In this paper the disturbances to sleep caused by road traffic noise are reviewed in the light of the latest published findings. First, a short presentation is made of what noise is in general. Then an exposition is made of the different characteristics of road traffic noise and how it may be measured and rated with various descriptors. In general terms, the continuous exposure of people to road traffic noise leads to suffering various kinds of discomfort, thereby reducing the number of well-being elements. However, this conclusion is made more complex to attain when non-acoustical factors such as socio-economic situation, age and gender are taken into account. In broad terms, nocturnal road traffic activity leads to difficulties in falling asleep for people and to a reduction of their sleep quality. This, however, depends strongly on physical measures of noise like for instance the intermittency of loud single noise events, their level relative to that of the background noise and the frequency and time of their occurrence. Several studies have also confirmed the fact that mood, too, is strongly affected after spending a night with significant noise exposure. Other psychological and physiological functions affected by night-time exposure to road traffic noise, such as performance the following day and cardiovascular reactivity are also reviewed.

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.

Previous studies of the association between occupational noise exposure and cardiovascular disease (CVD) or risk factors for CVD are primarily either cross-sectional or retrospective, whereas the design of the CORDIS study was both cross-sectional and longitudinal. It had three phases: Phase I was conducted during 1985-87 among 6,016 employees from 21 factories. Recorded were medical, ergonomic, environmental (including noise levels at the various work stations) and psychological data. Phase II was conducted during 1988-90, at 18 of the 21 original factories and included similar data collected from 3,509 subjects. Phase III was conducted during the years 1995-96 and 4,995 workers who participated in Phases I and II completed questionnaires pertaining to medical, occupational and life style variables. Mortality and cancer morbidity data were obtained over an 8 year follow-up period for all subjects. Results from Phase I, revealed no association between noise exposure and resting blood pressure. Positive association was found for serum lipids in women and in young men. Noise annoyance had an additive effect on this outcome. In addition, recurrent daily noise exposure was found to be associated with elevated acute resting heart rate. Results of Phase II showed that chronic exposure to high noise levels during the 2-4 years of the follow-up resulted in changes of 3.9 mmHg in SBP and 3.3 mmHg in DBP, among workers performing complex jobs. In workers performing simple jobs these changes were 0.3 and 0.4 mmHg. Thus the type of work performed appears to be a significant factor. Results of Phase III revealed that there was a trend for positive association between past noise exposure measured at Phase I and 8 years incidence of cardiovascular morbidity, mortality and total mortality. This trend was statistically significant for total mortality (hazard ratio = 1.97, 95% CI 1.28-4.54) even after controlling for possible confounders. In summary, tests for association between noise exposure and cardiovascular risk factors, or cardiovascular morbidity and mortality, and total mortality have yielded mixed results. Reasons for this are discussed, as well as suggestions for further research.

The psychobiology of stress has received increasing attention throughout the past two decades. Physiological pathways and subjective response patterns are described in more details aiming at a better understanding of the pathways leading to health or disease under prolonged periods of stress. Technical advances in the laboratory have significantly contributed to this development. One of these methodological advances is the measurement of cortisol in saliva which has promoted psychobiological stress research both in the laboratory and in the field. The present paper provides a brief methodological background and the use of salivary cortisol assessment as an indicator of stress in human studies from this research centre. It is suggested that research on health consequences of noise exposure should include salivary cortisol as a sensitive measure of allostatic load.

A new stress model, the Allostatic Load Model, refers to the ability to achieve stability through change. The various biological functions activated during stress serve an important role in the organism's adaptation to the environment by protecting and restoring the body but may, under certain conditions, also have health damaging consequences. Two different psychoneu­roendocrine stress systems are of particular interest: (1) the sympathetic adrenal medullary (SAM) and (2) the hypothalamic pituitary adrenocortical (HPA) systems. Sustained activation of the SAM system with overexposure to epinephrine (adrenaline) and norepinephrine (noradrenaline) is considered to contribute to the development of cardiovascular disease (CVD). Chronic stress exposure influencing the HPA-axis is associated with metabolic changes which also increase the risk of CVD but, in addition, also contribute to impaired immune function, diabetes, depressive symptoms and cognitive disturbances. The present paper is focused on the possible biological pathways between environmental stress and somatic illness, including the role of environmental stress for the development of musculoskeletal disorders. It is concluded that the SAM and the HPA systems play an important role in linking environmental stress to various negative health outcomes and that knowledge about these psychobiological pathways is of considerable importance for the possibilities to prevent and treat environmentally induced ill health.