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Stress hormones in the research on cardiovascular effects of noise
Division of Environment and Health, Federal Environmental Agency, 14191 Berlin, Germany
Department of Environment and Health, Federal Environmental Agency, P. O. Box 33 00 22, 14191 Berlin
In recent years, the measurement of stress hormones including adrenaline, noradrenaline and cortisol has been widely used to study the possible increase in cardiovascular risk of noise exposed subjects. Since endocrine changes manifesting in physiological disorders come first in the chain of cause-effect for perceived noise stress, noise effects in stress hormones may therefore be detected in populations after relatively short periods of noise exposure. This makes stress hormones a useful stress indicator, but regarding a risk assessment, the interpretation of endocrine noise effects is often a qualitative one rather than a quantitative one. Stress hormones can be used in noise studies to study mechanisms of physiological reactions to noise and to identify vulnerable groups. A review is given about findings in stress hormones from laboratory, occupational and environmental studies.
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Babisch W. Stress hormones in the research on cardiovascular effects of noise.Noise Health 2003;5:1-11
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Babisch W. Stress hormones in the research on cardiovascular effects of noise. Noise Health [serial online] 2003 [cited 2020 May 27 ];5:1-11
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Traffic noise causes stress reactions similar to other stressors in the occupational and ambient environment (Grunberg and Singer, 1990). In these situations of sympathetic and endocrine arousal, concentrations of stress hormones in the blood are increased. Energy and oxygen are mobilized in order to prepare the organism for fight-flight response to cope with the stressor (Ising and Braun, 2000, Spreng, 2000). During sleep even low indoor levels of traffic noise are sufficient to bring about such reactions. Stress research in general as well as noise stress research has shown that to a certain degree habituation leads to a reduction of acute stress effects, even when the stressful situation remains unchanged. However, this kind of adaptive behaviour may be associated in the long run with physiological costs (Sapolsky et al., 1986). Short-term studies on acute noise effects give only limited insight into the long-term health effects (Tafalla and Evans, 1997). With regard to decision making in public health, findings from epidemiological studies deserve particular attention.
Although not being a risk factor as such (in epidemiological terms), stress hormones like adrenaline, norepinephrine and cortisol can be viewed as reliable stress indicators (Vaernes et al., 1982, Grunberg and Singer, 1990, Baum and Grunberg, 1995). Stress hormones are easy to measure non-invasively, and appear to be an attractive outcome for epidemiological studies. They are particularly useful for investigating biological mechanisms, and play a crucial role in the metabolism of the organism, where they act as bio-messengers and neuro-transmitters in the regulation of autonomic and other physiological functions (Silbernagl and Despopoulos, 1991, Fauci et al., 1998). They are part of a complicated system of positive and negative feedback mechanisms affecting: the activity of the heart, blood pressure, blood lipids, blood glucose, blood clotting and blood viscosity. All these are established biological risk factors for hypertension, arteriosclerosis or myocardial infarction (Chrousos and Gold, 1992, Baum and Grunberg, 1995), when considering the causeeffect chain, i.e.: sound - annoyance (noise) - physiological arousal (stress indicators) - changes in biological risk factors - morbidity - mortality (Babisch et al., 2001). Long-term effects on the cardiovascular system are specifically focused in this respect (Anticaglia and Cohen, 1970, Cryer, 1980, Sapolsky et al., 1986, Cohen et al., 1995, Babisch, 2000). The important role of stress hormones in the haemostasis is summarized in [Table 1],[Table 2],[Table 3] regarding changes relevant for an increase in cardiovascular risk ("+" = increase, "-" = decrease).
In studies, free catecholamines have been analysed in plasma and urine using standard biochemical and electrochemical methods. Regarding corticosteroids, different procedures and derivates have been used to determine adrenal-cortical activity (total or free cortisol, hydroxycorticosteroids, ketosteroids). New studies have tended to focus on free cortisol in plasma or urine including certain metabolites such as 20α-dehydro-cortisol; a few have considered saliva. However, due to strong circadian and weekly rhythms of hormone excretion, epidemiological studies may suffer from methodological problems when only certain parts of the day/night are considered for sampling. Problems may also arise from too short observation periods in experiments regarding the longer half-life time constants (cortisol: about 70 minutes) of the hormone metabolism (Baum and Grunberg, 1995).
The potential health hazard of noise may be underestimated in epidemiological studies if effect-modifying factors such as: effort, discomfort, informational content, predictability and controllability of the noise, the individual's attitude towards the noise stressor and interactions with other stressors, are not taken into account (Westman and Walters, 1981, Lundberg, 1984, Breier et al., 1987, Tafalla and Evans, 1997).
Studies where industrial noise was the source of experimental noise exposure, revealed increases primarily in the norepinephrine levels of the exposed subjects (Levi, 1961, Levi, 1967, Ortiz et al., 1974, Andren et al., 1982, Buczynski and Kedziora, 1983, Tafalla and Evans, 1997). Increases in the adrenaline levels of the exposed subjects were also seen (Levi, 1961, Levi, 1967, Ortiz et al., 1974, Buczynski and Kedziora, 1983, Fruhstorfer et al., 1990). Regarding corticosteroids, only initial responses were seen during exposure sessions (Favino et al., 1973). Exposure to industrial noise was associated with higher corticoid excretion than for exposure to heat (Sakamoto, 1957). Generated broad-band noises (e.g., white or pink noise) and tonal sounds were associated with increases of catecholamines (Hawel and Starlinger, 1967, Arguelles et al., 1970, Slob et al., 1973, Klotzbiicher, 1976, Frankenhaeuser and Lundberg, 1977, Lundberg and Frankenhaeuser, 1978, Andren, 1982, Andren et al., 1983, Breier et al., 1987) and corticosteroids (Arguelles et al., 1962, Cantrell, 1974, Lundberg and Frankenhaeuser, 1978, Brandenberger et al., 1980, Follenius et al., 1980, Yamamura and Aoshima, 1980, Yamamura et al., 1982, Fruhstorfer et al., 1983, Iwamoto et al., 1985, Breier et al., 1987, Miki et al., 1998). Studies with aircraft noise often referred to sleep disturbances, showing increases in catecholamines (Osada et al., 1972, Maschke et al., 1992, Maschke et al., 1993, Maschke et al., 1995) and cortisol levels (Maschke et al., 1997, Maschke et al., 1998, Harder et al., 1999). However, decreases were also found (Atherley et al., 1970, Maschke et al., 1998, Harder et al., 1999). Other ambient noise sources including road traffic noise were associated with increases in catecholamines (Tatai et al., 1965, Verdun di Cantogno et al., 1976, Arvidsson and Lindvall, 1978, Ising et al., 1980a, Ising, 1983, Ising and Giinther, 1983, Tafalla and Evans, 1997, Ising and Braun, 2000) and corticosteroids (Tatai et al., 1965, Tafalla and Evans, 1997, Ising and Braun, 2000, Braun, 2001). High intensity sounds from jet engines or low flying military aircrafts evoked increases in cortisol or ACTH levels (Marth et al., 1988, Curio and Michalak, 1992, Curio and Michalak, 1993, Ising and Braun, 2000), but decreases were also observed (Bugard et al., 1953). Shooting sounds were associated with increases in catecholamines (Buczynski and Kedziora, 1983, Siegmann et al., 1999). Low frequency noise during sleep caused a decline of the awakening response of cortisol (Wiist et al., 2000) measured in saliva (Persson Waye et al., 2001). Music was associated with increases in norepinephrine and cortisol (Bergomi et al., 1991/92), and low frequency noise with a decrease in corticosteroids (Bondarev et al., 1970) (cited/reference in (Scheidt et al., 1986)) and an increase in adrenaline levels (Ising and Braun, 2000). Intermittent noise caused stronger effects than steady state noise (Yamamura et al., 1982, Buczynski and Kedziora, 1983). Negative findings (no noise effects) were also found in some laboratory studies (Tatai et al., 1967, Favino et al., 1971, Brandenberger et al., 1977, Sato et al., 1980, Yamamura et al., 1981, Carter et al., 1994, Gilbert et al., 1997).
There are indications that noise, particularly at lower levels, was associated with elevated stress hormones when interacting with mental tasks or other performances that require high concentration or effort (arithmetic tests, complex work, rush and critical control) (Levi, 1961, Tatai et al., 1965, Hawel and Starlinger, 1967, Levi, 1967, Tatai et al., 1967, Klotzbiicher, 1976, Frankenhaeuser and Lundberg, 1977, Arvidsson and Lindvall, 1978, Lundberg and Frankenhaeuser, 1978, Brandenberger et al., 1980, Ising et al., 1980a, Ising and Giinther, 1983, Breier et al., 1987, Tafalla and Evans, 1997, Miki et al., 1998, Ising and Braun, 2000). Increases of catecholamines were found in subjects performing physical exercise (Buczynski and Kedziora, 1983). Factors including gender (no clear picture) (Osada et al., 1972, Dugue et al., 1994, Harder et al., 1999, Braun, 2001), younger in age (Osada et al., 1972), low tolerance (Levi, 1961), high annoyance (Arvidsson and Lindvall, 1978), controllability of the noise (Lundberg and Frankenhaeuser, 1978, Breier et al., 1987), cardiovascular disorders (Arguelles et al., 1970, Andren, 1982, Andren et al., 1983), psychoneurotic problems (Arguelles et al., 1962), metabolic dysfunction (Verdun di Cantogno et al., 1976), well being (Maschke et al., 1998, Harder et al., 1999) and "negative Mgelectrolyte-balance" (Harder et al., 1999) were identified as potential effect modifiers. Modifiers of exposure such as the length of intermittent sound pulses (Yamamura and Aoshima, 1980) and window opening (Ising and Braun, 2000, Braun, 2001) had an impact on the excretion of stress hormones. Some studies gave some idea about the presence of a dose response relationship or threshold levels (Cantrell, 1974, Iwamoto et al., 1985, Maschke et al., 1993, Maschke et al., 1997).
[Table 4] summarises the results of epidemiological studeis on the association between noise and stress hormones. According to the model suggested by Ising (Ising and Braun, 2000), increases in norepinephrine levels in blood or urine are to be expected under habitual noise. This is a fairly consistent finding amongst cross-sectional studies on occupational noise (Manninen and Aro, 1979, Cesana et al., 1982, Bolm-Audorff et al., 1985, Cavatorta et al., 1987, Sudo et al., 1996, Ising and Braun, 2000). However, higher levels of adrenaline (Cavatorta et al., 1987, Sudo et al., 1996) and cortisol (Rai et al., 1981) were also found in body fluids as compared with subjects exposed to less noise. Interventional studies (field experiment) where noise exposure was manipulated by the use of ear protection in the occupational environment showed higher excretions of stress hormones under unprotected noise conditions (Ising et al., 1980b, Ising et al., 1980c, Bolm-Audorff et al., 1985, Melamed and Bruhis, 1996, Sudo et al., 1996). Community noise including road, air and rail traffic was associated with higher catecholamine (Evans et al., 1995, Evans et al., 1998, Babisch et al., 2001) and cortisol levels (Schulte and Otten, 1993, Evans et al., 2001, Ising and Ising, 2002) in urine where the subjects were exposed to higher noise levels. In a small pilot study a nonsignificant tendency towards higher salivary cortisol levels, particularly in the early afternoons and evenings, was seen in those subjects exposed to higher traffic noise levels than those exposed to lower noise levels (Poll et al., 2001). In contradiction to this, no or negative associations were reported in new aircraft noise studies. The concentrations of stress hormones in urine were lower despite the children and adults being exposed to higher noise levels (Kastka et al., 1999, Haines et al., 2001b, Stansfeld et al., 2001). In studies, where cortisol was measured in blood or saliva, no association or a tendency towards lower blood cortisol levels was found in the higher noise-exposed groups of subjects as compared to the lesser exposed (Babisch and Ising, 1986, Haines et al., 2001a, Stansfeld et al., 2001). However, this may partly be due to incomplete control of the circadian rhythm of cortisol excretion, or superimposing acute effects of momentary arousal, independent of noise, rather than a state of chronic stress.
A longitudinal study on changes of aircraft noise exposure after inauguration of a new airport revealed an increase in concentrations of stress hormones in children (Evans et al., 1998). One study did not show any noise effects in stress hormones, which may be due to too low exposure (Ising et al., 1999, Ising and Braun, 2000). Shift work (Cesana et al., 1982), fear of low flying jet fighters (Schulte and Otten, 1993) and coping styles (closing the window) (Babisch et al., 1996, Babisch et al., 2001) were identified as effect-modifiers. All in all, there seems to be fairly consistent results regarding occupational noise exposure, showing higher levels of stress hormones in higher exposed groups of subjects. As far as ambient noise levels are concerned, the results appear to be less convincing in this respect.
Activation of the neuroendocrine system usually depends upon the individual's recognition of a stressor as a threat (Westman and Walters, 1981, Vaernes et al., 1982). The auditory system, however, automatically activates the reticular activating system and hence can evoke autonomic-neuroendocrinic responses. Dysfunction resulting from sound stressors may be due to direct and/or indirect perceptions of sound (Westman and Walters, 1981, Babisch et al., 2001).
In experimental studies with humans carried out in the laboratory, unequivocal findings of noise exposure on the endocrine system have been sometimes observed. However, exposure conditions vary considerably between experiments. Metabolic time constants and clearance rates were not always taken adequately into account (Cryer, 1980, Baum and Grunberg, 1995). Problems arose from the fact that the experimental situation is stressful in itself and possibly masks the noise effect. Furthermore, secretory patterns of hormone excretion vary between individuals and are subject to pulsatile bursts, circadiane and weekly rhythms (Cryer, 1980, Baum and Grunberg, 1995, Maschke et al., 2000). This is a particular problem in the interpretation of findings for cortisol. Different biochemical methods and indicators of adrenal cortical activity applied make it often difficult to compare results from different studies.
Under habitual noise, increases in norepinephrine levels are to be expected. On the other hand, discomfort, emotional stress and non-habituated noise are associated with increased adrenaline excretion (Tafalla and Evans, 1997, Ising and Braun, 2000). Both mechanisms refer to the "defence" reaction (threat of control) (Henry and Stephens, 1977). Helplessness and depression are associated with increases of ACTH and corticosteroids (Checkley, 1996, Lundberg, 1999). This mechanism refers to the "defeat" reaction (loss of control) (Henry, 1992). However, it should be stated that this theoretical distinction between "defence" and "defeat" response is fluent. All three hormones tend to respond to stimuli that signal threat which may result in a defence and/or defeat response. Marked decreases in cortisol level may be due to a mild type of anxiety-depression syndrome where the anxiety is associated with increased sympathetic tonus and the depression reflects diminished adrenalcortical activity (Atherley et al., 1970). It was reported that in the absence of effort, noise does not increase physiological stress (Tafalla and Evans, 1997).
It is not clear as to what extent findings from experimental studies on endocrine responses of noise reflect a potential health hazard (Henry and Stephens, 1977, Cryer, 1980, Sapolsky et al., 1986). Using toxicological criteria, the observed effects may be interpreted in terms of "lowest observed effect levels" (LOEL). The results of epidemiological studies may reflect chronic states of stress, including processes of long-term compensation, habituation and physiological costs. As to what extent the findings can be interpreted in terms of „lowest observed adverse effect levels" (LOAEL), which would be relevant for a risk assessment, further clarification is needed (Babisch, 2002).
Integrating measurements of chronic stress response carried out in urine may be more reliable than spontaneous measurements of stress hormones at a particular point in time (plasma, saliva), because they are less susceptible to time patterns of hormone excretion (Baum and Grunberg, 1995). They may reflect better chronic dysfunction and a potential health risk, because the figures are not just a momentary state of arousal (Baum and Grunberg, 1995). A good correlation was found between the overnight collection and the total 24h collection of urinary catecholamines, if the ratio of catecholamine excretion to creatinine concentration is used to adjust for the renal filtration rate (Alessio et al., 1985, White et al., 1995). On the other hand, attempts have been made to improve the interpretation of short-term salivary cortisol measurements (Baum and Grunberg, 1995, Kirschbaum and Hellhammer, 1999). Changes of the steep increase ("morning rise") of cortisol within 45 minutes after awakening (preferable measured in saliva) may be a clinical manifestation of increased "allostatic load" (Lundberg, 1999, Wust et al., 2000a, Wiist et al., 2000b). Other authors suggest that a reduced decay of cortisol concentration during the early hours of sleep may be a clinical indicator of disturbed hypothalamo-pituitary-adrenal (HPA) axis activity, and thus a good indicator to assess acute and chronic stress effects due to noise (Born and Fehm, 2000). Small effects may best be detectable when the organism is at its nadir (minimum) of normal physiological arousal. The variability of free cortisol during the day, measured in saliva, was also used as an indicator of disturbed HPA axis regulation (Rosmond and Bjorntop, 2000). Under chronic stress the HPA axis becomes less plastic with less differences between morning and evening values (Dallman, 1993). In sleep-dept subjects relative rises of salivary cortisol levels in the afternoon and early evening were found (Spiegel et al., 1999). This may give a link to possible after-effects of noise disturbed sleep. Clinical research suggests that elevated plasma cortisol levels particularly in the evening may be adversely associated with glucose regulation, due to increases in serum insulin and reduced insulin clearance (Plat et al., 1999). Until now, it does not seem to be clear how the methods of cortisol measurement are related to one another, and which would to be the preferred one in epidemiological research to assess chronic noise induced stress effects. Saliva appears to be an attractive medium for the measurement of cortisol from a practical point of view. However, in large-scale studies only a few measurements throughout the day are applicable to assess changes in circadian patterns of cortisol excretion.
Current noise research in general, does not need to prove any longer the noise/stress hypothesis as such. It is common knowledge that noise is a psycho-social stressor that can affect physiological functioning. However, decisionmaking relies on quantitative risk assessment. This calls for standardized methods of the measurement of endocrine indicators of chronic stress on the one hand, and reliable clinical data on the other hand that allows the prediction of the quantitative impact of chronic changes in stress hormones on the subsequent development of diseases (incidence). Independent of any pathological manifestation, stress hormones may be particularly useful in identifying risk groups, interactions with other factors (combined exposures) or effect modifiers of the individual for coping with the noise stressor (Babisch et al., 2001). For example, stress hormones can be applied in experimental and epidemiological studies to answer questions such as:
Are noise-exposed subjects possibly at higher risk for stress-related diseases? Is train noise less harmful than road traffic noise?
Do males react stronger than females?
Are subjectively noise sensitive subjects a risk group?
Is sound insulation an effective measure to reduce noise-related stress reactions?
Has the attitude towards the noise source an impact on the stress response to noise? Which individual factors modify the reagibility towards noise?
Is there a dose-response relationship between exposure and perceived physiological stress? Etc.
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