they exceed certain stimulus level which need to be established properly.
• The routine measurement of infrasounds is grossly inadequate and it is important to know the ill effects of infrasounds, collectively known as vibroacoustic disease.
• The physicians need to be sensitized about the symptoms and signs of vibroacoustic disease.
• Significant research and proper legislation are needed to mitigate the effect of infrasound and low frequency noise (ILFN) on humans to reduce effect on health due to exposure to ILFN.