[Music listening habits of adolescents. With special reference to discothek exposure].
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Biomedical subjects
Publications and source records attributed to H Ising.
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The hypothesis that road traffic noise causes ischaemic heart disease (IHD) was tested in several epidemiological studies in middle-aged men. The studies carried out in Caerphilly (Wales) and Bristol-Speedwell (England) suggested the daytime (6-22 h) outdoor traffic noise level category 65-70 dB(A) as a threshold for noise effects detectable. Based on risk factors, a relative risk greater than 1 was calculated for the incidence of major IHD (RR = 1.1) in both samples for the subjects in this highest noise category, those in the quietest (51-56 dB(A)) serving as a reference using multiple models. Also the prevalence of myocardial infarction (RR = 1.2 and 1.1), ECG ischaemia (RR = 1.2 and 1.4) and any IHD disease (RR = 1.2 and 1.2) showed relative risks slightly greater than 1 in this noise group. In contradiction, the observed incidence of major IHD showed relative risks below 1 in both samples in this traffic noise group. The case-control studies carried out in Berlin revealed relative risks above 1 on the incidence (RR = 1.3 and 1.2) and the prevalence (RR = 1.2) of myocardial infarction at outdoor traffic noise levels in the range of 71-80 dB(A) serving the men in the category below 61 dB(A) as a reference. None of the findings was statistically significant. The relevance of the results is discussed.
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The auditory thresholds of about 60 anaesthetized guinea pigs were determined at 3 or 4 frequencies between 2 and 20 kHz using the acoustically evoked brain stem potentials. The animals were then exposed to electro-acoustically reproduced MLAF noise with peak levels between 120 and 130 dB(A). The exposure occurred either once or else four times within either 3 or 60 minutes. The level of noise increased at 7.5 and 75 dB/s (slow and fast increase). TTS was then determined. PTS was measured one week later. In over half the animals, exposure to rapidly increasing noise level with a peak of 126 dB(A) induced PTS > or = 30 dB for at least one frequency. Exposure to a slowly increasing noise level with the same peak provoked significantly smaller PTS. 4 exposures to a rapidly rising noise level within 3 minutes induced significantly smaller PTS than the same dosage within 60 minutes. Only in the latter case was PTS greater than TTS.
Guinea pigs were exposed once to MLAF noise (126 dB(A), 75 dB/s) and 12 cochleae were prepared for scanning electron microscopy 2 to 3 weeks after exposure. Qualitative analysis of the cilia of the outer hair cells revealed the types of damage already described in literature. The spatial distribution of cilia damage, however, differed essentially from the well known pattern: the damage was more or less pancochlear, beginning in the basal turn and increasing in frequency and severeness of damage till the end of the third turn. The most severe damage was visible in the outer row of the outer hair cells. This special pattern of cilia damage indicates that MLAF noise causes a different type of damage than the types described in literature. More studies are needed.
The influence of noise from night flying on electro-biological reactions and on the secretion of catecholamines (adrenaline and noradrenaline) was studied in eight healthy adults whose place of residence exposes them to day-time aircraft noise. The interrelationships were then analysed, with daytime noise exposure, personality traits and general day-to-day condition reflected in control variables. The subjects were each observed during five nights without noise exposure (Leq < 32 dB(A)) and five nights with noise exposure (Leq = 36 to 56 dB(A)), when the following factors were varied: number of flights (16, 32, 64 overflights with a constant maximum indoor sound level of 75 dB(A)); and sound level (64 overflights at a maximum indoor sound level of 55, 65 and 75 dB(A)). All these flights were transmitted electro-acoustically between the third and sixth hours of the night. When the various daytime exposures are taken into account, significant mean value differences between noisy and peaceful nights are demonstrated in 8-hour urine for both catecholamines. In the case of adrenaline, the original data already showed a significant increase with noise exposure. Furthermore, catecholamine concentration increases with sound level. The analysis confirms a close link between the volume of adrenaline in the urine collected and electro-biological reactions, with consideration given to personality traits and day-time alcohol consumption.
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The effect of oral Mg-supplementation as prophylaxis against noise-induced hearing loss was tested in a placebo-controlled double blind study involving 320 voluntary subjects during a 2-month period of military training. The hearing thresholds of all subjects were checked and only persons with normal hearing were accepted. Before and after the 2-month training, blood samples were collected and Mg was analysed in serum, erythrocytes and lymphocytes. Seven days after the last exposure to firearm noise, the audiograms of all test subjects were checked and permanent threshold shifts (PTS) were determined. The total group received a drink containing either 4g Mg granulate verum (6.7 mmol Mg aspartate) or placebo every working day during the 2-month training period. The primary source of noise exposure were firearms: 420 shots per person, mean peak level 164 dB(A). The recruits used ear plugs with a mean insertion loss of 25 dB. In both groups Mg-concentration in serum and in erythrocytes increased with time. Lymphocyte Mg increased in the Mg group only. In the placebo group the percentages of ears with PTS > 25 dB at 4 kHz/6 kHz and/or 8 kHz after exposure to firearm noise were twice as high as in the Mg group.
Rats maintained on normal Mg-containing diets for 12 weeks (plasma Mg = 0.96 +/- 0.02 mmole) and subjected to 85 dB(A), 12 h per day for 8 weeks; 95 dB(A), 16 h per day for 4 weeks demonstrated significant elevation in systolic and diastolic arterial blood pressure (ABP); plasma Mg showed a 15% decrease whereas aortic and portal vein muscle exhibited slight reductions in Mg content and elevation in Ca. Moderate (plasma Mg = 0.67 +/- 0.03 mmole) and more severely (plasma Mg = 0.28 +/- 0.01 mmole) Mg deficient animals not subjected to audiogenic stress (AS) also exhibited significant elevations in systolic and diastolic ABP; vascular tissue Mg content decreased whereas Ca content rose. Animals subjected to combined Mg deficiency and AS for 12 weeks exhibited the greatest deficits in plasma and vascular muscle Mg and the greatest elevations in systolic and diastolic ABP; vascular tissue Ca contents also showed the greatest increases. In-situ measurements of mesenteric arterioles, venules and precapillary sphincters in the various subgroups revealed negative correlation between the lumen sizes of these microvessels and plasma Mg. Also, there was an inverse correlation between plasma Mg and ABP. Capillary blood flow transit times were decreased in relation to the degree of plasma Mg reduction. A quantitative rarefication of true capillaries per mesentery was observed. In addition, vascular reactivity of terminal arterioles to constrictor agents (norepinephrine, angiotensin II, Ba2+) was in relation to the plasma and vascular tissue deficit in [Mg]. Reactivity to the dilator agent, histamine, decreased in proportion to Mg deficit. A rationale for therapeutic intervention with Mg may evolve from these studies.
It has been demonstrated that audiogenic stress (AS) can induce elevation of arterial blood pressure (ABP) in animals and humans and that noise-induced hearing loss may be associated with alterations in Mg metabolism. Experiments were designed to determine whether 1) there is a causal relationship among environmental noise stress, serum and vascular tissue (aortas and portal veins) Mg contents, and development of hypertension and 2) such noise-induced hypertension has a microcirculatory basis and what the mechanism may be. Rats maintained on normal Mg-containing diets for 12 wk (plasma [Mg] = 0.96 +/- 0.02 mM) and subjected to AS (85 dB(A), 12 h/day for 8 wk; 95 dB(A), 16 h/day for 4 wk) demonstrated significant elevation in systolic and diastolic ABP; plasma [Mg] showed a 15% deficit, whereas aortic and portal vein muscle exhibited slight reductions in Mg content and elevation in Ca. Moderate and more severely Mg-deficient animals not subjected to AS also exhibited significant elevations in systolic and diastolic ABP; vascular tissue Mg content decreased, whereas Ca content rose. Animals subjected to combined Mg deficiency and AS for 12 wk exhibited the greatest deficits in plasma and vascular muscle Mg and the greatest elevations in systolic and diastolic ABP; vascular tissue Ca contents also showed the greatest increases. In situ measurements of mesenteric arterioles, venules, and precapillary sphincters in the various subgroups revealed that the lower the plasma [Mg], the more constricted the microvessels, and the higher the ABP, the lower the plasma [Mg]. Capillary blood flow velocities were decreased in relation to the degree of plasma Mg deficit.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of noise of low-flying military jet aircraft were investigated from demoscopic and epidemiological points of view. Areas with different low-altitude flight noise exposure were compared with one another as to subjective annoyance, casual blood pressure and ear symptoms. With the same energy equivalent sound pressure level (Leq), the subjective disturbance caused by military low-altitude flight noise was essentially greater than that due to ordinary flight noise (in the neighbourhood of civil airports). A comparison of several areas revealed that frequencies of ear symptoms (tinnitus lasting more than one hour and permanent hearing threshold shifts of greater than 30 dB) were higher only in areas where maximal flight noise levels considerably exceeded 115 dB (A) accompanied by rapid noise level increases. Blood pressure measurements yielded significantly higher values (group difference 9 mm Hg systolic) in girls living in these highly exposed areas. Acoustic limits are proposed with respect to public health.
Volunteers aged 70 to 89 years living in a senior citizen's home in Haifa were exposed to flight noise via earphones while watching video films. Their blood pressure and heart rates were measured simultaneously. A high-quality recording and reproduction technique was employed. They were exposed to the noise of two to three overflights with Lmax = 99-114 dB(A) and slow sound pressure level increase (aircraft take off) or with Lmax = 95-112 dB(A) and a fast sound pressure level increase (low-altitude flight at high subsonic speed) at intervals of 10 to 15 min. The systolic and diastolic blood pressure was raised at Lmax = 112 dB(A) and high speed level increase at the average of 23 and 13 mmHg, respectively with individual maximal values of about 40 mm Hg (systolic). In order to prevent risks to the subjects' health, the noise exposure was not raised to levels above 112 dB(A) and fast level increase, although Lmax = 125 dB(A) has been measured in 75 m-low-altitude flight areas. The blood pressure response to a repeated single exposure increased in proportion to the preceding noise exposure. At high intensities and fast level increase an up to fourfold reaction intensification was detected in the majority of subjects. This change in reactivity is regarded as the result of sensitization toward the special type of noise and the implications of these observations for the long-term effects of chronic exposure to low-altitude flight noise are considered. On the basis of these results, proposals are made for limiting values for Lmax and for the speed of sound pressure level increase, the implementation of which would lead to a marked reduction in health risks from low-altitude flight noise.
Seven 24-hour ECG recordings and blood samples were taken within 3 weeks in 42 patients who had suffered an acute myocardial infarction (AMI). Ca, K and Mg concentrations in serum, and K and Mg in the erythrocytes, were determined by atomic absorption spectroscopy. One half of the patients were infused with 81 mval/day MgSO4 for 3 days. In patients who exhibited intense electrolyte alterations 10-20 days after AMI, there was a significantly higher rate in the frequency of couplets and/or tachycardia in the 2- to 20-day period after AMI. In patients infused with MgSO4, the fluctuation in serum electrolytes and the rate of arrhythmias were significantly reduced.
We examined whether healthy young swimmers improved performance during emotional and physical stress testing in the laboratory or during competition. Twenty four well trained healthy Caucasian pupils (14 boys and 10 girls, means = 16 years) were randomly treated either with 20 mmol Mg-aspartate-HCl/d or placebo for 3 months. After Mg supplementation serum Mg increased from 0.85 +/- 0.03 to 0.89 +/- 0.06 mmol/litre (P less than 0.05). Mg in red blood cells remained unchanged (4.79 +/- 0.35 mmol/kg dry weight before supplementation and 4.96 +/- 0.27 three months later, P = 0.32) whereas no increase in serum Mg or Mg in red blood cells was found in subjects who received placebo. Student's t test and analyses of variance revealed no significant differences in performance data either in the laboratory or during competition after supplementation with Mg.
The risk of hearing loss due to exposure to music in discotheques is discussed on the basis of VDI guideline No 2058, Bl 2. The hypothesis of a relationship was investigated in two empirical studies. In 204 pupils aged 13-19 years, a positive statistical relation of the 4 kHz hearing threshold on the music-hearing habits reported was observed. The difference between the extreme groups of noise exposure was approximately 4 dB (p less than 0.05) on a group average. The evaluation of audiograms of 3133 youths aged 16-20 years applying for a job performed during the medical tests required for employment, showed that those young people with a striking internal ear hearing loss of greater than 30 dB in the area of the C5 depression had spent significantly more time in discotheques than those without striking findings.
Noise-induced hearing loss appears to result from energy depletion in the hair cells. Cell membrane permeability is increased in hypomagnesemia, causing Na+ and Ca++ influx, with subsequent increase in energy-dependent ion-pumping. Energy exhaustion is further enhanced by hypomagnesemia-induced vasoconstriction. Dietary supplementation with magnesium was shown to lessen hearing loss in noise-exposed rats. It is postulated that the same mechanisms may act in man and the possible benefit of magnesium supplementation for noise-exposed workers should be investigated.