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EFFECTS ON HEALTH 63
cortisol (Berglund and Lindvall, 1995; Maschke, Rupp and Hecht, 2000; Babisch,
2003). Such changes also occur during sleep without the involvement of cortical
structures. The amygdala has the capacity to learn due to its plasticity, particularly
with respect to the meaning of sound stimuli (for example, danger of an approaching
lorry) (Spreng, 2000, 2004). Acoustic stimulation may act as an unspecific stressor
that arouses the autonomous nervous system and the endocrine system. The generalized
psychophysiological concept given by Henry and Stephens can be applied
directly to noise-induced stress reaction (Henry, 1992). The stress mechanism as such
is genetically determined but it may be modified by experience and environmental
factors. Its biological function is to prepare the organism to cope with a demanding
stressor. The arousal of the sympathetic and endocrine system is associated with
changes in physiological functions and the metabolism of the organism, including
BP, cardiac output, blood lipids (cholesterol, triglycerides, free fatty acids, phosphatides),
carbohydrates (glucose), electrolytes (magnesium, calcium), blood clotting
factors (thrombocyte aggregation, blood viscosity, leukocyte count) and others
(Friedman and Rosenman, 1975; Cohen, Kessler and Underwood Gordon, 1995;
Lundberg, 1999). In the long term, functional changes and dysregulation may occur,
thus increasing the risk of manifest diseases.
Fig. 4.3 shows the principal reaction schema used in epidemiological noise research
for hypothesis testing (Babisch, 2002). It simplifies the cause–effect chain, that is:
sound – annoyance (noise) – physiological arousal (stress indicators) – (biological)
risk factors – disease – and mortality (the latter is not explicitly considered in the
graph). The mechanism works “directly” through synaptic nervous interactions and
“indirectly” through the emotional and the cognitive perception of the sound. It
should be noted that the “direct” pathway is relevant even at low sound levels particularly
during sleep, when the organism is at its nadir of arousal. The objective
noise exposure (sound level) and the subjective noise “exposure” (annoyance) may
serve independently as exposure variables in the statistical analyses of the relationship
between noise and health end points.
Principally, the effects of environmental noise cannot directly be extrapolated from
results of occupational noise studies. The two noise environments cannot simply be
merged into one sound energy-related dose–response model (for example, a simple
24-hour average noise level measured with a dose-meter). Noise effects are not only
dependent on the sound intensity but also on the frequency spectrum, the time pattern
of the sound and the individuals’ activities which are disturbed. Therefore, epidemiological
studies carried out under real-life conditions can provide the basis for
a quantitative risk assessment provided that there is adequate control over confounding
and exposure variables. Other noise sources might act as confounders
and/or effect modifiers on the association of interest. The effects of road traffic noise
(at home) were shown to be stronger in subjects who were also exposed to high noise
levels at work (Babisch et al., 1990).
4.5.3 PREVIOUS REVIEWS ON ENVIRONMENTAL NOISE AND
CARDIOVASCULAR RISK
Causality in epidemiology can never be completely proven (Schlesselman, 1987;
Christoffel and Teret, 1991; Weed, 2000). It is a gradual term for which evidence is
increasing with the increasing number of facts. However, the magnitude of effect, the
presence of a dose–response relationship and consistency with other studies in different
populations and with different methodology and biological plausibility are
NIGHT NOISE GUIDELINES FOR EUROPE