https://www.healio.com/psychiatry/journals/psycann/1976-12-6-12/{806b8887-c02e-40c8-a228-57f1cdb2bdba}/the-stress-of-life.pdf

The stress of life

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(02)11280-3.pdf

Association between mortality and indicators of traffic-related air pollution in the Netherlands: a cohort study

WHO Regional Office for Europe.

Significant advances in our knowledge about interventions to prevent cardiovascular disease (CVD) have occurred since publication of the first female-specific recommendations for preventive cardiology in 1999.1 Despite research-based gains in the treatment of CVD, it remains the leading killer of women in the United States and in most developed areas of the world.2–3 In the United States alone, more than one half million women die of CVD each year, exceeding the number of deaths in men and the next 7 causes of death in women combined. This translates into approximately 1 death every minute.2 Coronary heart disease (CHD) accounts for the majority of CVD deaths in women, disproportionately afflicts racial and ethnic minorities, and is a prime target for prevention.1–2 Because CHD is often fatal, and because nearly two thirds of women who die suddenly have no previously recognized symptoms, it is essential to prevent CHD.2 Other forms of atherosclerotic/thrombotic CVD, such as cerebrovascular disease and peripheral arterial disease, are critically important in women. Strategies known to reduce the burden of CHD may have substantial benefits for the prevention of noncoronary atherosclerosis, although they have been studied less extensively in some of these settings.

In the wake of the reports of the Women’s Health Initiative and the Heart and Estrogen/Progestin Replacement Study (HERS), which unexpectedly showed that combination hormone therapy was associated with adverse CVD effects, there is a heightened need to critically review and document strategies to prevent CVD in women.4–7 These studies underscore the importance of evidence-based practice for chronic disease prevention. Optimal translation and implementation of science to improve preventive care should include a rigorous process of evaluation and clear communication about the quantity and quality of evidence used to support clinical recommendations. Recently, there has been an increase in the …

Evidence-Based Guidelines for Cardiovascular Disease Prevention in Women

Noise is a prominent feature of the environment including noise from transport, industry and neighbours. Exposure to transport noise disturbs sleep in the laboratory, but not generally in field studies where adaptation occurs. Noise interferes in complex task performance, modifies social behaviour and causes annoyance. Studies of occupational and environmental noise exposure suggest an association with hypertension, whereas community studies show only weak relationships between noise and cardiovascular disease. Aircraft and road traffic noise exposure are associated with psychological symptoms but not with clinically defined psychiatric disorder. In both industrial studies and community studies, noise exposure is related to raised catecholamine secretion. In children, chronic aircraft noise exposure impairs reading comprehension and long-term memory and may be associated with raised blood pressure. Further research is needed examining coping strategies and the possible health consequences of adaptation to noise.

/pdf/noise-pollution-non-auditory-effects-on-health-5fmte691k3.pdf

Noise pollution: non-auditory effects on health

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

Traffic Noise and Risk of Myocardial Infarction

Traffic noise is the most important source of environmental annoyance. According to the Environmental Expert Council of Germany, severe annoyance persistent over prolonged periods of time is to be regarded as causing distress. Previously, extraaural noise effects were mostly assessed using a paradigm in which the sound level played the major role. On the basis of this paradigm the relatively low sound level of environmental noise was not considered to be a potential danger to health. In contrast to this numerous empirical results have shown long-term noise-induced health risks. Therefore a radical change of attitude - a change of paradigm - is necessary. For an immediate triggering of protective reactions (fight/flight or defeat reactions) the information conveyed by noise is very often more relevant than the sound level. It was shown recently that the first and fastest signal detection is mediated by a subcortical area - the amygdala. For this reason even during sleep the noise from aeroplanes or heavy goods vehicles may be categorised as danger signals and induce the release of stress hormones. In accordance with the noise stress hypothesis chronic stress hormone dysregulations as well as increases of established endogenous risk factors of ischaemic heart diseases have been observed under long-term environmental noise exposure. Therefore, an increased risk of myocardial infarction is to be expected. The results of individual studies on this subject in most cases do not reach statistical significance. However, according to the Environmental Expert Council, these studies show a consistent trend towards an increased cardiovascular risk if the daytime immission level exceeds 65 dB(A). Most of the previous studies on the extraaural effects of occupational noise have been invalidated by exposure misclassifications. In future studies on health effects of noise a correct exposure assessment is one of the most important preconditions.

Health effects caused by noise : Evidence in the literature from the past 25 years

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.

Ear damage caused by leisure noise.

Increased catecholamine levels in urine in subjects exposed to road traffic noise: The role of stress hormones in noise research

This is a review of the research into endocrine effects of noise since the early 1980s at the Institute for Water, Soil and Air Hygiene. According to our knowledge, no other group has studied systematically the endocrine effects of acute and chronic noise exposure. Mechanisms of acute noise-induced stress reactions as well as long-term increase of stress hormones in animal and persons under chronic noise exposure were studied. Our theoretical background was Henry's psychophysiological stress model with the two reaction alternatives : (i) The fight-flight reaction, characterised by an increase in adrenalin and noradrenaline (ii) The defeat reaction with increased cortisol. Extremely intense acute noise exposure near the threshold of pain caused an increased release of cortisol from the suprarenal cortex but acute noise exposure with levels between 90 and 100 dB(A) caused an increase of catecholamines. Non-habituated noise increased primarily the release of adrenalin from the suprarenal medulla, whereas habituated noise caused a chronic increase of noradrenaline from the sympathetic synapses under longterm noise exposure at work. Environmental noise exposure (Leq >/= 60 dB(A)) caused catecholamine increase if activities such as conversation, concentration, recreation etc were disturbed through noise. In sleeping persons, traffic noise with only Leq >/= 30 dB (A) and Lmax >/= 55 dB(A) caused significant acute increase of cortisol, which developed into chronic increase if the noise exposure was repeated consistently. Parallel to cortisol, chronic noradrenaline increase was also observed. Based upon the empirical results, a noise stress model was developed which is a first step forward in the theoretical understanding of endocrine noise effects.

H. Ising

Papers

Traffic Noise and Risk of Myocardial Infarction

Health effects caused by noise : Evidence in the literature from the past 25 years

Ear damage caused by leisure noise.

Increased catecholamine levels in urine in subjects exposed to road traffic noise: The role of stress hormones in noise research

Acute and chronic endocrine effects of noise : Review of the research conducted at the Institute for water, soil and air hygiene