Green space may improve health by enabling physical activity and recovery from stress or by decreased pollution levels. We investigated the association between residential green (greenness or green space) and mortality in adults using the Swiss National Cohort (SNC) by mutually considering air pollution and transportation noise exposure. To reflect residential green at the address level, two different metrics were derived: normalised difference vegetation index (NDVI) for greenness, and high resolution land use classification data to identify green spaces (LU-green). We used stratified Cox proportional hazard models (stratified by sex) to study the association between exposure and all natural cause mortality, respiratory and cardiovascular disease (CVD), including ischemic heart disease, stroke and hypertension related mortality. Models were adjusted for civil status, job position, education, neighbourhood socioeconomic position (SEP), geographic region, area type, altitude, air pollution (PM 10), and transportation noise. From the nationwide SNC, 4.2 million adults were included providing 7.8 years of follow-up and respectively 363,553, 85,314 and 232,322 natural cause, respiratory and CVD deaths. Hazard ratios (and 95%-confidence intervals) for NDVI [and LU-green] per interquartile range within 500m of residence were highly

Most studies published to date consider single noise sources and the reported noise metrics are not informative about the peaking characteristics of the source under investigation. Our study focuses on the association between cardiovascular mortality in Switzerland and the three major transportation noise sources-road, railway and aircraft traffic-along with a novel noise metric termed intermittency ratio (IR), expressing the percentage contribution of individual noise events to the total noise energy from all sources above background levels. We generated Swiss-wide exposure models for road, railway and aircraft noise for 2001. Noise from the most exposed façade was linked to geocodes at the residential floor height for each of the 4.41 million adult (>30 y) Swiss National Cohort participants. For the follow-up period 2000-2008, we investigated the association between all noise exposure variables [L(Road), L(Rail), L(Air), and IR at night] and various cardiovascular primary causes of death by multipollutant Cox regression models adjusted for potential confounders including NO. The most consistent associations were seen for myocardial infarction: adjusted hazard ratios (HR) (95% CI) per 10 dB increase of exposure were 1.038 (1.019-1.058), 1.018 (1.004-1.031), and 1.026 (1.004-1.048) respectively for L(Road), L(Rail), and L(Air). In addition, total IR at night played a role: HRs for CVD were non-significant in the 1st, 2nd and 5th quintiles whereas they were 1.019 (1.002-1.037) and 1.021 (1.003-1.038) for the 3rd and 4th quintiles. Our study demonstrates the impact of all major transportation noise sources on cardiovascular diseases. Mid-range IR levels at night (i.e. between continuous and highly intermittent) are potentially more harmful than continuous noise levels of the same average level.

Exposure to traffic noise is associated with stress and sleep disturbances. The World Health Organization (WHO) recently concluded that road traffic noise increases the risk for ischemic heart disease and potentially other cardiometabolic diseases, including stroke, obesity, and diabetes. The WHO report focused on whole-day noise exposure, but new epidemiological and translational field noise studies indicate that nighttime noise, in particular,is an important risk factor for cardiovascular disease (CVD) through increased levels of stress hormones and vascular oxidative stress, leading to endothelial dysfunction and subsequent development of various CVDs. Novel experimental studies found noise to be associated with oxidative stress–induced vascular and brain damage, mediated by activation of the NADPH oxidase, uncoupling of endothelial and neuronal nitric oxide synthase, and vascular/brain infiltration with inflammatory cells. Noise-induced pathophysiology was more pronounced in response to nighttime as compared with daytime noise. This review focuses on the consequences of nighttime noise.

BackgroundEpidemiological studies have inconsistently linked transportation noise and air pollution (AP) with diabetes risk. Most studies have considered single noise sources and/or AP, but none has investigated their mutually independent contributions to diabetes risk.MethodsWe investigated 2631 participants of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA), without diabetes in 2002 and without change of residence between 2002 and 2011. Using questionnaire and biomarker data, incident diabetes cases were identified in 2011. Noise and AP exposures in 2001 were assigned to participants’ residences (annual average road, railway or aircraft noise level during day-evening-night (Lden), total night number of noise events, intermittency ratio (temporal variation as proportion of event-based noise level over total noise level) and nitrogen dioxide (NO2) levels. We applied mixed Poisson regression to estimate the relative risk (RR) of diabetes and their 95% confidence intervals (CI) in mutually-adjusted models.ResultsDiabetes incidence was 4.2%. Median [interquartile range (IQR)] road, railway, aircraft noise and NO2 were 54 (10) dB, 32 (11) dB, 30 (12) dB and 21 (15) μg/m3, respectively. Lden road and aircraft were associated with incident diabetes (respective RR: 1.35; 95% CI: 1.02–1.78 and 1.86; 95% CI: 0.96–3.59 per IQR) independently of Lden railway and NO2 (which were not associated with diabetes risk) in mutually adjusted models. We observed stronger effects of Lden road among participants reporting poor sleep quality or sleeping with open windows.ConclusionsTransportation noise may be more relevant than AP in the development of diabetes, potentially acting through noise-induced sleep disturbances.

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