Review articleRoad traffic noise effects on cardiovascular, respiratory, and metabolic health: An integrative model of biological mechanisms
Introduction
Non-auditory health effects of noise have been widely investigated over the past decades. Field studies provide strong evidence for risk associations and causal relationships. The biological plausibility of such associations is reasonably well documented, which leads to the consideration of noise pollution as a true risk factor for disease and, given its frequency in the population, a major public health issue (WHO, 2000).
Of interest in urban environments is road traffic noise, given the large exposed population and the long exposure time-periods. Some 20% and 30% of the EU population are exposed to noise levels higher than 65 dBA in the daytime and 55 dBA in the night-time, respectively (WHO, 2011). For such noise levels, a number of studies have reported significant associations with cardiovascular diseases (Selander et al., 2009), respiratory diseases (Niemann et al., 2006), type 2 diabetes (Sørensen et al., 2013), and adverse birth outcomes (Díaz and Linares, 2015). Moreover, short-term associations with cardiovascular, respiratory, and diabetes-related outcomes including mortality have been found (Tobías et al., 2001, Tobías et al., 2014, Tobías et al., 2015a, Tobías et al., 2015c, Linares et al., 2006).
Road traffic noise ranks second – only behind fine particles – among the nine environmental risk factors with highest health impact in European countries, which means a loss of 400–1500 healthy life years due to ischemic heart disease per million people (Hänninen et al., 2014). In the city of Madrid (Spain) a health impact study reported a reduction of nearly 200 and 300 deaths per year due to cardiovascular and respiratory causes, respectively, for a 1 dBA decrease in diurnal noise levels, comparable to the death rate reduction obtained with an equivalent decrease in fine particle concentration (Tobías et al., 2015b).
First we review the various biological mechanisms whereby exposure to environmental noise is likely to cause or aggravate cardiovascular, respiratory, and metabolic disorders. Second we briefly look at the neuroendocrine processes triggered by noise as a stressor, and their implications for autonomic balance. Third we present an integrative model comprising all reviewed psychological and pathophysiological mechanisms involved in the onset and development of noise-induced adverse effects on cardiovascular, respiratory, and metabolic health.
Section snippets
Methods
First we searched PubMed databases for articles with combinations of the following keywords in the title: “noise”, “cardiovascular”, “heart disease”, “atherosclerosis”, “infarction”, “stroke”, “hypertension”, “blood pressure”, “heart rate”, “diabetes”, “respiratory”, “annoyance”, and “sleep”, from January 2000 to March 2015. Then we manually searched for appropriate articles – i.e. those dealing with specific physiological or psychological mechanisms – included in the references within the
Noise and cardiovascular health
Over the years, evidence has grown for the hypothesis of a long-term association between road traffic noise exposure in large cities and the occurrence of ischemic heart disease and cerebrovascular disease, in the light of the results from a recent meta-analysis of cross-sectional studies (Banerjee et al., 2014) and from longitudinal studies with increasing statistical power (Babisch et al., 2005, Selander et al., 2009, Argalášová-Sobotová et al., 2013, Sørensen et al., 2011a, Sørensen et al.,
Noise and respiratory health
Unlike the case of cardiovascular disease, research on respiratory morbidity associated with environmental noise is rather scarce. Some time ago, a few pioneering studies reported long-term significant associations with respiratory outcomes such as bronchitis and asthma (Ising et al., 2003, Ising et al., 2004, Niemann et al., 2006). Regarding short-term associations, a time series study found that 4.7% of hospital admissions due to pneumonia in children could be attributed to a 1 dBA increase in
Noise as a source of stress
All proposed mechanisms whereby noise exposure may cause cardiovascular, respiratory, and metabolic alterations rest on the assumption that noise is primarily a psychological stressor (Prasher, 2009). Noise, like any other psychological stimulus, activates the CNS structures of emotional processing and may be a threat for homeostasis. According to the stress model described by McEwen (1998), an individual achieves stability through “allostasis”, which denotes adaptation to environmental
Towards a new integrative model
At this point we are ready to propose an up-to-date stress model comprising all the investigated mechanisms that link noise with cardiovascular, respiratory, and metabolic health outcomes.
The new model allows for an adaptive mechanism that enables coping with sustained psychological stress; this implies diversion of stress from the prefrontal cortex to the central autonomic network for physical processing, reducing the psychological load at the cost of elevating the allostatic load. By doing
Conclusions
The possible biological pathways linking road traffic noise with health outcomes are well documented in noise research. However, some small-scale mechanisms need to be investigated in greater detail, such as those relating noise exposure to systemic inflammation, endothelial dysfunction, and alterations in the immune system. Again, further research is needed to elucidate the role of both the central nervous system structures and the neuroendocrine system in noise stress management, provided
Acknowledgments
We thank Aurelio Tobías for his support and valuable comments.
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