Environmental Engineering Reference
In-Depth Information
nature of sleep to compensate for disturbance), it appears difficult to deprive sleep
sufficiently to produce adverse health effects in most situations. However, when noise
pollution is so severe as to disturb sleep on a regular unrelenting basis, this would con-
stitute a hazard to one's health. Critical questions that remain include what is the
function of sleep and its benefit to health and how does sleep disturbance manifest
itself in terms of ill health and well-being?
Stress response
There is considerable debate as to whether the non-auditory factors associated with
noise could have detrimental health consequences due to a general stress syndrome.
Such mechanisms are not new. Selye (1956) proposed a general adaptation syndrome
for stress with three stages: alarm reaction, resistance and a stage of exhaustion.
There are health consequences associated with the final stages of this schema. At the
low to moderate levels of stress, where adaptation in the resistance stage can occur,
there may still be a 'price to pay', including, for example, lowered resistance to infec-
tion, gastrointestinal ulcers and cardiovascular disease. Besides the reductionist bio-
medical models of stress-induced disease, there are other more recent models of stress
that include psychological and social components, as well as biological components
(ie the bio-psychosocial or psychosomatic model of disease that include the concepts
of coping; Oken, 2000).
Noise, particularly loud and unexpected, is known to have an undesirable phys-
iological effect on the recipient. How much this and the slower responses lead to a
generalized stress response via the hypothalamic pituitary adrenal (HPA) axis, sym-
pathetic (adrenomedullary) nervous system (SNS) and cardiovascular reactivity is
controversial. The HPA axis and SNS have central roles in the ongoing homeostatic
regulatory processes of the body in the face of the changing environmental stimuli
that an individual encounters. This provides the body with the physiological survival
mechanism commonly termed 'fight or flight', which can be activated in situations
where the individual is unable to cope adequately with an extreme and potentially
threatening set of stimuli. Furthermore, it has been suggested that excessive activa-
tion of this system, as with chronic noise exposure, can lead to patho-physiological
processes, such as elevated blood pressure, high serum cholesterol, diabetes and
cardiovascular disease.
It is known that noise can cause release of 'stress hormones' Babisch (1998,
2000), and Ising et al (1999) discovered that subjects exposed to noise show elevated
levels of stress hormones in the blood. This is supported by Maschke et al (1993),
who found that subjects exposed to aircraft noise with maximum levels of 55-65
dB(A) showed increased cortisol levels. The link between stress and cardiovascular
disease is well documented - for example, Morrell et al (1997) report evidence for
an association between perceived stress and fatal/non-fatal coronary artery events.
This is supported by epidemiological evidence that chronic noise exposure increases
the risk of ischaemic heart disease (Schwartz and Thompson, 1993).
The long-term activation of the HPA system and increased release of cortisol can
result in a number of health problems, including immuno-suppression, insulin resis-
tance, osteoporosis and intestinal problems. It is also thought that noise exposure
can lead to increased systemic glycerol and non-sterified fatty acids, thus raising the
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