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| Year : 2004
| Volume
: 6 | Issue : 22 | Page
: 35-47 |
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| Noise induced nocturnal cortisol secretion and tolerable overhead flights |
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M Spreng
Dept. Physiology and Experimental Pathophysiology, University of Erlangen, Germany
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Mainly dependent on level and dynamic increase sound produces over-shooting excitations which activate subcortical processing centers (e.g. the amygdala, functioning as fear conditioning center) besides cortical areas (e. g. arousing annoyance, awakenings) as well. In addition there exist very close central nervous connections between subcortical parts of the auditory system (e.g. amygdala) showing typical plasticity effects (sensitization) and the hypothalmic-pituitary-adrenal (HPA)-axis. Using that causal chain noise induce cortisol excretion even below the awakening threshold.
Thus repeated noise events (e.g. overflights during night time) may lead to accumulation of the cortisol level in blood. This can happen because its time-constant of exponential decrease is about 50 to 10 times larger than that one for adrenaline and noradrenaline. This fact and the unusual large permeability of cortisol through the cell membranes opens a wide field of connections between stress-dependent cortisol production and the disturbance of a large number of other endocrine processes, especially as a result of long-term stress activation by environmental influences such as environmental noise.
Based upon a physiological model calculating the cortisol accumulation starting at a nightly threshold of physiological over-proportional reactions around L max =53 dB(A) the number of tolerable noise events (over-flights in a nightly time range) can be estimated for given indoor peak sound pressure levels, keeping the cortisol increase within the normal range. Examples of results for 8 hours in the night are for instance number and level combinations (NAL-values) of 13 events with 53 dB(A) indoor peak level or 6 events with 70 dB(A) indoor peak level repectively. Keywords: aircraft noise, auditory system, vegetative system, amygdala, cortisol, number and level combinations, tolerable over-flights
How to cite this article:
Spreng M. Noise induced nocturnal cortisol secretion and tolerable overhead flights. Noise Health 2004;6:35-47 |
| Introduction | |  |
The sense of hearing - ten times more sensitive than the eye in humans as well - is the most decisive warning and communications organ. This is why it remains open to the environment day and night, and is unable to deny access to sound stimuli in the same way as the eye with its lids closed against impinging light (Spreng, 1980). This is the reason why sounds from the environment are constantly picked up, whether awake or asleep, and trigger massive stimulation of the processing sections of the brain, particularly the subcortical regions, which instigate various noise effects and ultimately the sensation of "noise". Noise effects are not only experienced as disturbing, irritating or stressful, but may also be associated with after-effects in terms of health. This was clearly indicated by earlier measurements with reference to the health effects of rail track noise (Osada et al., 1972).
In laboratory experiments Osada et al. had presented track noise with peak levels of 50 and 60 dB(A) and a duration of 20 seconds (corresponding to the passage of a fast goods train) to persons during their night's sleep. Sound exposure in the first hour of sleep was every 5 minutes, in the second hour every 10 minutes and in the third hour every 20 minutes.
In the remaining 3 hours the sequence was presented in the reverse order. This resulted in 42 track noise episodes per night.
The results of the early-morning blood test showed significant reductions of the percentage rise in eosinophilic and basophilic granulocytes and an accelerated decline in leukocytes as compared to a normal collective group. More distinct results were found in similar experiments with peak levels ranging between 50 and 80 dB(A) respectively, but using only 18 track noise episodes per night (Osada et al., 1974).
The occasional objection that fluctuations of this kind cannot occur in one night (PasschierVermeer, 1993) is untenable since it is already known physiologically and in terms of the circadian rhythm that fluctuations of these values between -20% and +40% around the 24-hour mean value may occur. The normal formation processes are clearly influenced negatively by the impact of nocturnal track noise, however, this being essentially dependent on the glucocorticoids (cortisol) released, as has also been pointed out for a long time already (Spreng, 1984).
| Direct reactions of the organism to sound | | |
As is clearly apparent from the much simplified scheme of [Figure - 1], the sounds striking the ear are converted to neural stimulation by the hearing sensory cells in the inner ear, whose nervous pathways are centrally directed towards the different processing centers of the brain (Spreng, 1994).
At this point, damage to the sensory cells (aural noise effects), which cannot be regenerated or medicinally treated as a rule, may already have been incurred by high-pitched sound pressure levels of longer duration (greater than 80 dB(A)) and highly dynamic sound pressure changes (steep sides of the noise peaks). Hazards of this nature are not present where normal environmental noise is concerned, which is also the case for overhead flights which are not too close - generally ignoring the reduced recovery time of the ear induced by noise exposure of longer duration.
With a view to understanding noise effects, at least two special features of peripheral processing in the auditory system, starting behind the highly susceptible sensory cells of the inner ear and transforming the mechanical sound activation into the body's own nerve signals (action potentials), have to be born in mind. First of all, the proportional-differential behavior of the sensory receptors, over-emphasizing the stimulus dynamics, has to be taken into special account. Excess stimulation (over-shooting), dependent on the dynamics of the volume increase of sound, always occurs immediately behind the ear's sensory cells, which in turn accesses the entire periphery and central system ([Figure - 1], bottom left shows the over-shooting number of action potentials after stimulus onset). This dynamic increase is notably high for aircraft sounds with approx. 6 -10 dB(A) per second as compared to other types of noise.
These excess stimulation effects then unfold in many areas of the brain in the course of further central nervous processing, where it is less the auditory center of the cerebral cortex (e.g. perception of the noise components, direction of the noise, speech recognition etc.) which is of importance, but rather more the areas shown in [Figure - 1] which are emphasized as the reticular formation and above all as the amygdala (almond-shaped structure).
Also worthy of note are the extremely fast nervous processing tracts. Fast monosynaptic nervous pathways exist which activate the neurons of the quadrigeminal plate (inferior colliculus) located in the brainstem after 5 ms, and the so-called geniculate body (corpus geniculatum), as an additional important thalamic synaptic center after 7 ms, prior to reaching the cortical regions ([Figure - 1], bottom left shows the fast brainstem response in a human subject after click stimulation) (Spreng, 1984; 1985 and 1994).
Noise effects essentially influencing the direct processing routes or levels and ultimately the auditory cortical center and other areas of the central nervous system should not be neglected at all, however, since these involve the excitations induced by the noise, which, although having no effect on health, determine to a massive extent the degree of annoyance of the exposed person and produce reported awakenings.
Relevant in terms of influence on health, however, is the primary activation system of the reticular formation, responsible for asleep-awake synapses, for maintaining coordinated motorial programs (conflict, escape) in readiness, and basically for taking care of enhanced watchfulness (state of alertness).
Of particular importance, not taken into proper consideration so far, is above all that part of the brain specially emphasized in [Figure - 1], the socalled amygdala (almond kernel) which is associated with sections of the auditory pathway and correspondingly subject to the same exitation. This system, also functioning as fear conditioning center, is marked by its unusual plasticity (learning capacity), specifically with regard to adverse i.e. negative assessment of combined, repetitive or conditioning noise stimuli (Spreng, 2000a).
| Non-aural noise effects on the organism General vegetative noise effects | | |
All organisms possess the ability to react in an appropriate manner to adverse environmental stimuli, e.g. when loud noises occur. In the same way that the flow of information between sensorial uptake and motorial reaction is not based exclusively on purely cortical neural contacts, but includes the subcortical regions to a large extent, a bridge is set up between sensorial activation and vegetative reactions by subcortical processing tracts of the brain. These zones contain limbic and hypothalamic mechanisms which on their part can influence the autonomic nervous system and special hormone stress reactions via rapid links. These mechanisms react frequently, even when lacking introspective knowledge about the actual cause of the emotional response, in fact even without conscious perception, while asleep for example.
Of decisive importance for understanding noise effects in this context is detailed knowledge of the exitation processes and synaptic principles, not only with regard to the peripheral but also the central processing system of audition or brain respectively.
Two systems need to be distinguished in the central nervous sensory/vegetative activation processes, both of which are mainly under subcortical control: the ascending reticular activating system (ARAS) and the vegetative nervous system (VNS).
The ascending reticular activating system (ARAS) activates the cerebral cortex, regulating the waking-sleeping rhythm of the brain among other items, and contributes to the alertness control. Playing a leading part in this system is the reticular formation (formatio reticularis) in the subcortex [Figure - 1], a network of neurons extending from the brainstem to the diencephalon and mainly containing neurons regulating the circulation. It is activated by sensory stimuli on the one hand, and by the limbic system, the so-called "emotional brain", on the other. In this way both internal and external stimuli are in a position to influence the organism, awake or asleep.
In this manner, the adrenal medulla, an important central organ of vegetative activation, is stimulated via the nervous pathways (sympathetic nervous system), whereby the catecholamines, adrenaline and noradrenaline for example, are released into the blood immediately. Among other things - in addition to the relatively fast nervously controlled activation - the said catecholamines bring about a flexible reaction of the organism to stress stimuli, of somewhat longer duration (several minutes), as well as emotional stress situations such as annoyance, fear or pleasure, particularly affecting the cardiovascular system, respiration, intestinal activity, metabolism, pupillary reflexes and the central nervous system (CNS). Direct connection with the motoricity (e.g. changes in muscular tension) via the central gray substance takes place alongside this [Figure - 1].
The equally important main reaction line of the vegetative nervous system (VNS) starts from the central regulatory system of the hypothalamus and accesses practically all the effector systems responsible for hormone balance: e.g. via the pituitary, the adrenal gland system.
An important causal chain is notably present here, of significance in understanding the health hazards which may arise from the effects of adverse sounds (noise). This is primarily responsible for the release of stress conditioned hormones (e.g. cortisol).
| Causal chain auditory pathway (Amygdala) hypothalamus - stress hormone release | | |
The lateral area of the amygdala (almond kernel) core is part of the auditory system. An abundance of findings exists which indicate that the core region of the amygdala is to be denoted as a critical structure in the brain, playing a significant role in the experiences of fear and the emotional process of learning. It is a fact today that the fast monosynaptic thalamus-amygdala tract is taken as responsible for the direct transmission of responses to fear triggered by acoustic stimuli ([Figure - 1], left hand side). This has been corroborated by a series of conditioning experiments with animals (LeDoux, 1990 and 1995; Masterton, 1996), and it has also been successfully shown recently (LaBar et al., 1998) that during conditioned learning-to-fear in humans, a clear contribution to exitation arising from structures of the amygdala can be observed using echo-planar functional nuclear magnetic resonance.
As mentioned already, this system acting as a fear conditioning center is distinguished by an unusual capacity to learn (plasticity), particularly with regard to adverse sound stimuli, i.e. those combined with negative assessment (Edeline and Weinberger, 1992; Lennartz and Weinberger, 1992; Quirk et al., 1995; Rogan and LeDoux, 1995).
The said plasticity is apparent, for example, in the shortening of reaction times and the hooking up (recruitment) of additional rapidly reacting neurons. Of great importance alongside this increased reaction agility is a change with regard to the frequency information of the conditioning (adverse) noises. It could be shown (Edeline and Weinberger, 1992) that the selectivity of the neuronal elements adapts itself with particular sensitivity to the specific frequencies characteristic of the impinging sound [Figure - 2].
It is also of particular importance that a very close activating connection exists between the amygdala and the brain region of the hypothalamus (Feldman and Weidenfeld, 1998; Gray, 1991). The hypothalamus is the predominant center for vegetative-nervous or hormone regulation of the entire organism. This means that it is primarily responsible for rapid changes via the vegetative nervous system (e.g. in the cardiovascular system: increased heart rate, blood pressure) and for shifts of the hormone balance (e.g. stress hormone release).
A causal chain of peripheral and central (subcortical) activating systems is thus on hand, allowing explanation of the irritating and health impairing effects of longer term or often repeated sounds (Spreng, 2000a). It should be understood in front of this background why longer acting noises which cannot be influenced, of lower to average intensity but with specific frequencies (e.g. aircraft noises), can induce irritating stimulation and reactions which are otherwise only to be observed when the sound episodes are louder.
Very simply formulated and based on the plasticity of the amygdala, one can imagine the generation of noise effects from repeated undesirable sounds as follows: as a result of the stimulation sparked off by the impinging sounds, the amygdala will undergo such plastic changes under the influence of the simultaneously activated cerebral cortex (analysis of the sound episode: e.g. steep increase, characteristic frequency components) and that of the hippocampus, responsible for the more complex cognitive processes (analysis of the sound source: e.g. aircraft arrival, aircraft departure) that the entire organism becomes more sensitive to noises of this type. The end effect is that the pathway is cleared to a very fast and crude processing system which reacts to complex stimulants (e.g. aircraft sounds) with direct access to vegetative and hormone functional units as well as to emotional zones. This is without the time otherwise needed to become cognitively fully conscious of the situation, or semantically process the significance of the sounds in detail [Figure - 2].
It should be added that the functioning reaction system, routed this way but without appreciable conscious processing, will be almost fully active even during sleep, indeed it has to be fully active, based on evolutionary history (noises from hostile surroundings).
| Stress hormone, cortisol | | |
The stress hormone most important for noise effects, released as part of the causal chain auditory tract - amygdala - hypothalamus is cortisol. Key substance in this process is the corticotropin-releasing hormone (CRH), formed in the hypothalamus and several other regions of the brain with the purpose of coordinating stress and immune reactions, and the beginning of a hormone cascade. It reaches the pituitary gland via a special vascular system. The pituitary gland responds by secretion into the blood of corticotropin (ACTH: adrenocorticotropic hormone) produced in the POMC cells (proopiomelanocortin cells), which in turn stimulates the adrenal glands to release cortisol (hydrocortisone) and aldosterone. These most important stress hormones belong to the steroid hormones and, for example, step up the heart rate, sensitize the blood vessels for the hormones adrenaline and noradrenaline, and also influence many metabolic functions. The Aldosterone, released on stress stimulation, itself affects the peripheral regulatory mechanisms of the kidney (renin-angiotensin-aldosterone mechanism) and also enhances the excitability of the blood-vessel muscular system. This means that peripheral fine regulatory systems may be brought out of balance (e.g. reduction of the sensitivity of the regulatory effects of the baroreceptors by circulating angiotensin in the medulla) as a result of environmental influences, e.g. noise, or drowned out or over-activated by longer sound duration (Spreng, 1984). The effects of the antidiuretic hormone (ADH) also released from the hypothalamus may, under certain circumstances, be viewed as comparable to CRH, meaning a possible potentiation of the cortisol production, and via the kidney cause increase of the blood volume (hypertension).
Physiologically speaking, the cortisol level in the blood is subject to certain fluctuations, depending on the time of day. These circadian rhythm changes are observable beforehand in the concentration characteristics of the regulatory hormone, ACTH, which itself stimulates the cortisol secretion of the adrenal cortex cells. This pronounced endogenously fixed rhythm of the blood cortisol level during the day (with a range of approx. 5-30 µg/dl in the plasma) shows clearly higher values in the late morning than in the evening. It must be noted that these fluctuations are not dependent on sleeping habits and that any changes induced by sleep reversal (e.g. shift work, jet lag) are only slight and very slow to take effect. It should also be noted that the secretion of cortisol by the adrenal cortex of every human is episodic (peaks of up to 20 µg/dl), based on an equally episodic ACTH secretion (Voigt, 1994; Yasuda and Nakamura, 1997). Such episodes occur more frequently at night and in the early hours, leading to higher cortisol levels when stress instigating stimulation (e.g. noises at night) is of course particularly effective.
It is generally known for the organism that its regulatory systems, corresponding to the circadian rhythms governing them, react particularly strongly to stimulation in the early hours of the morning, and exhibit particularly weak retroactive regulation attributes (Spreng, 1997).
The negative health effects of a persistently elevated CRH and cortisol level have been known for some time, where direct and indirect effects of cortisol secretion in the fields of hemodynamics, endocrinopathy, metabolism and anthropometry have been described (for more details see Spreng, 2000b). Negative influences of this kind are observed in spite of the generally inhibitory feedback regulation of the hypothalamus-pituitary-adrenocortical axis, and are most probably due to a shift in the operational pivot of the system, basically caused by the influence of stress or over-activation (e.g. by the massive amygdala excitation inflow). In addition adrenalin and noradrenalin also produced under stress conditions to a certain extent counteract against the cortisol feedback regulation, which after all may be less sensitive during sleep.
Alongside this clearly defined causal chain, a further area of the hypothalamus (regio arcuata), able to produce the adrenocorticotropic hormone (ACTH) from corresponding precursors without a detour via the pituitary [Figure - 1], should not be neglected. ACTH produced this way, as well as the beta-endorphin which is also released there (Khachaturian et al., 1995), is transported into wide extra-hypothalamic regions of the brain via axonal transport mechanisms. As recently shown (Barna, 1997; Gomez-Sanchez et al., 1997), corticosteroids and aldosterone can be additionally produced this way in those regions of the brain reached.
| Conclusion | | |
Based on the causal chain closed by the amygdala as functional component between increased stimulation of the auditory system and increased activation of the hypothalamuspituitary-adrenocortical system (axis), as well as based on the triggering of extra-hypothalamic hormone effects, it can be explained why frequent sound stimulation, even below the limit of aural damage (noise deafness limit) and below the awakening threshold, may have health relevant effects (see below).
In addition, it also becomes clear that extra-aural noise effects of enormous diversity may occur in the vegetative sphere, and that over a longer period of time a large number of physiological regulatory mechanisms may be drowned out or destabilized, as a result of which numerous chronic functional disturbances or illnesses may arise.
This fact opens a wide field of connections between stress-dependent cortisol production and the disturbance of a large number of other endocrine processes, especially as a result of long-term stress activation by environmental influences such as environmental noise. In situations of this kind it has to be expected that negative influences on the entire hormone balance of the organism may occur [Figure - 1].
| Health impairment | | |
Sleep disturbances
Basically speaking, all changes in sleep characteristics caused by unwelcome sounds are to be regarded as sleep disturbances, not solely the process of awakening (UBA, 1992). Sleep disturbances are present, for example, if four subconscious arousal reactions occur in the night (arousal reactions fluctuate between 1 and 16 a night in the course of a natural, undisturbed night's sleep), one of which steps into the realm of consciousness. The same is true if an awake phase during the night lasts more than 20 to 30 minutes and a re-onset of sleep is not achieved. One also refers to sleep disturbances if the initial onset of sleep is delayed (longer than half an hour).
Sleep disturbances may in fact be assessed more quantitatively in terms of 2 criteria: on the one hand, the frequency of reactions (changes in the different sleep phases, distinguishable in the EEG between light and deep sleep), and on the other hand arousal reactions (Griefahn, 1990; Griefahn and Spreng, 2003).
With regard to noise impingement during sleep, particularly flight noise, a recommendation worthy of sensory physiological underlining is that orientation refer exclusively to the maximum level and not to the average level as in the awake state. Studies have shown that changes in sleep depth occur approx. from maximum levels of 55 dB(A) (frequency rises in EEG, lowering of peripheral circulation). The decisive role here is played by the sound level or sound level peaks. To a certain extent, however, the sound dynamics (steepness of the increase; difference to the background level), frequency components and informational content of the sound are also of significance, the duration of the individual sections less so.
If an additional awake phase is induced by noise, movements occur to a greater extent or deep sleep phases are shortened, which can be regarded as abnormal or damaging to health. Without a doubt, sleep disturbances of this nature can be compensated subsequently, provided they only occur occasionally. Longer deprivation of sleep on the other hand leads to detection of changes in the organism relevant to health risks (e.g. loss of vitamin B1, sinking iron level).
| Stress hormone secretions (especially at night) | | |
Particularly problematic, in fact, are not primarily the changes in depth of sleep, awake phases, movement increases etc., instigated by the exposure to sound during sleep, but rather the massive activation of the amygdala and consequently the hypothalamus which also occurs during sleep, as shown in [Figure - 2], and, above all, the stress hormone release (ACTH, adrenaline, noradrenaline, cortisol etc.) involuntarily activated as a result. Newer investigations (Maschke et al., 1995 and 1996) more specifically emphasize the increased cortisol secretion induced by exposure to the sound of flight noise at night, which, contrary to the adrenaline characteristics, is partially above the normally expected range (Spreng, 1996 and 1997), and as a result of its notably larger metabolizing time constants (cortisol: 60-130 min; adrenaline: < 3 min; noradrenaline: 7-12 min) may be cumulative during the night.
Taking into account the unusual large permeability of cortisol through the cell membranes and its immediate influence upon transcription processes widespread health effects may be assumed.
In contrast to an increased adrenaline concentration, a cortisol level permanently enhanced by noise effects signifies the risks of health impairment, e.g. the inhibition of glucose functions (diabetes), amplified protein and bone degeneration (osteoporosis), decline of immunoactive substances (immunosuppression, prolongation of the healing phase), increased effects of blood pressure raising hormones (hypertonia), buildup of blood cholesterol (cardiovascular damage, myocardial infarction), increased secretion of gastric juices (gastric ulcer) (Spreng, 1997 and 2000b).
Explicitly worthy of attention here are the studies of Samra et al. (1998), where effects on the regulation of lipolysis were found in cases of physiologically invoked hypercortisolism.
Generally speaking, as shown in [Figure - 2], the close linking of the key components, amygdala (fear conditioning center) in the auditory tract branch with the vegetative regulatory center of the hypothalamus is responsible for a wide range of changes in the homeostatic balance of the organism, which may in turn trigger other serious health disorders (Spreng, 1984 and 2000b).
The fact that the hypercritical values of cortisol secretion already mentioned were incurred in a noise situation of 16 overhead flights with peak levels of 55 dB(A) on the ear of the person asleep (Maschke et al., 1995), and were no longer significantly enhanced by level increases (e.g. 65 dB(A)) or frequency increases (e.g. 74 overhead flights), has to be assessed as an indication of the health risk of night-flight noise, at least between midnight and 4 a.m.
In addition to the above, the studies also question the current criterion of the awakening threshold (maximum level at least 60 dB(A)) (see below) and indicate the significance of a nocturnal vegetative threshold of physiological overproportional reactions, otherwise derived (see below), with a maximum level of 53 dB(A) on the ear of the person asleep.
| Estimation of a tolerable number of overhead flights at night | | |
The criterion 6 × 60 dB(A) on the ears of the person asleep was popularly used in the past for the assessment of nocturnal disturbances by aircraft noise (Jansen, 1973, Jansen et al.,1995). It maintains that 6 overhead flights with a maximum level of 60 dB(A) indoors at night are just about tolerable with regard to the avoidance of health risks.
This criterion is based on a predefined awakening threshold of L max = 60 dB(A) and a definition with reference to a once-only awakening provoked by 6 episodes of this kind. Since this value of 60 dB(A) is tagged at least with a standard deviation of +/- 7 dB(A), this itself would be a reason for arriving at a preventive specification of 53 dB(A). In addition to this, values for arousal thresholds quoted in the literature vary between 35 dB(A) and 65 dB(A) (e.g. Pearson et al., 1989; Griefahn, 1990; Hofmann, 1991; Ollerhead et al., 1992).
Finally, the above definition is based on handling a diffuse cloud of points, derived from several different studies, with the aid of simply adjusted compensatory/approximation straight lines (Griefahn et al., 1976). The use of more up-todate procedures (e.g. non-linear regression among others) is very likely to result in lower values for an arousal threshold derived from this original data.
Above all, however, the criterion 6 × 60 dB(A) says nothing about how many nocturnal flight episodes involving lower maximum levels (e.g. L max = 59 dB(A)) without health impairment are still tolerable. With the objective of tackling this problem at least as an estimation, a simple physiological model, exclusively based on cortisol secretion at night has been proposed (Spreng, 2002).
A summation (accumulation) of the cortisol increases during time T (in minutes) at night, derived from individual cortisol increases (ci), both initial and dependent on the level induced by flight episodes (equidistant intervals) after exponential degradation in each case (time constant t = 64 min) is calculated. This should not exceed a maximum tolerable normal value (C tol) - based on an average normal cortisol value in plasma (c m ). The toleration range defined this way (C tol - c m ) can be thought of in its first approximation as an addition in each case to the slow circadian changes of the plasma cortisol concentration.
The interconnection formulated in [Figure - 3] is the result, wherein the level dependency of the initial cortisol jumps, c i (assumed to be independent of the absolute concentration as a starting simplification), applies, in accordance with the direct and close relationship between cortical excitation and activation of the hypothalamic areas described at the outset. A quantitative relation can be derived in this respect, based on the stimulation-excitation link resulting from the auditory evoked response measurements in the human being (Spreng, 1976) (power function with exponent k = 0.32). A comparable exponent also results from psychophysical scaling experiments on auditory perception conducted by the Harvard psychologist Stevens (1961).
If a night-time vegetative threshold of overproportional reaction(L o ), itself still fully within the physiological range, is set with a maximal level value of L o = 53 dB(A) then values are found [Figure - 3] which permit a quantitative estimation of tolerable night-time overhead flights using the model proposed.
The setting of a vegetative threshold of physiological over-proportional reaction is based on the widely accepted fact that clear and readily measurable central nervous and vegetative changes with maximum levels between 60 and 65 dB(A) occur during noise exposure in the daytime. If the more central areas are observed in greater detail, a vegetative threshold of physiological over-proportional reaction of the central excitation system of a person awake is shown to occur under acute exposure to sound, with average momentary levels of 63 dB(A), on account of deviation of the evoked potentials from the normal characteristics of a person awake, shifts in frequencies of the characteristic currents emanating from the brain (EEG), as well as the appearance of secondary skinpotential changes instigated by the central excitation (Keidel and Spreng 1976: faster EEG alpha-rhythm equals slower EEG alpha-rhythm, deviations in the intensity function of the evoked potentials, significant skin current changes; Rovekamp, 1983: heart rate changes; Jansen et al., 1999: finger pulse amplitude). Of additional interest, the range of the loudest human voice at a distance of 2-4 m has levels around L max = 61-69 dB(A).
Since agreement also exists that the sensitivity of the organism is at least 10 dB lower (DiNisi et al., 1990, Jansen et al., 1995), the specification of a night-time vegetative over-proportional reaction threshold at L max = 53 dB(A) is entirely plausible.
If one uses this value [Figure - 3] a correlation is found to exist between the tolerable number of overhead flights at night and the maximum levels, as shown in [Table - 1] where the maximum range of sound levels on the ear of the person asleep, between L max = 70 dB(A) and L max = 40 dB(A), is listed.
It is particularly worth emphasizing that conversion of these values of tolerable maximum levels and overhead flight numbers, estimated with a physiological model, into equivalent continuous sound levels is in no way permissible.
The results of this purely physiologically based, and currently still very simplified model are in the upper range of levels are in fact present, the total number of night-time overhead flight episodes (even at lower sound level values) may never exceed the number recorded in [Table - 1]. In other words, if 6 episodes with a maximum level of 70 dB(A) occur in the 8 hours at night for example, then absolutely no further noise effects are tolerable, even with clearly lower maximum levels. This rigid statement may be effective only in case the physiological model will be improved taking into account for instance feedback regulations and other incidents.
In spite of its marked simplification the model presented here gains in plausibility if one extrapolates the calculation on one side to a single still tolerable night-time episode. The result obtained (for a 10 dB(A)-down-time of 20 sec duration) is SEL = 125 dB(A) (SEL=Sound Exposure Level), corresponding well to the limiting value, below which aural damage to the sense of hearing in the inner ear is highly unlikely (Spreng et al., 1992).
On the other hand - although this is not allowed in principle - the values calculated from the lower maximum level range of the model roughly approach that of an equivalent continuous sound level of L eq < 30 dB(A). This value serves the purpose of avoiding sleep disturbances in living quarters and should not be exceeded according to the specification of the interdisciplinary working circle of the Federal Environment Agency (UBA, 1982).
Comparison with the relatively few individual literature quotations of the number of tolerable overhead flights at night, which are not, however, based on a purely physiological estimation procedure, also reveals values confirming the present model.
Griefahn (1990), for example, has published a critical maximum level L max = 53 dB(A) which, among other aspects, should not be exceeded during as few as 10 overhead flights per night. The present model yields a tolerable value of 13 overhead flights at night for the said value of L max = 53 dB(A).
Vallet and Vernet (1993) require that indoor values of L max = 40 dB(A) for between 20 and 25 night-time overhead flights should not be exceeded. In terms of the physiological model a tolerable number of 23 overhead flights at night are to be found in [Table - 1] for a level of L max = 40 dB(A).
Finally, the results published by Maschke et al., 1995 who determined increased cortisol nighttime values after 16 aircraft noise episodes with L max = 55 dB(A) within 4 hours at night, also fits the model. Recalculation using the reduced scale of effect of only 4 hours at night (instead of 8 hours) produces a tolerable number of only 8 aircraft noise episodes for the chosen maximum level of L max = 55 dB(A). The night-time cortisol level increases induced by aircraft noise and ascertained by Maschke et al., 1995 are most probably attributable to the fact that the twice as many episodes were used in these experiments than would have been tolerable from the physiological conditions.
At least it should be mentioned that the results of the physiological model match almost perfectly the number and level values (NALvalues) determined for the probabilities of awakenings in the largest study ever done on the effect of aircraft noise on sleep (Basner et al., 2001; Griefahn and Spreng, 2003).
| Acknowledgment | | |
Dedicated with gratitude to my honored mentor, Prof. Dr., Dr. h. c. W. D. Keidel, on the occasion of his 85 th birthday[50]
| References | | |
| 1. | Barna, I.; Koenig, J. I.; Makara, G. B. (1997) Effects of anterolateral and posterolateral cuts around the medial hypothalamus on the immunoreactive ACTH and Beta-Endorphin levels in selected brain regions of the rat. Brain Res. Bull. 42: 353-357  |
| 2. | Basner M., Buess H., Luks N., Maa3 H., Mawet L., Muller E.W., Muller U., Piehler C., Plath G., Quehl J., Rey E., Samel A., Schulze M., Vejvoda M. and Wenzel J. (2001) Nachtfluglarmwirkungen - eine Teilauswertung von 64 Versuchspersonen in 832 Schlaflabornachten. DLRForschungsbericht, 2001-26, ISSN 1434-8454 |
| 3. | DiNisi, J., Muzet, A., Ehrhart, J.,Libert, J. P.(1990) Comparison of cardiovascular responses to noise during waking and sleeping in humans. Sleep, 13: 108-120 |
| 4. | Edeline, J-M.; Weinberger, N. M. (1992) Associative retuning in the thalamic source of input to the amygdala and auditory cortex: Receptive field plasticity in the medial division of the medial geniculate body. Behav. Neurosci. 106: 81-105 |
| 5. | Feldman, S. ; Weidenfeld, J. (1998) The excitatory effects of the amygdala on hypothalamic-pituitary- adrenocortical responses are mediated by hypothalamic norepinephrine, serotonin, and CRF-41. Brain Res. Bull., 45: 389-393 |
| 6. | Gomez-Sanchez, C. E.; Zhou, M. Y.; Cozza, E. N.; Morita, H.; Foeking, M. F.; Gomez-Sanchez, E. P. (1997) |
| 7. | Aldosteron biosynthesis in the rat brain. Endocrinology, 13: 3369-3373 |
| 8. | Gray, T. S. (1991) Amygdala role in autonomic and neuroendocrine responses to stress. In Stress, neuropeptides an systemic disease. Academic Press, New York, pp 37-53 |
| 9. | Griefahn, B., Jansen, G., Klosterkotter, W. (1976) Zur Problematik larmbedingter Schlafstorungen - eine Auswertung von Schlafliteratur. Umweltbundesamt, Berichte 4/76, Berlin |
| 10. | Griefahn, B. (1990) Praventivmedizinische Vorschlage fur den nachtlichen Schallschutz. Z. Larmbekampfung, 37: 4 -14 |
| 11. | Griefahn, B; Spreng, M. (2004) Disturbed sleep patterns and limitation of noise. Noise and Health 6(22): 27-33 |
| 12. | Hofmann, W. (1991) Vliegtuiglawaai, sleep en gezondheid. Een literatuurstudie. Gezondheidsraad (Publikatie Nr. A91/01), Den Haag |
| 13. | Jansen, G. (1973) Grenz- und Richtwerte in der Larmbekampfung. Kampf dem Ldrm, 3: 71-78 |
| 14. | Jansen, G., Linnmeier, A., Nitzsche, M. (1995) Methodenkritische Uberlegungen und Empfehlungen zur Bewertung von Nachtfluglarm. Z. f. Larmbekampfung, 42: 91-106 |
| 15. | Jansen, G., Notbohm, G., Schwarze, S. (1999) Gesundheitsbeeintrachtigungen durch umweltbedingten Larm. In Umwelt und Gesundheit, Rat der Sachverstandigen fur Umweltfragen, ed., MetzlerPoeschel, Stuttgart, pp. 249-343 |
| 16. | Keidel, W. D., Spreng, M. (1976) Neuro-elektrophysiologische Larmbewertung. Forschungsbericht BMI/UB II 5520-01, (Techn. Inf. Biblio. AC 2890, Hannover) Inst. Physiologie u. Biokybernetik, Uni Erlangen |
| 17. | Khachaturian, H.; Lewis, M. E.; Tsou, K.; Watson, S.J.(1995) Beta-endorphin, Alpha-MSH, ACTH, and released peptites. In : Handbook of Chemical Neuroanatomy. Vol. 4. BjOrklund, A. and Hokfelt, T., eds. Elsevier, Amsterdam, pp 216-272 |
| 18. | LaBar, K. S.; Gatanby, J. C.; Gore, J. C.; LeDoux, J. E.; Phelps, E.A.(1998) Human amygdala activation during conditioned fear aquisition and extinction: A mixed-trial fMRI study. Neuron, 20: 937-945 |
| 19. | LeDoux, J. E. (1990) Information flow from sensation to emotion: Plasticity in the neural computation of stimulus value. In Learning and Computational Neuroscience: Functions of Adaptive Networks. Gabriel, M and Moore, J. eds. MIT-Press, Cambride etc., pp 2-51 |
| 20. | LeDoux, J. E. (1995) Emotion: Clues from the brain. Ann. Rev. Psychol., 46: 209-235 |
| 21. | Lennartz, R. C.; Weinberger, N. M. (1992) Frequency-specific receptive field plasticity in the medial geniculate body induced by Pavlovian fear conditioning is expressed in the anesthesized brain. Behav. Neurosci. ,106: 484-497 |
| 22. | Maschke, C.; Ising, H.; Arndt, D. (1995) Nachtlicher Verkehrslarm und Gesundheit: Ergebnisse von Labor- und Feldstudien. Bundesgesundheitsblatt , 4: 130-137 |
| 23. | Maschke, C.; Arndt, H.; Ising, H.; Laude, D.; Thierfelder, W,; Contzens, S.(1995) Nachtfluglarmwirkungen auf Anwohner. G. Fischer, Stuttgart |
| 24. | Maschke, C.; Pleines, F. (1996) Nachtfluglarmwirkungen und ihr EinfluB auf die Gesundheit. In DAL, Hrsg.: Der Luftverkehr im Spannungsfeld zwischen Gesundheit, Politik und Wirtschaft. DAL Informationszentrum, Dusseldorf, pp. 21-38 |
| 25. | Masterton, R. B. (1996) Role of the mammalian forebrain in hearing. In Acoustical Signal Processing in the Central Auditory System. Syka, J.,ed. Plenum Press, New York-London, pp 1-17 |
| 26. | Ollerhead, J. B., Jones, C. J.,Cadoux, R. E. et al. (1992) Report of a field study of aircraft noise and sleep disturbance. Civil Aviation Authority, London |
| 27. | Osada, Y., Tsunashima, S., Yoshida, K. (1972) Effects of train and jet aircraft noise on sleep. Bull. Inst. Public Health (Tokyo), 21: 133-138 |
| 28. | Osada, Y., Ogawa, S., Ohkubo, Ch., Miyazaki, K. (1974) Experimental study of sleep interference by train noise. Bull. Inst. Of Public Health (Tokyo), 23: 171-177 |
| 29. | Passchier-Vermeer, W. (1993) Noise and Health. Health Council of the Netherlands (Pub. A93/02E), Den Haag, Pearson, K. S., Barber, D. S., Tabacknick, B. G. (1989) Analysis of predictability of noise-induced sleep disturbance. BBN Systems and Technologies Co., Canoga Park |
| 30. | Quirk, G. J., Repa, J. C., LeDoux, J. E. (1995) Fear conditioning enhances short-latency auditory responses of lateral amygdala neurons: Parallel recordings in the freely behaving rat. Neuron ,15: 1029-1039 |
| 31. | Rovekamp, A. J. M. (1983) Physiological effects of environmental noise on normal and more sound-sensitive human beings. In Noise as a Public Health Problem, Vol.1, Rossi, G. ed., Edizione Tecniche (Amplifon), Milano, pp 605-614 |
| 32. | Rogan, M. T,, LeDoux, J. E. (1975) LTP is accompanied by commensurate enhancement of auditory-evoked responses in a fear conditioning circuit. Neuron, 15: 127-136 |
| 33. | Samra, J. S.; Clark, M. L.; Humphreys, S. M.; MacDonald, I. A.; Bannister, P. A.; Frayn, K. N. (1998) Effects of physiological hypercorticosolemia on the regulation of lipolysis in subcutaneous adipose tissue. J. clin. Endocrinol. Metab., 83: 626-631 |
| 34. | Spreng, M. (1976) Grenzen der sensorischen Informationsverarbeitung des Menschen. Naturwiss. Rundschau, 29: 377-386 |
| 35. | Spreng, M. (1980) Addition verschiedener Larmeinflusse In Ldrmschdden des Ohres, Berg, M. .ed. Thieme, Stuttgart, pp 71 - 76 |
| 36. | Spreng, M. (1984) Risikofaktor Larm - Physiologische Aspekte. Therapiewoche, 34: 3765-3772 and In Risikofaktoren der Umwelt. von Eiff, A. W. ed., Schattauer-Verlag, Stuttgart-New York |
| 37. | Spreng, M. (1985) Noise effects on auditory and vegetative control systems in man. In Proc. Inter-Noise °85, Federal Inst. Occup. Safety, ed., Wirtschaftsverlag NW Bremerhaven, pp 969-972 |
| 38. | Spreng, M. (1994) Physiologie des GehOrs. In PhoniatriePadaudiologie Biesalski, P; Frank, F. eds., Thieme, Stuttgart, pp 1 - 47 |
| 39. | Spreng, M. (1996) Gutachterliche Stellungnahme Verwaltungsrechtstreit Flughafen Hahn (7C 11843/93.OVG Koblenz). Erlangen |
| 40. | Spreng, M. (1997) Kritische Betrachtung des Schienenbonus anhand horphysiologischer/medizinischer Fakten. Tagungsband: Fachseminar Schienenldrm Institut far Okologische Studien, Munchen, pp. 19-29 |
| 41. | Spreng, M. (2000a) Central nervous system activation by noise . Noise and Health, 7: 49-57 |
| 42. | Spreng, M. (2000b) Possible health effects of noise induced cortisol increase. Noise and Health, 7: 59-63 |
| 43. | Spreng, M. (2002) Cortical excitation, cortisol excretion, and estimation of tolerable nightly over-flights Noise and Health , 4, 16: 39-46 |
| 44. | Spreng, M., Leupold, S., Firsching, P. (1992) Gehorschaden durch Impulslarm. Schriftenreihe der Bundesanstalt fiir Arbeitsschutz Fb 630, Wirtschaftsverlag NW, Bremerhaven, 1991 and |
| 45. | Gehorschadensrichtige Bewertung impulsiver und tonaler Industrieschalle: Versuch eines Einwertzuschlags. Z. f. Larmbekampfung, 39: 31-38 |
| 46. | Stevens, S. S. (1961) The psychophysics of sensory function. In Sensory Communication, Rosenblith, W. A. ed., MIT Press and John Wiley 6 Sons, Inc., New York - London, pp. 1-33 |
| 47. | UBA, Interdiziplinarer Arbeitsskreis fur Larmwirkungsfragen. (1982) Beeintrachtigung des Schlafs durch Larm. Z. f. Larmbekampfung 29: 13-16 |
| 48. | Vallet, M, Vernet, I. (1996) Night aircraft noise index and sleep research. In Noise and Disease, Ising, H., Kruppa, B, eds.. Gustav Fischer Verlag, Stuttgart-New York, pp 467468 |
| 49. | Voigt, K. (1994) Endokrines System. In Lehrbuch der Physiologie, Klinke, R; Silbernagel, S., eds., Thieme, Stuttgart_New York |
| 50. | Yasuda, N.; Nakamura, K. (1997) Heterogeneity of corticotropin-releasing factor (CRF). Jap. J. Physiol., 47: 147-159 |
Correspondence Address:
M Spreng
Dept. Physiology/Biocybernetics, University of Erlangen, Universitaetsstrasse 17,D-91054 Erlangen
Germany
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 15070527 
[Figure - 1], [Figure - 2], [Figure - 3]
[Table - 1] |
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