Laurie Thiesse

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

Abstract 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.

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.

Diurnal variability of transportation noise exposure and cardiovascular mortality : a nationwide cohort study from Switzerland

BACKGROUND Most epidemiological noise studies consider 24 h average noise exposure levels. Our aim was to exploratively analyze the impact of noise exposure at different time windows during day and night on cardiovascular mortality. METHODS We generated Switzerland-wide exposure models for road traffic, railway and aircraft noise for different time windows for the year 2001. Combined noise source equivalent continuous sound levels (Leq) for different time windows at the most exposed façade were assigned to each of the 4.41 million Swiss National Cohort adult participants. Follow-up period was from 2000 to 2008. Hazard ratios (HR) of noise effects on various cardiovascular primary causes of death were computed by Cox regression models adjusted for potential confounders and NO2 levels. RESULTS For most cardiovascular causes of death we obtained indications for a diurnal pattern. For ischemic heart disease the highest HR was observed for the core night hours from 01 h to 05 h (HR per standard deviation of Leq: 1.025, 95% CI: 1.016-1.034) and lower HR for the daytime 07 h to 19 h (1.018 [1.009-1.028]). Heart failure and daytime Leq yielded the highest HR (1.047 [1.027-1.068]). CONCLUSION For acute cardiovascular diseases, nocturnal intermittent noise exposure tended to be more relevant than daytime exposure, whereas it was the opposite for chronic conditions such as heart failure most strongly associated with continuous daytime noise. This suggests that for acute diseases sleep is an important mediator for health consequences of transportation noise.

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.

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.

0096 TEMPORAL VARIATION OF TRANSPORTATION NOISE DURING SLEEP IMPACTS ON GLUCOSE METABOLISM

Intermittency ratio (IR) has been proposed as a new metric to reflect short-term temporal variations of noise exposure. As transportation noise is linked to higher risk for incident type 2 diabetes, we investigated the short-term effect of IR on glucose metabolism. Twenty-three volunteers (age: 24.6±0.7y; BMI: 22.1±0.4; 11 females) participated in a laboratory study starting with a noise-free baseline night followed by four nights with night-time noise scenarios differing in IR (low IR: distant highway, dense traffic vs. high IR: short distance, residential street or railway line) with a constant hourly Leq of 45 dB(A) at the ear of the sleeper. The study ended with a noise-free recovery night. Glucose levels significantly increased after four nights of nocturnal transportation noise compared to baseline. After one recovery night glucose returned to baseline levels for low IR, but not for high IR. Four nights of nocturnal traffic noise significantly impaired glucose tolerance in lean young volunteers. We have first evidence that short-term effect of highly intermittent night noise is more deleterious for glucose metabolism than low intermittency.