The role of noise as an environmental pollutant and its impact on health are being increasingly recognized. Beyond its effects on the auditory system, noise causes annoyance and disturbs sleep, and it impairs cognitive performance. Furthermore, evidence from epidemiologic studies demonstrates that environmental noise is associated with an increased incidence of arterial hypertension, myocardial infarction, and stroke. Both observational and experimental studies indicate that in particular night-time noise can cause disruptions of sleep structure, vegetative arousals (e.g. increases of blood pressure and heart rate) and increases in stress hormone levels and oxidative stress, which in turn may result in endothelial dysfunction and arterial hypertension. This review focuses on the cardiovascular consequences of environmental noise exposure and stresses the importance of noise mitigation strategies for public health.

https://www.klein-winternheim.de/lokale-agenda/d43d5e550c96630fc05d6c66ec88f0f4_Elsner-eurheartj.ehu030.full.pdf

Cardiovascular effects of environmental noise exposure

To update the current state of evidence and assess its quality, we conducted a systematic review on the effects of environmental noise exposure on the cardio-metabolic systems as input for the new WHO environmental noise guidelines for the European Region. We identified 600 references relating to studies on effects of noise from road, rail and air traffic, and wind turbines on the cardio-metabolic system, published between January 2000 and August 2015. Only 61 studies, investigating different end points, included information enabling estimation of exposure response relationships. These studies were used for meta-analyses, and assessments of the quality of evidence using the Grading of Recommendations Assessment, Development and Evaluation (GRADE). A majority of the studies concerned traffic noise and hypertension, but most were cross-sectional and suffering from a high risk of bias. The most comprehensive evidence was available for road traffic noise and Ischeamic Heart Diseases (IHD). Combining the results of 7 longitudinal studies revealed a Relative Risk (RR) of 1.08 (95% CI: 1.01-1.15) per 10 dB (LDEN) for the association between road traffic noise and the incidence of IHD. We rated the quality of this evidence as high. Only a few studies reported on the association between transportation noise and stroke, diabetes, and/or obesity. The quality of evidence for these associations was rated from moderate to very low, depending on transportation noise source and outcome. For a comprehensive assessment of the impact of noise exposure on the cardiovascular and metabolic system, we need more and better quality evidence, primarily based on longitudinal studies.

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WHO Environmental Noise Guidelines for the European Region: A Systematic Review on Environmental Noise and Cardiovascular and Metabolic Effects: A Summary.

To evaluate the quality of available evidence on the effects of environmental noise exposure on sleep a systematic review was conducted. The databases PSYCINFO, PubMed, Science Direct, Scopus, Web of Science and the TNO Repository were searched for non-laboratory studies on the effects of environmental noise on sleep with measured or predicted noise levels and published in or after the year 2000. The quality of the evidence was assessed using GRADE criteria. Seventy four studies predominately conducted between 2000 and 2015 were included in the review. A meta-analysis of surveys linking road, rail, and aircraft noise exposure to self-reports of sleep disturbance was conducted. The odds ratio for the percent highly sleep disturbed for a 10 dB increase in Lnight was significant for aircraft (1.94; 95% CI 1.61–2.3), road (2.13; 95% CI 1.82–2.48), and rail (3.06; 95% CI 2.38–3.93) noise when the question referred to noise, but non-significant for aircraft (1.17; 95% CI 0.54–2.53), road (1.09; 95% CI 0.94–1.27), and rail (1.27; 95% CI 0.89–1.81) noise when the question did not refer to noise. A pooled analysis of polysomnographic studies on the acute effects of transportation noise on sleep was also conducted and the unadjusted odds ratio for the probability of awakening for a 10 dBA increase in the indoor Lmax was significant for aircraft (1.35; 95% CI 1.22–1.50), road (1.36; 95% CI 1.19–1.55), and rail (1.35; 95% CI 1.21–1.52) noise. Due to a limited number of studies and the use of different outcome measures, a narrative review only was conducted for motility, cardiac and blood pressure outcomes, and for children’s sleep. The effect of wind turbine and hospital noise on sleep was also assessed. Based on the available evidence, transportation noise affects objectively measured sleep physiology and subjectively assessed sleep disturbance in adults. For other outcome measures and noise sources the examined evidence was conflicting or only emerging. According to GRADE criteria, the quality of the evidence was moderate for cortical awakenings and self-reported sleep disturbance (for questions that referred to noise) induced by traffic noise, low for motility measures of traffic noise induced sleep disturbance, and very low for all other noise sources and investigated sleep outcomes.

WHO Environmental Noise Guidelines for the European Region: A Systematic Review on Environmental Noise and Effects on Sleep.

In metropolitan areas, road traffic is a major contributor to ambient air pollution and the dominant source of community noise. The authors investigated the independent and joint influences of community noise and traffic-related air pollution on risk of coronary heart disease (CHD) mortality in a population-based cohort study with a 5-year exposure period (January 1994-December 1998) and a 4-year follow-up period (January 1999-December 2002). Individuals who were 45-85 years of age and resided in metropolitan Vancouver, Canada, during the exposure period and did not have known CHD at baseline were included (n = 445,868). Individual exposures to community noise and traffic-related air pollutants, including black carbon, particulate matter less than or equal to 2.5 μm in aerodynamic diameter, nitrogen dioxide, and nitric oxide, were estimated at each person's residence using a noise prediction model and land-use regression models, respectively. CHD deaths were identified from the provincial death registration database. After adjustment for potential confounders, including traffic-related air pollutants or noise, elevations in noise and black carbon equal to the interquartile ranges were associated with 6% (95% confidence interval: 1, 11) and 4% (95% confidence interval: 1, 8) increases, respectively, in CHD mortality. Subjects in the highest noise decile had a 22% (95% confidence interval: 4, 43) increase in CHD mortality compared with persons in the lowest decile. These findings suggest that there are independent effects of traffic-related noise and air pollution on CHD mortality.

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Association of Long-term Exposure to Community Noise and Traffic-related Air Pollution With Coronary Heart Disease Mortality

Environmental factors can act as facilitators of chronic non-communicable diseases. Ambient noise and air pollution collectively outrank all other environmental risk factors in importance, contributing to over 75% of the disease and disability burden associated with known environmental risk factors. In the first part of this review, we discussed the global burden and epidemiologic evidence supporting the importance of these novel risk factors as facilitators of cardiometabolic disease. In this part, we will discuss pathophysiological mechanisms responsible for noise and air pollution-mediated effects. Akin to traditional cardiovascular risk factors, a considerable body of evidence suggests that these environmental agents induce low-grade inflammation, oxidative stress, vascular dysfunction, and autonomic nervous system imbalance, thereby facilitating the development of diseases such as hypertension and diabetes. Through their impact on traditional risk factors and via additional novel mechanisms, environmental risk factors may have much larger impact on cardiovascular events than currently appreciated. In the second part of this review, we discuss deficiencies and gaps in knowledge and opportunities for new research.

/pdf/environmental-stressors-and-cardio-metabolic-disease-part-ii-10na44bt54.pdf

Environmental stressors and cardio-metabolic disease: part II-mechanistic insights.

BackgroundSeveral studies show an association between exposure to aircraft or road traffic noise and cardiovascular effects, which may be mediated by a noise-induced release of stress hormonesObje

/pdf/saliva-cortisol-and-exposure-to-aircraft-noise-in-six-5bddt9v07r.pdf

Saliva Cortisol and Exposure to Aircraft Noise in Six European Countries

Objectives Studies on the health effects of aircraft and road traffic noise exposure suggest excess risks of hypertension, cardiovascular disease and the use of sedatives and hypnotics. Our aim was to assess the use of medication in relation to noise from aircraft and road traffic. Methods This cross-sectional study measured the use of prescribed antihypertensives, antacids, anxiolytics, hypnotics, antidepressants and antasthmatics in 4,861 persons living near seven airports in six European countries (UK, Germany, the Netherlands, Sweden, Italy, and Greece). Exposure was assessed using models with 1dB resolution (5dB for UK road traffic noise) and spatial resolution of 250×250m for aircraft and 10×10m for road traffic noise. Data were analysed using multilevel logistic regression, adjusting for potential confounders. Results We found marked differences between countries in the effect of aircraft noise on antihypertensive use; for night-time aircraft noise, a 10dB increase in exposure was associated with ORs of 1.34 (95% CI 1.14 to1.57) for the UK and 1.19 (1.02 to 1.38) for the Netherlands but no significant associations were found for other countries. For day-time aircraft noise, excess risks were found for the UK (OR 1.35; CI: 1.13 to 1.60) but a risk deficit for Italy (OR 0.82; CI: 0.71 to 0.96). There was an excess risk of taking anxiolytic medication in relation to aircraft noise (OR 1.28; CI: 1.04 to 1.57 for daytime and OR 1.27; CI: 1.01 to 1.59 for night-time) which held across countries. We also found an association between exposure to 24hr road traffic noise and the use of antacids by men (OR 1.39; CI 1.11 to 1.74). Conclusion Our results suggest an effect of aircraft noise on the use of antihypertensive medication, but this effect did not hold for all countries. Results were more consistent across countries for the increased use of anxiolytics in relation to aircraft noise.

https://oem.bmj.com/content/oemed/68/7/518.full.pdf?with-ds=yes

Maria Chiara Antoniotti

Papers

Saliva Cortisol and Exposure to Aircraft Noise in Six European Countries

Medication use in relation to noise from aircraft and road traffic in six European countries: results of the HYENA study.

Aircraft Noise Exposure and Use of Medication