Validation of an Automatic Arousal Detection Algorithm for Whole-Night Sleep EEG Recordings.

Arousals during sleep are transient accelerations of the EEG signal, considered to reflect sleep perturbations associated with poorer sleep quality. They are typically detected by visual inspection, which is time consuming, subjective, and prevents good comparability across scorers, studies and research centres. We developed a fully automatic algorithm which aims at detecting artefact and arousal events in whole-night EEG recordings, based on time-frequency analysis with adapted thresholds derived from individual data. We ran an automated detection of arousals over 35 sleep EEG recordings in healthy young and older individuals and compared it against human visual detection from two research centres with the aim to evaluate the algorithm performance. Comparison across human scorers revealed a high variability in the number of detected arousals, which was always lower than the number detected automatically. Despite indexing more events, automatic detection showed high agreement with human detection as reflected by its correlation with human raters and very good Cohen's kappa values. Finally, the sex of participants and sleep stage did not influence performance, while age may impact automatic detection, depending on the human rater considered as gold standard. We propose our freely available algorithm as a reliable and time-sparing alternative to visual detection of arousals.

Ultradian modulation of cortical arousals during sleep: effects of age and exposure to nighttime transportation noise.

STUDY OBJECTIVES: The present study aimed at assessing the temporal non-rapid eye movement (NREM) EEG arousal distribution within and across sleep cycles and its modifications with aging and nighttime transportation noise exposure, factors that typically increase the incidence of EEG arousals. METHODS: Twenty-six young (19-33 years, 12 women) and 16 older (52-70 years, 8 women) healthy volunteers underwent a 6-day polysomnographic laboratory study. Participants spent two noise-free nights and four transportation noise exposure nights, two with continuous and two characterized by eventful noise (average sound levels of 45 dB, maximum sound levels between 50 and 62 dB for eventful noise). Generalized mixed models were used to model the time course of EEG arousal rates during NREM sleep and included cycle, age, and noise as independent variables. RESULTS: Arousal rate variation within NREM sleep cycles was best described by a u-shaped course with variations across cycles. Older participants had higher overall arousal rates than the younger individuals with differences for the first and the fourth cycle depending on the age group. During eventful noise nights, overall arousal rates were increased compared to noise-free nights. Additional analyses suggested that the arousal rate time course was partially mediated by slow wave sleep (SWS). CONCLUSIONS: The characteristic u-shaped arousal rate time course indicates phases of reduced physiological sleep stability both at the beginning and end of NREM cycles. Small effects on the overall arousal rate by eventful noise exposure suggest a preserved physiological within- and across-cycle arousal evolution with noise exposure, while aging affected the shape depending on the cycle.

Transportation noise impairs cardiovascular function without altering sleep: The importance of autonomic arousals.

AIMS: Chronic exposure to nocturnal transportation noise has been linked to cardiovascular disorders with sleep impairment as the main mediator. Here we examined whether nocturnal transportation noise affects the main stress pathways, and whether it relates to changes in the macro and micro structure of sleep. METHODS AND RESULTS: Twenty-six young healthy participants (12 women, 24.6 ± 0.7 years, mean ± SE) spent five consecutive 24-h days and one last morning in the laboratory. The first (baseline) and last (recovery) nights comprised a quiet ambient scenario. In-between, four different noise scenarios (low/medium/high intermittent road or rail scenarios with an identical equivalent continuous sound level of 45 dB) were randomly presented during the 8-h nights. Participants felt more annoyed from the transportation noise scenarios compared to the quiet ambient scenario played back during the baseline and recovery nights (F5,117 = 10.2, p < 0.001). Nocturnal transportation noise did not significantly impact polysomnographically assessed sleep macrostructure, blood pressure, nocturnal catecholamine levels and morning cytokine levels. Evening cortisol levels increased after sleeping with highly intermittent road noise compared to baseline (p = 0.002, noise effect: F4,83 = 4.0, p = 0.005), a result related to increased cumulative duration of autonomic arousals during the noise nights (F5,106 = 3.4, p < 0.001; correlation: rpearson = 0.64, p = 0.006). CONCLUSION: Under controlled laboratory conditions, highly intermittent nocturnal road noise exposure at 45 dB increased the cumulative duration of autonomic arousals during sleep and next-day evening cortisol levels. Our results indicate that, without impairing sleep macrostructure, nocturnal transportation noise of 45 dB is a physiological stressor that affects the hypothalamic-pituitary-adrenal axis during the following day in healthy young good sleepers.

Self-Reported Sleep Disturbance from Road, Rail and Aircraft Noise: Exposure-Response Relationships and Effect Modifiers in the SiRENE Study.

This survey investigates the cross-sectional association between nighttime road, rail and aircraft noise exposure and the probability to be highly sleep disturbed (%HSD), as measured by self-report in postal and online questionnaires. As part of the Swiss SiRENE study, a total of 5592 survey participants in the entire country were selected based on a stratified random sample of their dwelling. Self-reported sleep disturbance was measured using an ICBEN-style 5-point verbal scale. The survey was carried out in four waves at different times of the year. Source-specific noise exposure was calculated for several façade points for each dwelling. After adjustment for potential confounders, all three noise sources showed a statistically significant association between the nighttime noise level LNight at the most exposed façade point and the probability to report high sleep disturbance, as determined by logistic regression. The association was strongest for aircraft noise and weakest for road traffic noise. We a priori studied the role of a range of effect modifiers, including the "eventfulness" of noise exposure, expressed as the Intermittency Ratio (IR) metric, bedroom window position, bedroom orientation towards the closest street, access to a quiet side of the dwelling, degree of urbanization, sleep timing factors (bedtime and sleep duration), sleep medication intake, survey season and night air temperature. While bedroom orientation exhibited a strong moderating effect, with an Leq-equivalent of nearly 20 dB if the bedroom faces away from the nearest street, the LNight-%HSD associations were not affected by bedroom window position, sleep timing factors, survey season, or temperature.

Associations of Various Nighttime Noise Exposure Indicators with Objective Sleep Efficiency and Self-Reported Sleep Quality: A Field Study.

It is unclear which noise exposure time window and noise characteristics during nighttime are most detrimental for sleep quality in real-life settings. We conducted a field study with 105 volunteers wearing a wrist actimeter to record their sleep during seven days, together with concurrent outdoor noise measurements at their bedroom window. Actimetry-recorded sleep latency increased by 5.6 min (95% confidence interval (CI): 1.6 to 9.6 min) per 10 dB(A) increase in noise exposure during the first hour after bedtime. Actimetry-assessed sleep efficiency was significantly reduced by 2%-3% per 10 dB(A) increase in measured outdoor noise (Leq, 1h) for the last three hours of sleep. For self-reported sleepiness, noise exposure during the last hour prior to wake-up was most crucial, with an increase in the sleepiness score of 0.31 units (95% CI: 0.08 to 0.54) per 10 dB(A) Leq,1h. Associations for estimated indoor noise were not more pronounced than for outdoor noise. Taking noise events into consideration in addition to equivalent sound pressure levels (Leq) only marginally improved the statistical models. Our study provides evidence that matching the nighttime noise exposure time window to the individual's diurnal sleep-wake pattern results in a better estimate of detrimental nighttime noise effects on sleep. We found that noise exposure at the beginning and the end of the sleep is most crucial for sleep quality.

Façades, floors and maps - Influence of exposure measurement error on the association between transportation noise and myocardial infarction.

BACKGROUND: Epidemiological research on transportation noise uses different exposure assessment strategies based on façade point estimates or regulatory noise maps. The degree of exposure measurement error and subsequent potentially biased risk estimates related to exposure definition is unclear. We aimed to evaluate associations between transportation noise exposure and myocardial infarction (MI) mortality considering: assumptions about residential floor, façade point selection (loudest, quietest, nearest), façade point vs. noise map estimates, and influence of averaging exposure at coarser spatial scales (e.g. in ecological health studies). METHODS: Lden from the façade points were assigned to >4 million eligible adults in the Swiss National Cohort for the best match residential floor (reference), middle floor, and first floor. For selected floors, the loudest and quietest exposed façades per dwelling, plus the nearest façade point to the residential geocode, were extracted. Exposure was also assigned from 10 × 10 m noise maps, using "buffers" from 50 to 500 m derived from the maps, and by aggregating the maps to larger areas. Associations between road traffic and railway noise and MI mortality were evaluated by multi-pollutant Cox regression models, adjusted for aircraft noise, NO2 and socio-demographic confounders, following individuals from 2000 to 2008. Bias was calculated to express differences compared to the reference. RESULTS: Hazard ratios (HRs) for the best match residential floor were 1.05 (1.02-1.07) and 1.03 (1.01-1.05) per IQR (11.3 and 15.0 dB) for road traffic and railway noise, respectively. In most situations, comparing the alternative exposure definitions to this reference resulted in attenuated HRs. For example, assuming everyone resided on the middle or everyone on first floor introduced little bias (%Bias in excess risk: -1.9 to 4.4 road traffic and -4.4 to 10.7 railway noise). Using the noise grids generated a bias of approximately -26% for both sources. Averaging the maps at a coarser spatial scale led to bias from -19.4 to -105.1% for road traffic and 17.6 to -34.3% for railway noise and inflated the confidence intervals such that some HRs were no longer statistically significant. CONCLUSION: Changes in spatial scale introduced more bias than changes in residential floor. Use of noise maps to represent residential exposure may underestimate noise-induced health effects, in particular for small-scale heterogeneously distributed road traffic noise in urban settings.

A systematic analysis of mutual effects of transportation noise and air pollution exposure on myocardial infarction mortality: a nationwide cohort study in Switzerland.

AIMS: The present study aimed to disentangle the risk of the three major transportation noise sources-road, railway, and aircraft traffic-and the air pollutants NO2 and PM2.5 on myocardial infarction (MI) mortality in Switzerland based on high quality/fine resolution exposure modelling. METHODS AND RESULTS: We modelled long-term exposure to outdoor road traffic, railway, and aircraft noise levels, as well as NO2 and PM2.5 concentration for each address of the 4.40 million adults (>30 years) in the Swiss National Cohort (SNC). We investigated the association between transportation noise/air pollution exposure and death due to MI during the follow-up period 2000-08, by adjusting noise [Lden(Road), Lden(Railway), and Lden(Air)] estimates for NO2 and/or PM2.5 and vice versa by multipollutant Cox regression models considering potential confounders. Adjusting noise risk estimates of MI for NO2 and/or PM2.5 did not change the hazard ratios (HRs) per 10 dB increase in road traffic (without air pollution: 1.032, 95% CI: 1.014-1.051, adjusted for NO2 and PM2.5: 1.034, 95% CI: 1.014-1.055), railway traffic (1.020, 95% CI: 1.007-1.033 vs. 1.020, 95% CI: 1.007-1.033), and aircraft traffic noise (1.025, 95% CI: 1.006-1.045 vs. 1.025, 95% CI: 1.005-1.046). Conversely, noise adjusted HRs for air pollutants were lower than corresponding estimates without noise adjustment. Hazard ratio per 10 µg/m³ increase with and without noise adjustment were 1.024 (1.005-1.043) vs. 0.990 (0.965-1.016) for NO2 and 1.054 (1.013-1.093) vs. 1.019 (0.971-1.071) for PM2.5. CONCLUSION: Our study suggests that transportation noise is associated with MI mortality, independent from air pollution. Air pollution studies not adequately adjusting for transportation noise exposure may overestimate the cardiovascular disease burden of air pollution.

Adverse impact of nocturnal transportation noise on glucose regulation in healthy young adults: Effect of different noise scenarios.

BACKGROUND: Epidemiological evidence indicates an association between transportation noise exposure and a higher risk of developing type 2 diabetes. Sleep disturbances are thought to be one of the mechanisms as it is well established that a few nights of short or poor sleep impair glucose tolerance and insulin sensitivity in healthy good sleepers. OBJECTIVES: The present study aimed to determine the extent to which exposure to nocturnal transportation noise affects glucose metabolism, and whether it is related to noise-induced sleep alterations. METHODS: Twenty-one young healthy volunteers (nine women) participated in a six-day laboratory study starting with a noise-free baseline night, then four nights sleeping with randomly-presented transportation noise scenarios (three road and one railway noise scenario) with identical average sound level of 45dB but differing in eventfulness and ending with a noise-free recovery night. Sleep was measured by polysomnography. Glucose tolerance and insulin sensitivity were measured after the baseline, the last noise night and the recovery nights with an oral glucose tolerance test using Matsuda and Stumvoll insulin sensitivity indexes. Eleven participants were assigned a less eventful noise scenario during the last noise night (LE-group), while the other ten had a more eventful noise scenario (ME-group). Baseline metabolic and sleep variables between the two intervention groups were compared using a non-parametric Mann-Whitney U test while mixed models were used for repeated measure analysis. RESULTS: All participants had increased glucoseAUC (mean±SE, 14±2%, p<0.0001) and insulinAUC (55±10%, p<0.0001) after the last noise night compared to the baseline night. 2h-glucose level tended to increase only in the ME-group between baseline (5.1±0.22mmol·L-1) and the last noise night (6.1±0.39mmol·L-1, condition: p=0.001, interaction: p=0.08). Insulin sensitivity assessed with Matsuda and Stumvoll indexes respectively decreased by 7±8% (p=0.001) and 9±2% (p<0.0001) after four nights with transportation noise. Only participants in the LE-group showed beneficial effects of the noise-free recovery night on glucose regulation (relative change to baseline: glucoseAUC: 1±2%, p=1.0 for LE-group and 18±4%, p<0.0001 for ME-group; Stumvoll index: 3.2±2.6%, p=1.0 for LE-group and 11±2.5%, p=0.002 for ME-group). Sleep was mildly impaired with increased sleep latency of 8±2min (<0.0001) and more cortical arousals per hour of sleep (1.8±0.6arousals/h, p=0.01) during the last noise night compared to baseline. No significant associations between sleep measures and glucose tolerance and insulin sensitivity were found. CONCLUSION: In line with epidemiological findings, sleeping four nights with transportation noise impaired glucose tolerance and insulin sensitivity. Based on the presented sound exposure, the eventfulness of the noise scenarios seems to play an important role for noise-induced alterations in glucose regulation. However, we could not confirm our hypothesis that transportation noise impairs glucose regulation via deterioration in sleep quality and quantity. Therefore, other factors, such as stress-related pathways, may need to be considered as potential triggers for noise-evoked glucose intolerance in future research.

Long-term exposure to transportation noise and its association with adiposity markers and development of obesity.

The contribution of different transportation noise sources to metabolic disorders such as obesity remains understudied. We evaluated the associations of long-term exposure to road, railway and aircraft noise with measures of obesity and its subphenotypes using cross-sectional and longitudinal designs. We assessed 3796 participants from the population-based Swiss Cohort Study on Air Pollution and Lung and Heart Diseases (SAPALDIA), who attended the visits in 2001 (SAP2) and 2010/2011 (SAP3) and who were aged 29-72 at SAP2. At SAP2 we measured body mass index (BMI, kg/m2). At SAP3 we measured BMI, waist circumference (centimetres) and Kyle body Fat Index (%) and derived overweight, central and general obesity. Longitudinally for BMI, we derived change in BMI, incidence of overweight and obesity and a 3-category outcome combining the latter two. We assigned source-specific 5-year mean noise levels before visits and during follow-up at the most exposed dwelling façade (Lden, dB), using Swiss noise models for 2001 and 2011 and participants' residential history. Models were adjusted for relevant confounders, including traffic-related air pollution. Exposure to road traffic noise was significantly associated with all adiposity subphenotypes, cross-sectionally (at SAP3) [e.g. beta (95% CI) per 10 dB, BMI: 0.39 (0.18; 0.59); waist circumference: 0.93 (0.37; 1.50)], and with increased risk of obesity, longitudinally (e.g. RR = 1.25, 95% CI: 1.04; 1.51, per 10 dB in 5-year mean). Railway noise was significantly related to increased risk of overweight. In cross-sectional analyses, we further identified a stronger association between road traffic noise and BMI among participants with cardiovascular disease and an association between railway noise and BMI among participants reporting bad sleep. Associations were independent of the other noise sources, air pollution and robust to all adjustment sets. No associations were observed for aircraft noise. Long-term exposure to transportation noise, particularly road traffic noise, may increase the risk of obesity and could constitute a pathway towards cardiometabolic and other diseases.

Transportation noise exposure, noise annoyance and respiratory health in adults: A repeated-measures study.

Transportation noise leads to sleep disturbance and to psychological and physiological sustained stress reactions, which could impact respiratory health. However, epidemiologic evidence on associations of objective transportation noise exposure and also perceived noise annoyance with respiratory morbidity is limited. We investigated independent associations of transportation noise exposure and noise annoyance with prevalent respiratory symptoms and incident asthma in adults. Using 17,138 observations (from 7049 participants) from three SAPALDIA (Swiss Cohort Study on Lung and Heart Diseases in Adults) surveys, we assessed associations of transportation noise exposure and noise annoyance with prevalent respiratory symptoms, and with incident asthma (in 10,657 nested observations from 6377 participants). Annual day-evening-night transportation noise comprising road, railway and aircraft Lden (Transportation Lden) was calculated for the most exposed façade of participants' residence using Swiss noise models. Transportation noise annoyance was assessed using an 11-point scale, and participants reported respiratory symptoms and doctor-diagnosed asthma at each survey. We estimated associations with transportation Lden (as well as source-specific Lden) and noise annoyance, independent of air pollution and other potential confounders, using mutually-adjusted mixed logistic and Poisson models and applying random intercepts at the level of the participants. Prevalent respiratory symptoms ranged from 5% (nocturnal dyspnoea) to 23% (regular cough/phlegm). Transportation noise annoyance, but not Lden, was independently associated with respiratory symptoms and current asthma in all participants, with odds ratios (OR) and 95% confidence intervals (CI) ranging between 1.03 (95%CI: 1.01, 1.06) and 1.07 (95% CI: 1.04, 1.11) per 1-point difference in noise annoyance. Both noise annoyance and Lden showed independent associations with asthma symptoms among asthmatics, especially in those reporting adult-onset asthma [ORLden: 1.90 (95% CI: 1.25, 2.89) per 10 dB; p-value of interaction (adult-onset vs. childhood-onset): 0.03; ORnoise annoyance: 1.06 (95%CI: 0.97, 1.16) per 1-point difference; p-value of interaction: 0.06]. No associations were found with incident asthma. Transportation noise level and annoyance contributed to symptom exacerbation in adult asthma. This suggests both psychological and physiological noise reactions on the respiratory system, and could be relevant for asthma care. More studies are needed to better understand the effects of objective and perceived noise in asthma aetiology and overall respiratory health.

Sleep spindle characteristics and arousability from nighttime transportation noise exposure in healthy young and older individuals.

Study Objectives: Nighttime transportation noise elicits awakenings, sleep-stage changes, and electroencephalographic (EEG) arousals. Here, we investigated the potential sleep-protective role of sleep spindles on noise-induced sleep alterations. Methods: Twenty-six young (19-33 years, 12 women) and 18 older (52-70 years, 9 women) healthy volunteers underwent a repeated measures polysomnographic 6-day laboratory study. Participants spent one noise-free baseline night, followed by four transportation noise-exposure nights (road traffic or railway noise; continuous or intermittent: average sound levels of 45 dB, maximum sound levels of 50-62 dB), and one noise-free recovery night. Sleep stages were scored manually and fast sleep spindle characteristics were quantified automatically using an individual band-pass filtering approach. Results: Nighttime exposure to transportation noise significantly increased sleep EEG arousal indices. Sleep structure and continuity were not differentially affected by noise exposure in individuals with a low versus a high spindle rate. Spindle rates showed an age-related decline along with more noise-induced sleep alterations. All-night spindle rates did not predict EEG arousal or awakening probability from single railway noise events. Spindle characteristics were affected in noise-exposure nights compared to noise-free nights: we observed a reduction of the spindle amplitude in both age groups and of the spindle rate in the older group. Conclusions: We have evidence that spindle rate is more likely to represent a trait phenomenon, which does not seem to play a sleep-protective role in nighttime transportation noise-induced sleep disruptions. However, the marked reduction in spindle amplitude is most likely a sensitive index for noise-induced sleep alterations.

Exposure to Night-Time Traffic Noise, Melatonin-Regulating Gene Variants and Change in Glycemia in Adults.

Traffic noise has been linked to diabetes, with limited understanding of its mechanisms. We hypothesize that night-time road traffic noise (RTN) may impair glucose homeostasis through circadian rhythm disturbances. We prospectively investigated the relationship between residential night-time RTN and subsequent eight-year change in glycosylated hemoglobin (ΔHbA1c) in 3350 participants of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA), adjusting for diabetes risk factors and air pollution levels. Annual average RTN (Lnight) was assigned to participants in 2001 using validated Swiss noise models. HbA1c was measured in 2002 and 2011 using liquid chromatography. We applied mixed linear models to explore RTN-ΔHbA1c association and its modification by a genetic risk score of six common circadian-related MTNR1B variants (MGRS). A 10 dB difference in RTN was associated with a 0.02% (0.003-0.04%) increase in mean ΔHbA1c in 2142 non-movers. RTN-ΔHbA1c association was modified by MGRS among diabetic participants (Pinteraction = 0.001). A similar trend in non-diabetic participants was non-significant. Among the single variants, we observed strongest interactions with rs10830963, an acknowledged diabetes risk variant also implicated in melatonin profile dysregulation. Night-time RTN may impair glycemic control, especially in diabetic individuals, through circadian rhythm disturbances. Experimental sleep studies are needed to test whether noise control may help individuals to attain optimal glycemic levels.

Exposure to Road, Railway, and Aircraft Noise and Arterial Stiffness in the SAPALDIA Study: Annual Average Noise Levels and Temporal Noise Characteristics.

BACKGROUND: The impact of different transportation noise sources and noise environments on arterial stiffness remains unknown. OBJECTIVES: We evaluated the association between residential outdoor exposure to annual average road, railway, and aircraft noise levels, total noise intermittency (IR), and total number of noise events (NE) and brachial-ankle pulse wave velocity (baPWV) following a cross-sectional design. METHODS: We measured baPWV (meters/second) in 2,775 participants (49-81 y old) at the second follow-up (2010-2011) of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA). We assigned annual average road, railway, and aircraft noise levels (Ldensource), total day- and nighttime NEtime and IRtime (percent fluctuation=0%, none or constant noise; percent fluctuation=100%, high fluctuation) at the most exposed façade using 2011 Swiss noise models. We applied multivariable linear mixed regression models to analyze associations. RESULTS: Medians [interquartile ranges (IQRs)] were baPWV=13.4 (3.1) m/s; Ldenair (57.6% exposed)=32.8 (8.0) dB; Ldenrail (44.6% exposed)=30.0 (8.1) dB; Ldenroad (99.7% exposed): 54.2 (10.6) dB; NEnight=123 (179); NEday=433 (870); IRnight=73% (27); and IRday=63.8% (40.3). We observed a 0.87% (95% CI: 0.31, 1.43%) increase in baPWV per IQR of Ldenrail, which was greater with IRnight>80% or with daytime sleepiness. We observed a nonsignificant positive association between Ldenroad and baPWV in urban areas and a negative tendency in rural areas. NEnight, but not NEday, was associated with baPWV. Associations were independent of the other noise sources and air pollution. CONCLUSIONS: Long-term exposure to railway noise, particularly in an intermittent nighttime noise environment, and to nighttime noise events, mainly related to road noise, may affect arterial stiffness, a major determinant of cardiovascular disease. Ascertaining noise exposure characteristics beyond average noise levels may be relevant to better understand noise-related health effects. https://doi.org/10.1289/EHP1136.

Transportation noise exposure and cardiovascular mortality: a nationwide cohort study from Switzerland.

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 [Lden(Road), Lden(Rail), Lden(Air), and IR at night] and various cardiovascular primary causes of death by multipollutant Cox regression models adjusted for potential confounders including NO2. 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 Lden(Road), Lden(Rail), and Lden(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.

Long-term exposure to transportation noise and air pollution in relation to incident diabetes in the SAPALDIA study.

Background: Epidemiological 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. Methods: We 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. Results: Diabetes 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. Conclusions: Transportation noise may be more relevant than AP in the development of diabetes, potentially acting through noise-induced sleep disturbances.

Visual information and rubber hand embodiment differentially affect reach-to-grasp actions.

During the "rubber hand illusion" (RHI) participants feel touch originating from an artificial hand, which is felt to belong to the own body. The perceived location of the real hand is shifted towards the location of the artificial hand. However, evidence as to whether the RHI is accompanied by alterations of hand action is mixed. We found that the perceived size of one's own hand was affected by the size of the artificial hand that was used to elicit the illusion. Moreover, we tested a possible transfer of the RHI to a reach-to-grasp action. We observed that hand transport (i.e., reach) errors after RHI induction were independent of artificial hand size, showing that the parameter which is important for these reaching errors is the hand's perceived location. Results thus show that the RHI affects not only perceptual, but also action processing. In contrast, grip aperture was affected by artificial hand size independent of the RHI, suggesting that visual information about hand size affects grasping independent of embodiment of the artificial hand. Grip size increased with artificial hand size; this effect is explained by a higher reliance on proprioceptive information during blind reaching after receiving distorted visual information.