M Spreng

Bio: M Spreng is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Electroencephalography & Fear processing in the brain. The author has an hindex of 10, co-authored 17 publications receiving 645 citations.

Ear damage caused by leisure noise.

Abstract: Noise is a health risk. Recent findings suggest that leisure noise is a substantial danger especially to children, teenagers and young adults. Epidemiological studies of teenagers with no occupational noise exposure show an increasing number with a substantial and measurable irreversible inner ear damage. This is basically due to the wide spread exposition to very loud toys (pistols and squibs), crackers and exposure to electronically amplified music, e.g. from personal cassette players (PCP), at discos or concerts etc. Protection against irreversible ear damage by leisure noise has an important impact in preventive medical care. Therefore the general public must be informed that loud leisure activities may cause damage to the ear. In order to protect children, young people and adults, the legislature ought to set limits for sound levels in discos, concert halls and for music equipment and toys by establishing the necessary standards and regulations.

Possible health effects of noise induced cortisol increase

Abstract: The auditory system is permanently open - even during sleep. Its quick and overshooting excitations caused by noise signals are subcortically connected via the amygdala to the hypothalamic-pituitary-adrenal-axis (HPA-axis). Thus noise causes the release of different stress hormones (e.g. corticotropin releasing hormone: CRH; adrenocorticotropic hormone: ACTH) especially in sleeping persons during the vagotropic night/early morning phase. These effects occur below the waking threshold of noise and are mainly without mental control. Animal experiments show noise-induced changes in sensitivity of cellular cortisol receptors by increase of heat-shock proteins, and ultrastructural changes in the tissue of the heart and the adrenal gland. Increased cortisol levels have been found in humans when exposed to aircraft noise or road traffic noise during sleep. The effects of longer-lasting activation of the HPA-axis, especially long term increase of cortisol, are manifold: immuno suppression (e.g. eosinopenia), insulin resistance (e.g. diabetes), cardiovascular diseases (e.g. hypertension and arteriosclerosis), catabolism (e.g. ostoeporosis), intestinal problems (e.g. stress ulcer) etc. Even worse may be the widespread extrahypothalamical effects of CRH/and/or ACTH which have the potential to influence nearly all regulatory systems, causing for example stress-dysmenorrhea etc. as signs of disturbed hormonal balance.

Central nervous system activation by noise

Abstract: Connections between thalamic structures of the auditory system and subcortical areas (amygdala, hippocampus, hypothalamus) had been hypothesized to act as a fast reacting "memory chain" establishing and enhancing adverse excitations during noise exposure. Recent studies prove that the lateral amygdala is an important part of a second separate pathway to the telencephalic projections of the auditory system. This fast, monosynaptic thalamo-amygdala tract is responsible for full-blown "fear responses" evoked by auditory stimuli as shown by several conditioning experiments in animals: A fear memory system. The appertaining basic processes of plasticity in the amygdala are reductions of latencies of neuronal excitations and recruiting of more elements with shorter latency, long-term potentiation causing enhancement of auditory-evoked responses by repeated stimulation, as well as sharpening of primary broad tuning curves of elements. Very recently a study using Functional-Magnetic-Resonance-Imaging (fMRI) demonstrated that an amygdalar contribution to conditioned fear learning can be revealed in normal human subjects too. These findings were supported by Positron-Emission-Tomography (PET) studies in depressive persons showing that amygdala metabolic abnormality predicted the cortisol concentration in blood. Using connections via central amygdala, lateral and medial hypothalamus to parts named nuclei paraventriculares and regio arcuata, the sound evoked excitations reach two essential components of endocrine functioning: a) the well-known hypothalamic-pituitary-adrenal (HPA) system with a subsequent rise (via Corticotropin-Releasing Hormone: CRH) in Corticotropin (Adreno-CorticoTropin Hormone: ACTH) and the corticosterone levels; b) the synthesis of ACTH and beta-endorphine-like substances in the arcuate region being axonally transported to extrahypothalamic brain regions. Longer-lasting activation of the HPA-axis, especially abnormally increased or periodically elevated levels of cortisol and the widespread extrahypothalamically distributed CRF/ACTH may lead to disturbed hormonal balance and even to severe diseases.

Disturbed sleep patterns and limitation of noise.

Abstract: Due to the undisputable restorative function of sleep, noise-induced sleep disturbances are regarded as the most deleterious effects of noise. They comprise alterations during bedtimes such as awakenings, sleep stage changes, body movements and after-effects such as subjectively felt decrease of sleep quality, impairment of mood and performance. The extents of these reactions depend on the information content of noise, on its acoustical parameters and are modified by individual influences and by situational conditions. Intermittent noise, that is produced by air traffic, rail traffic and by road traffic during the night is particularly disturbing and needs to be reduced. Suitable limits are suggested.

Noise induced nocturnal cortisol secretion and tolerable overhead flights.

Abstract: 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 Lmax = 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 respectively.

Burden of Disease from Environmental Noise: Quantification of Healthy Life Years Lost in Europe

Abstract: The health impacts of environmental noise are a growing concern. At least one million healthy life years are lost every year from traffic-related noise in the western part of Europe. This publication summarises the evidence on the relationship between environmental noise and health effects, including cardiovascular disease, cognitive impairment, sleep disturbance, tinnitus, and annoyance. For each one, the environmental burden of disease methodology, based on exposure-response relationship, exposure distribution, background prevalence of disease and disability weights of the outcome, is applied to calculate the burden of disease in terms of disability-adjusted life-years. Data are still lacking for the rest of the WHO European Region. This publication provides policy-makers and their advisers with technical support in their quantitative risk assessment of environmental noise. International, national and local authorities can use the procedure for estimating burdens presented here to prioritize and plan environmental and public health policies.

Cardiovascular effects of environmental noise exposure

Abstract: The role of noise as an environmental pollutant and its impact on health are being increasingly recognized. Beyond its effects on the auditory system, noise causes annoyance and disturbs sleep, and it impairs cognitive performance. Furthermore, evidence from epidemiologic studies demonstrates that environmental noise is associated with an increased incidence of arterial hypertension, myocardial infarction, and stroke. Both observational and experimental studies indicate that in particular night-time noise can cause disruptions of sleep structure, vegetative arousals (e.g. increases of blood pressure and heart rate) and increases in stress hormone levels and oxidative stress, which in turn may result in endothelial dysfunction and arterial hypertension. This review focuses on the cardiovascular consequences of environmental noise exposure and stresses the importance of noise mitigation strategies for public health.

Traffic Noise and Risk of Myocardial Infarction

Abstract: Background:The biologic plausibility for noise stress-related cardiovascular responses is well established. Epidemiologic studies on the relationship between transportation noise and ischemic heart disease suggest a higher risk of myocardial infarction in subjects exposed to high levels of traffic n

How and why environmental noise impacts animals: an integrative, mechanistic review.

Abstract: Ecology Letters (2011) 14: 1052–1061 Abstract The scope and magnitude of anthropogenic noise pollution are often much greater than those of natural noise and are predicted to have an array of deleterious effects on wildlife. Recent work on this topic has focused mainly on behavioural responses of animals exposed to noise. Here, by outlining the effects of acoustic stimuli on animal physiology, development, neural function and genetic effects, we advocate the use of a more mechanistic approach in anthropogenic environments. Specifically, we summarise evidence and hypotheses from research on laboratory, domestic and free-living animals exposed to biotic and abiotic stimuli, studied both observationally and experimentally. We hope that this molecular- and cellular-focused literature, which examines the effects of noise on the neuroendocrine system, reproduction and development, metabolism, cardiovascular health, cognition and sleep, audition, the immune system, and DNA integrity and gene expression, will help researchers better understand results of previous work, as well as identify new avenues of future research in anthropogenic environments. Furthermore, given the interconnectedness of these physiological, cellular and genetic processes, and their effects on behaviour and fitness, we suggest that much can be learned from a more integrative framework of how and why animals are affected by environmental noise.

The noise/stress concept, risk assessment and research needs

Abstract: In principle, the noise/stress hypothesis is well understood: Noise activates the pituitary-adrenal-cortical axis and the sympathetic-adrenal-medullary axis. Changes in stress hormones including epinephrine, norepinephrine and cortisol are frequently found in acute and chronic noise experiments. The catecholamines and steroid hormones affect the organism's metabolism. Cardiovascular disorders are especially in focus for epidemiological studies on adverse noise effects. However, not all biologically notifiable effects are of clinical relevance. The relative importance and significance of health outcomes to be assessed in epidemiological noise studies follow a hierarchical order, i.e. changes in physiological stress indicators, increase in biological risk factors, increase of the prevalence or incidence of diseases, premature death. Decision-making and risk management rely on quantitative risk assessment. Epidemiological methods are the primary tool for providing the necessary information. However, the statistical evidence of findings from individual studies is often weak. Magnitude of effect, dose-response relationship, biological plausibility and consistency of findings among studies are issues of epidemiological reasoning. Noise policy largely depends on considerations about cost-effectiveness, which may vary between populations. Limit or guideline values have to be set within the range between social and physical well-being - between nuisance and health. The cardiovascular risk is a key-outcome in non-auditory noise effects' research because of the high prevalence of related diseases in our communities. Specific studies regarding critical groups, different noise-sources, day/evening/night comparisons, coping styles and other effect-modifying factors, and the role of annoyance as a mediator of effect are issues for future research in this field.