Noise has the potential to cause stress reactions. Chronic noise-induced stress accelerates the ageing of the myocardium and thus increase the risk of myocardial infarction. The involved pathomechanisms include acute increase of catecholamines or cortisol under acute noise exposure and an interaction between endocrine reactions and intracellular Ca/Mg shifts. Chronic noise exposure of animals on a diet with suboptimal magnesium content led to increase of connective tissue and calcium, and decrease of magnesium in the myocardium. These changes were correlated to noradrenaline and normal ageing. Post mortem studies of hearts from victims of ischemic heart diseases confirmed the importance of Ca/Mg shifts in humans. Recent epidemiological studies support the importance of noise as a risk factor in circulatory and heart diseases, especially in myocardial infarction.
Keywords: stress, catecholamines, cortisol, calcium, ageing, myocardial infarction.
|How to cite this article:|
Ising H, Babisch W, Kruppa B. Noise-induced endocrine effects and cardiovascular risk. Noise Health 1999;1:37-48
| Introduction|| |
There is increasing epidemiological evidence that chronic noise exposure increases the cardiovascular risk, especially the risk of ischemic heart disease. (For recent reviews see Schwarze and Thompson, 1993; Babisch, 1998 a and b). The theoretical basis of the epidemiological noise and health studies is the non-specific stress effect of noise. For methodological reasons much of the work was concentrated on noise-induced vasoconstriction and increase of blood pressure. However, the epidemiological evidence is pointing more to a noise-related risk increase of myocardial infarction (MI) than of hypertension (Babisch, 1998 a and b). Since hypertension is only one of a long list of risk factors in MI, noise seems to affect other risk factors more than the blood pressure. One of the most important risk factors in MI is age, or more precisely the biological age of the heart. In the following we will study some effects of acute and chronic noise exposure on several risk factors in MI, including some parameters which are related to the biological age of the heart. To limit the length of this paper we will omit noise effects on vasoconstriction and blood pressure.
Noise-induced stress reactions
Acute exposure to maximal sound pressure levels above 90 dB(A) has the potential to cause inner ear hearing loss and to stimulate the sympathetic nervous system into increasing the release of adrenaline and noradrenaline. We found an increase of noradrenaline in persons exposed to habitual work noise. [Figure - 1] shows the differences of noradrenaline (NA) in 14 workers who were exposed to noise levels of Leq = 95 - 102 dB(A), when working for one day without ear protectors and Leq = 82 -99 dB(A) and for one day with ear protectors. In the subgroup of persons with low Mg content in the erythrocytes, the noise induced increase of noradrenaline was nearly double as compared with persons with high erythrocytes-Mg (Ising et al. 1980a).
In contrast to this, non habitual noise caused an increase of adrenaline. 51 test persons worked for 2 days under exposure to car racing noise with Lmax = 100 dB(A) and Leq = 85 dB(A) and for one day in quiet conditions (Leq < 50 dB(A)). A significant increase of adrenaline excretion was observed. This was accompanied by a decrease in erythrocytes-Mg and increase in Serum-Mg, Mg-excretion and total cholesterol in blood serum. The latter is a risk factor of myocardial infarction (MI) see [Table - 1] (Ising et al. 1980b).
Noise levels above 120 dB(A) increase cortisol in humans and animals (Ising et al. 1990).Twenty Wistar rats were exposed to military low-altitude flight noise with Lmax = 125 dB(A) for 10 s each during a period of 12 h with stochastic varying pauses. After the exposure cortisol in the blood was significantly increased in the exposed animals as compared with the controls. The urine, adrenaline and noradrenaline values were slightly decreased and the Mg-excretion was increased. The results are listed in [Table - 2].
In dogs exposed to 3 min. noise of an alarm clock (75 dB) the plasma concentrations of adrenaline, noradrenaline, adrenocorticotropic hormone (ACTH) and cortisol were studied. Both catecholamines increased within 1 min. after the onset of the noise to more than threefold of the pre-exposure value. ACTH was increased for 5 to 15 min. after the onset of the noise by a factor of 1.4. Cortisol reached its maximum, 11 times higher concentration as compared to the pre-exposure value, 12 min. after the exposure. This is an example of an acute noise-induced increase of the hormone reaction from the suprarenal medulla as well as the cortex (Engeland et al. 1990).
In a rat experiment a dose response relationship of stress hormones under exposure to traffic noise was demonstrated. The plasma concentration of cyclic adenosine, 3´, 5´,monophosphate (c-AMP) was measured after 4 h. exposure to recorded traffic noise with levels of 60, 80 and 100 dB(A). Traffic noise of 60 dB(A) as well as 80 dB(A) caused a 30% increase of c-AMP while 100dB(A) traffic noise resulted in an 50% increase of c-AMP (Okada et al., 1985).
Stress-Induced Myocardial Injury
From animal experiments we know that immobilisation acts as a stressor and causes an increase of cortisol (Sapolsky, et al. 1986).
Ceremuzynski et al. (1991) studied the injury of pigs' myocardium after 24 h of immobilization stress. Electromicroscopic examination revealed microtraumata of the myocardium. Among other biochemical alterations they observed decrease of mitochondrial ATP and increased generation of free radicals which may be components of the stress-induced myocardial injury.
In earlier experiments infusions of adrenaline into healthy dogs resulted in a marked decrease in myocardial ATP (Ceremuzynski et al., 1978). Catecholamines i.e. adrenaline and noradrenaline stimulate the activity of c-AMP. Furthermore catecholamines increased via c-AMP and tromboxan the influx of Ca 2 + into the smooth muscle cells thus increasing the risk of a coronary artery spasm (Ceremuzynski et al. 1981).
However these effects reported by Ceremuzynski were caused by massive increase of stress hormones, i.e. cortisol and catecholamines, which will hardly be caused by acute noise exposure. But since in real life even moderate environmental noise exposure can increase the acute release of stress hormones (Klotzbucher, Fichtel; 1967; Ising, Gunther: 1983; Maschke et al. 1995), this might have long-term effects on health.
In an experiment with 181 Wistar rats, the effects on the heart rate and the ECG ST interval were studied after 1h of exposure to 100 dB(A) continuous broad band noise (Zhao et al. 1990). ST eliminations are caused by myocardial ischemia.
A special technique was applied to measure the ECG in conscious unrestricted rats. Each rat was monitored for 1h before exposure, 1h of noise exposure and 2h after the exposure on three consecutive days. In 55% of the rats, the heart rate decrease and the ST interval increase was reproducable during noise exposure and normalized directly after the end of the exposure. The noise-induced increase of the ECG ST segment was similar to ST increase during myocardial ischemia, caused by injections of isoprenaline or occlusion of a coronary artery. Therefore it can be concluded from these results that the described acute noise exposure caused a short-term reversible and reproducable myocardial ischemia in about half of the experimental rats.
Long term health effects of chronic noise stress in animals
Carefully controlled animal model studies were used to develop the hypothesis of noise as a cardiovascular risk factor. In order to be able to apply animal results to humans, acute and direct noise-induced increase of stress hormones i.e. catecholamines and cortisol in humans and animals, were compared and shown to be qualitatively similar (Ising, 1993). Long-term health effects of directly noise-induced stress can be studied qualitatively in the animal model.
In an animal study with persistently repeated noise exposure a chronic increase of noradrenaline was found (Giinther et al. 1978). In this experiment, 6 groups of rats were fed diets with normal, suboptimal, or deficient content of magnesium respectively, of which 3 groups were used as noise controls. Magnesium deficiency was used as a model for a stressor which acts synergistically with noise. After one month on these diets, noise exposure of 3 groups was started and continued for 3 months: Traffic noise (maximal level 86 dB) with quiet intervals and a mean noise level of 69 dB ( frequency weighted according to the frequency characteristic of the rat's hearing threshold) for 2 groups and for the 3rd. group a constant noise with a mean level of 75 dB was added.
Mg-deficient diet alone resulted in a marked chronic increase of noradrenaline excretion (444%) as compared to the controls [Table - 3], which increased further with noise (69 dB: 32%; 75 dB: 76%). This shows that Mg-deficiency and noise are stressors which act synergistically. During the experiment, the body weight of the controls increased from 200g to 402g and 335g respectively, for both of the groups on the suboptimal Mg diets. However, it was constant in the Mg-deficient group without noise and was seen to decrease when the noise was applied. Using noradrenaline as an indicator of the total stress, the death rate, Ca content and the collagen (indicated by hydroxyproline) of the myocard, and the quotient of Ca/Mg increased while the Mg-content decreased with increasing stress. It is obvious that even moderate chronic noise exposure increases the quotient of Ca/Mg and the collagen content in the heart, and also decreases the lifespan.
Similar Ca/Mg shifts were found in the vascular walls of chronically noised-stressed rats (Altura et al .1992).
However chronic noise exposure is often not causing chronic increase of stress hormones. Quite often the organism is able to adapt to the noise to such a degree that no negative health effects are detectable.
A lifelong night-time noise exposure experiment with rats did not show any negative health effects of noise, not even a difference of the mean body weight. Frequency-varying band noise bursts of 1s duration, and pauses of 1s, with two mean levels of Leq = 80 or 100 dB(A) were used as noise exposure. In this experiment the rats received a diet with optimal Mg-supply and drinking water ad libitum (Borg 1981). No long-term noise related stress effects occurred, since adaptation to such a kind of noise is possible at a lower cost to the organism than noise bursts with unpredictable occurrences (Glass et al, 1969; de Boer et. al., 1989).
In another experiment with rats on a diet with optimal magnesium content it was shown that also noise bursts at unpredictable times with Leq = 92 dB resulted in no stress effects during 12 weeks of exposure (Ising et al.1981).
In the following experiments a diet with suboptimal Mg-content (200mg/kg) was used and the influence of the noise level increase velocity was studied. Controls and two experimental groups were compared after 12 weeks of nighttime noise exposure. One group was exposed to slowly increasing noise signals (dL/dt = of 5 dB/s), the other to rectangular pulses (dL/dt > 1000 dB/s), both with Leq = 80 dB and stochastic varying pauses with a mean pause duration of 40 s.
As indicators of noise-induced stress, the excretion of c-AMP during the experiment and the body weight at the end of the experiment were measured. Long-term exposure to slowly increasing noise signals caused a 20% increase in c-AMP and a 5% decrease in body weight while suddenly switched on noise pulses leads to 62% c-AMP increase and 9% lesser body weight. Both noise types caused no increase of collagen in the myocard.
In a similar experiment the noise level of the suddenly switched on pulses was varied (Leq = 80, 86 and 92 dB). The body weight showed at the end of the experiment, level dependent decrease of 9%, 14% and 23% .The collagen content of the myocardium was increased by 5% and 8% at 86 and 92 dB respectively (Nawroth, 1984).
In an experiment of 52 weeks duration, the effect of noise in normal Wistar rats (NWR) and spontaneous hypertensive rats (SHR) were compared. The result of the noise stress was a significant decrease in body weight only in the SHR and a significant increase of cardiac fibroses (collagen fibres in the interstitial space of myocardium), again only in the spontaneous hypertensive rats. (Hermann et.al., 1994). The collagen increase was similar to that in our experiments (Ising et al., 1979).
Interaction of stress and Ca/Mg shifts
Further analysis of the experimental results led to an interaction model between chronic stress and intracellular electrolyte shifts (Ising et al., 1986; Ising et al., 1985) [Figure - 2]. Chronic stress caused a loss of extracellular and intracellular Mg and an increase of intracellular Ca (Gunther et al., 1978). A decrease of Mg was correlated to an increased physiological noise sensitivity, i.e. to more severe noradrenaline releases in animals and humans under noise exposure (Gunther et al., 1978, Ising et al., 1980a, Ising et al., 1986). We found a positive feedback mechanism between stress - caused by noise and/or other stressors - and intracellular Ca/Mg shifts which may increase the cardiovascular risk.
The importance of Ca/Mg shifts was confirmed by post mortem studies of hearts from victims of ischemic heart diseases (IHD, ICD 410-414*)). The tissue samples were taken from areas of the myocardium not affected by the infarction and the results were stable after controlling for several confounders (Elwood et al. 1980). The results in [Table - 4] show that in humans the ratio of Ca/Mg increases with age. A differentiation between ischemic heart disease (IHD) death and non-IHD death revealed that the myocardium of IHD death looked older with respect to Ca/Mg increase. Since chronic noise stress increased the ratio of Ca/Mg and the collagen content of the rat myocardium, (which can be interpreted as accelerated ageing (Ising et al. 1981)) and increased Ca/Mg-ratios were found in the myocardium of IHD deaths, we concluded that chronic noise stress also accelerates the ageing of the heart in humans.
*) ICD 410: acute myocardial infarction, ICD 411-414: other acute and chronic ischemic heart diseases
Chronic noise stress, Mg-balance and cardiovascular risk
In several studies, it was shown that chronic noise exposure has the potential to cause chronically increased noradrenaline and/or cortisol. Acute and chronic occupational noise exposure led to acute (Ising et al., 1980a) and chronic increase of noradrenaline (Ising et al., 1999) and cortisol. The increase of cortisol was accompanied by a vanishing of the circadian rhythm similar to patients with Cushing syndrom. A noise exposure reduction of about 30 dB by consequent use of ear protectors for one week led to a normalization of cortisol as well as the circadian rhythm of cortisol (Melamed and Bruhis, 1996).
Persons under long-term road traffic noise exposure had significantly increased excretions of noradrenaline and/or cortisol during the night as compared to controls (Babisch et al., 1996; Ising 1999).
Children developed increased adrenaline and noradrenaline excretions within 1 1/2 years after the onset of flight noise exposure due to the opening of the new Munich airport (Evans et al., 1997).
Six weeks of experimental night time flight noise exposure (Leq = 32 dB(A), Lmax = 65dB(A) 32 times per night) resulted in an acute increase of cortisol excretion, followed by about two weeks of normalization and subsequent long-term increase of cortisol in males (Maschke et al., 1998). In this experiment blood samples were taken before and after the noise exposure. Among other biochemical parameters the Mg concentration of the erythrocytes (EMg) was analysed by atomic absorption spectroscopy. In one of the 16 test-persons EMg decreased, indicating a negative Mg-balance during the 6 weeks of night-time noise exposure. Five other persons had unusually low EMg already at the beginning of the experiment and it remained low. Most of those persons had long-term cortisol increase during the last three weeks, in contrast to persons with normal EMg at the beginning and no EMg-losses, the majority of which showed a constant cortisol excretion in the last three weeks (Harder et al., 1998).
A cohort study on the relation of noise, Mg and blood pressure revealed a significant negative correlation between EMg and blood pressure (Ising et al., 1985). The pathophysiological mechanisms involved in the development of hypertension under noise exposure, in combination with optimal and sub-optimal Mgintake were studied by Altura et.al. (1992). Besides the already mentioned Ca/Mg shifts in the vascular walls, an increased vasoconstriction under the action of noradrenaline was observed. This effect was confirmed in humans by measuring the increase of the total peripheral resistance (TPR) during infusion of noradrenaline. The noradrenaline induced TPR increase was reduced by Mg-injections (Ising et al.1992).
These injections increased the serum Mg concentration (SMg) to such a degree that also was observed during acute stress of rats on a diet with optimal Mg content. Rats exposed to a combination of sub-optimal Mg input and stress for 12 weeks, had a significantly reduced SMg and reacted to acute stress with significantly reduced SMg increase (Ising et al 1986).
The acute myocardial infarction is an extremely severe stressor. It was observed that infarction size and complications after the infarction depend upon the increase of catecholamines caused by the infarction (Ceremuzynski et al., 1981).
In another study it was demonstrated that about 1/3 of the patients with acute MI had a significant reduction of SMg 2 + several hours after the MI (beginning of the severe chest pain (Bertschat et al.,1995)) and thus with a Smg increase. An organism with optimal Mg supply will react with a substantial release of stored Mg, under the influence of an acute and severe stressor. It is reasonable therefore to argue that probably a long-term sub-optimal Mg supply will have reduced the effect of an SMg 2 + release directly after the MI. It is not surprising that patients with reduced SMg2+ after the MI had an increased risk of complications during two weeks after the MI as compared to MI patients with constant or increased SMg2+ on day 1 of the MI as compared to the long term average of Smg2+ (Jeremias et al.,1996).
| Discussion|| |
Long-term health effects of noise can be studied in the animal model, if intensive noise causes directly an increase of stress hormones. Noise with moderate levels has the potential to disturb activities i.e. concentration, communication and sleep and therefore to cause indirectly stress hormone increase. Noise-induced indirectly transmitted stress reactions can not be studied in animals as a model for humans; however, the long-term health effects of directly and indirectly increased stress hormones will be qualitatively similar in humans and animals. Animal models can therefore be used to study this part of the problem too.
Animal studies show that chronic noise exposure does not always lead to chronic stress hormone increase.
Several conditions increase the risk for chronic noise-induced stress reations:
- Noise is not the only stressor: in combination with other synergic stressors i.e. cold (Heroux et al., 1977), suboptimal Mg intake (Gunther et al.,1978, Ising et al.,1981), nicotine and / or caffeine (Naworth, 1984), overcrowding (Henry and Stevens 1977).
- Persistent noise may lead to an excedence of the individual potential of adaption to stressors.
- Hereditary defects, for example in spontaneous hypertensive rats lower the stress tolerance.
- Some noise characteristics: sudden and unpredictably occuring noise events cause nonhabituable shock reactions (Glass et al.1969). If such a kind of noise exposure is high enough to increase the risk of noise-induced hearing loss it will also cause chronic stress in active animals (Ising et al.,1993).
- During sleep the levels that cause noiseinduced stress reactions are much lower than in the active phase.
- The information which is transmitted by the type of noise: This effect is deduced from Henry's psychophysiological stress model (Henry and Stevens, 1977), which stresses the importance of „early experience". To test this hypothesis the following experiments proposed
:Rats are conditioned to two types of noise, one of these is conditioned negatively by an electric shock, the other neutrally. After conditioning, two subgroups are exposed during sleep to one or the other type of noise. The hypothesis is tested that only the negatively conditioned noise type will lead to chronically increased cortisol.
- In humans acute and chronic stress hormone increase can be caused indirectly by environmental noise via disturbance of activities such as concentration, communication, circulation and sleep.
Based on the results of the above demonstrated experiments, we developed a model of noise effects [Figure - 3] and also formulated the hypothesis that chronic noise exposure, even with quite low levels, has the potential to cause chronic stress hormone increase in humans and thus accelerates the ageing of the myocardium and the vascular walls. These effects are related to an increased risk of myocardial infarction and other health effects i.e. immunosuppression.
As mentioned in the introduction, there is some epidemiological evidence in the literature for a noise related increase of the risk in myocardial infarction (Babisch 1998 a and b). Although the relative risk increase due to environmental noise exposure seems to be quite low - between 1.1 and 1.5 - and therefore difficult to prove, noiseinduced health effects might be important for medicine because of the high number of exposed people. In West Europe, a total of 50-70 million persons are exposed to mean traffic noise levels above 65 dB(A) at daytime.This daytime level corresponds to a nighttime level of 55 dB(A). The epidemiological studies indicate that at this noise-exposure a dose-dependent risk increase of myocardial infarction begins and that the nighttime noise is more detrimental to health than noise exposure during the day.
| Conclusions|| |
From these findings we conclude, that traffic noise exposure, especially at night time, has the potential to cause chronic increase of noradrenaline and cortisol. In a certain percentage of the population cortisol may be increased above the normal range.
Based on the results of the above demonstrated experiments, we developed a model of noise effects [Figure - 3] and formulated the hypothesis that chronic noise exposure accelerates the ageing of the myocardium and the vascular walls, and therefore increases the risk of myocardial infarction.
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Federal Environmental Agency, Institute for Water, Soil and Air Hygiene, Corrensplatz 1, D - 14191 Berlin
Source of Support: None, Conflict of Interest: None
[Figure - 1], [Figure - 2], [Figure - 3]
[Table - 1], [Table - 2], [Table - 3], [Table - 4]