Increased catecholamine levels in urine in subjects exposed to road traffic noise: The role of stress hormones in noise research
Introduction
Traffic noise causes considerable disturbance and annoyance in exposed subjects Gierke and Eldred, 1993, Miedema and Vos, 1998, Schwela, 2000. Besides the psychosocial effects of community noise, there is concern about the impact of noise on public health, particularly regarding cardiovascular outcomes (Suter, 1992, Gezondheitsraad, 1994, Berglund and Lindvall, 1995, Babisch, 1998, Porter et al., 1998; Passchier-Vermeer and Passchier, 2000). Fig. 1 describes the reaction model and the hypotheses to be tested in epidemiological studies. Noise activates the sympathetic and endocrine system of the organism. The mechanism works either directly through the synaptic nervous interactions in the reticular activating system and parts of the between brain (including the hypothalamus) or indirectly through the emotional and the cognitive perception of the sound via the cortical and subcortical structures (including the limbic region; Andersson and Lindvall, 1988, Spreng, 2000a). According to the general stress model, neuroendocrine arousal affects the humoral and metabolic state of the organism and acts as a mediator along the pathway from the perceived sound to the stress-related disease (Henry, 1993). In principle, a variety of well known and established risk factors may be affected. Many are well recognized as risk factors for ischemic heart disease such as blood lipids, glucose level, and haemodynamic and haemostatic factors.
The role of stress hormones in the reaction model is crucial. Although not being a risk factor as such (in epidemiological terms), stress hormones like adrenaline and noradrenaline can be viewed as stress indicators (Grunberg and Singer, 1990) when considering the cause–effect chain, i.e. sound, annoyance (noise), physiological arousal (stress indicators), (biological) risk factors, and disease.
In general, noise epidemiology can be focussed on three levels of outcome when investigating the relationships between noise and health. These levels are stress indicators (e.g. stress hormones), risk factors (e.g. blood pressure, blood lipids, and haemostatic factors), and manifest diseases (e.g. hypertension and ischemic heart disease).
Noise effects in stress indicators have at the moment no direct clinical relevance in terms of health. It would be difficult to assess the increase in risk for a certain disease due to changes in physiological indicators of stress (arousal). Stress indicators, however, are particularly useful for investigating biological mechanisms because they are short-term reacting parameters, which occur at the beginning of the reaction chain. (The significance to health of increased cortisol levels due to noise is currently discussed (Spreng, 2000b).)
In contrast to this, noise effects in established biological risk factors have a direct relevance to health (per definition). Since these are mostly continuous variables, even small nonpathological mean (average) changes in populations may be relevant to assess the relationship between noise and health in relatively small samples. However, for a quantitative risk assessment, external sources of data would have to be used. For example, what does an “x%” increase in cholesterol level in the exposed group mean with regard to the risk of myocardial infarction?
Noise effects with regard to the prevalence or incidence of the manifest disease as a statistical endpoint clearly have a relevance to health. From the collected data, it is possible to directly carry out a quantitative risk assessment. However, since distinct rare events are the basis, large samples are needed for achieving statistically significant results.
As part of an environmental research project on physiological and biochemical factors and health determinants in young women, the concentrations of the catecholamines epinephrine (adrenaline) and norepinephrine (noradrenaline) were measured in the total urine night sample. The women were living in the city of Berlin in streets subject to different levels of traffic noise. The impact of effect modifiers on the association between noise and stress hormones was tested by comparing the different abilities of the subjects in coping with the noise.
Section snippets
Methods
In 1993/1994, the city of Berlin (Department of Health and Social Affairs) conducted an environmental survey. In two areas of inner city districts, 801 female subjects were screened with regard to a large variety of biochemical parameters measured in blood and urine, including heavy metals, pesticides, polyaromatic hydrocarbons, immunoglobulins, and standard clinical blood parameters (Fromme and Beyer, 1996). The collection of data comprised health-related factors, determinants of the home
Results
Traffic volume varied from 170 to 38,000 vehicles per day on the streets. It was estimated that these exposure figures correspond to nighttime average sound pressure levels at the facades of the homes from approximately 40 to 75 dB(A). Assuming an increase in noise level of 3 dB(A) per doubling of traffic volume, a difference of 23 dB(A) of the Leq, 24 h between the noisiest and the quietest streets is obtained. One-third of the women lived in streets with more than 20,000 vehicles/day,
Discussion
Acute endocrine changes, including catecholamines and glucocorticoids levels in urine, due to exposure to transportation noise or industrial noise have been seen in several experimental studies (Ising et al., 1980, Borg, 1981, Ising et al., 1990, Maschke et al., 1992; Melamed and Bruhis, 1996; Maschke et al., 1998). Intraindividual comparisons were made by comparing the subjects' responses to the noise on days of different exposure. The studies were carried out under laboratory or field
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2022, Journal of Veterinary BehaviorCitation Excerpt :Therefore, increases in DA likely acts to prime appropriate behavioral responses to the stressor (LeBlanc and Ducharme, 2007; Belujon and Grace, 2015). A considerable body of previous research indicates elevations in peripheral circulating levels of the catecholamine E accompanies acute stressors, for example, (Ward et al., 1983; Beerda et al., 1996, 2000; Babisch et al., 2001; LeBlanc and Ducharme, 2007), but contrary to our prediction, there was no significant difference in Boarding dog group E levels compared to Home group dogs in the current study. Acute stress causes a relatively brief burst of E from the adrenal medulla, and its short half-life may indicate that E is not the optimal marker for evaluation of a stressor lasting many hours (Kennedy et al., 2001).