Health impact assessment of traffic noise in Madrid (Spain)
Introduction
According to a recent study by the World Health Organisation Regional Office for Europe (WHO, 2011), 20% of the population of EU countries is exposed to traffic noise levels of above 65 dBA during the day and 30% is exposed to levels of over 55 dBA at night, which translates as a loss of 61,000 disability-adjusted life years (DALYs). For levels above these values, which are considered health-protective, many studies report statistically significant associations between exposure to noise and cardiovascular diseases (Niemann et al., 2006; Coghlan, 2007; Van Kempen et al., 2002; Davies et al., 2005; Schwela at al., 2005; Stansfeld et al., 2005), respiratory system diseases (Niemann et al., 2006; Ising et al., 2003, Ising et al., 2004) and connective tissue diseases (arthritis) (Niemann et al., 2006). According to a recent meta-analysis, traffic noise would rank among the four environmental factors having the greatest health impact and causing anywhere from 400 to 1500 DALYs per million population in Europe (Hänninen et al., 2014).
It is estimated that 3% of cases of ischaemic heart disease in large cities are attributable to road traffic noise (Babisch, 2008). There are ever more studies that point to a significant association between urban noise and severe cardiovascular events, such as myocardial infarction and stroke (Babisch, 2006; Selander et al., 2009; Sørensen et al., 2011). The risk factors which are directly related to cerebrovascular accident are hypertension, arteriosclerosis and low heart-rate variability index.
Furthermore, the degree of acceptance of environmental noise is determined by psychosocial and demographic aspects, such as time of residence, sensitivity, attitude and personality (Paunovic et al., 2009, Guski, 1999). This response is channelled by the limbic system to the hypothalamus, in an endocrine process that culminates in the adrenal cortex with the release of cortisol. Exposure to nocturnal noise produces sleep interruptions and electroencephalography (EEG) arousal, which cause a lack of deep, repairing slow-wave sleep (SWS), as well as affecting rapid eye movement (REM) sleep (Eberhardt, 1988, Belojevic et al., 1997). A reduction in the time of repairing sleep causes an increase in cortisol levels on the following day (Leproult et al., 1997, Vgontzas et al., 1999, 2003; Spiegel et al., 2003; Ising et al., 2004). All studies report a generalised long-term inability on the part of individuals to adapt to nocturnal noise, which may lead to chronification of cortisol overproduction (Maschke et al., 2002, Maschke, 2003, Ising and Ising, 2002). Hypercortisolaemia is associated with the development or exacerbation of atherosclerosis. Indeed, cortisol activates the adipose tissue metabolism in order to increase the supply of energy to the body in response to stress. Lypolisis of triglycerides increases the quantity of fatty acids in the arteries, favouring the irreversible accumulation of plaques that increase the risk of cerebrovascular accident due to ischaemia or thrombosis (Samra et al., 1998, Spreng, 2000a, Spreng, 2000b).
Lastly, one of the most surprising effects of exposure to noise, and one that has been investigated for some years now, is the increased risk of respiratory diseases among children. While a study undertaken in 2002 in the city of Madrid concluded that noise was a risk factor for daily all-cause emergency hospital admissions (Tobias et al., 2001) across all age groups, another undertaken in 2006 reached the same conclusion for children under the age of 10 years in respect of hospital admissions due to all causes, respiratory diseases and, more specifically, pneumonia (Linares et al., 2006). In other studies, bronchitis and other respiratory symptoms, such as bronchial asthma, were associated with the sensation of noise annoyance, both severe and moderate, as well as sleep disturbances caused by nocturnal noise, particularly in children (Niemann et al., 2006; Ising et al., 2004).
Health outcomes deriving from long-term exposure to noise include both cardiovascular and respiratory events, a phenomenon that has been well documented by cohort studies undertaken in recent years (Hart et al., 2013), but short-term studies which link traffic noise to short-term mortality due to the above-described causes are practically non-existent. Recent research conducted in the city of Madrid links short-term circulatory (Tobías et al., 2014a) and respiratory mortality (Tobías et al., 2014b) in the over-65 age group to traffic noise, regardless of the effects of chemical air pollution. The above association was quantified using relative risk (RR), rather than an indicator that might give an idea of the real impact on population health, such as assessment of the direct impact on annual mortality. This study now calculates the impact on annual mortality attributed to traffic noise among subjects aged over 65 years and compares it to PM2.5-related mortality, which is the indicator of traffic-related chemical pollution recommended by the WHO for ascertaining health impacts (WHO, 2005).
Section snippets
Context and study population
The city of Madrid is a densely populated metropolitan area situated in the central region of Spain. In the period 2003–2005, it had a mean population of 3,099,834, and of this total, 2,507,563 (80%) were aged under 65 years (National Statistics Institute/Instituto Nacional de Estadística); both groups formed the target population for this study. The vehicle fleet exceeded 2 million vehicles, which had a mean daily intensity of 2.4 million cars that peaked in May (2.5 million) and fell to a
Results
Table 1 shows the descriptive statistics for the variables considered in the study and Fig. 1 depicts the histograms and box plot.
WHO guideline values (WHO, 2000) were exceeded on 52% of days and 100% of nights across the period analysed.
In order to ensure that the impacts of noise and PM2.5 were comparable, an increase of qLeqD=1 dBA was considered for the average diurnal noise level. For the purposes of comparison, annual deaths attributable to an increase of qPM2.5=10 μg/m3 in PM2.5
Discussion
Despite having the same source, noise levels and air pollutants in Madrid have similar and independent effects on health (Tobías et al., 2014a, Tobías et al., 2014b). As Table 2 showed, if avoidable mortality attributable to noise is compared to avoidable PM2.5-related mortality, it will be observed that both figures are very similar in the case of cardiovascular cause mortality and that the effect of noise on respiratory mortality was practically double that attributable to PM2.5, though these
Acknowledgements
This was a strategic health action funded by the SEPY-1037/14 and FIS Project: ENPY 1001/13.
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