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Background: Few epigenome-wide association studies (EWAS) on air pollutants exist, and none have been done on transportation noise exposures, which also contribute to environmental burden of disease., Objective: We performed mutually independent EWAS on transportation noise and air pollution exposures., Methods: We used data from two time points of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA) from 1,389 participants contributing 2,542 observations. We applied multiexposure linear mixed-effects regressions with participant-level random intercept to identify significant Cytosine-phosphate-Guanine (CpG) sites and differentially methylated regions (DMRs) in relation to 1-y average aircraft, railway, and road traffic day-evening-night noise (Lden); nitrogen dioxide ( NO 2 ); and particulate matter (PM) with aerodynamic diameter < 2.5 μ m ( PM 2.5 ). We performed candidate (CpG-based; cross-systemic phenotypes, combined into "allostatic load") and agnostic (DMR-based) pathway enrichment tests, and replicated previously reported air pollution EWAS signals., Results: We found no statistically significant CpGs at false discovery rate < 0.05 . However, 14, 48, 183, 8, and 71 DMRs independently associated with aircraft, railway, and road traffic Lden; NO 2 ; and PM 2.5 , respectively, with minimally overlapping signals. Transportation Lden and air pollutants tendentially associated with decreased and increased methylation, respectively. We observed significant enrichment of candidate DNA methylation related to C-reactive protein and body mass index (aircraft, road traffic Lden, and PM 2.5 ), renal function and "allostatic load" (all exposures). Agnostic functional networks related to cellular immunity, gene expression, cell growth/proliferation, cardiovascular, auditory, embryonic, and neurological systems development were enriched. We replicated increased methylation in cg08500171 ( NO 2 ) and decreased methylation in cg17629796 ( PM 2.5 )., Conclusions: Mutually independent DNA methylation was associated with source-specific transportation noise and air pollution exposures, with distinct and shared enrichments for pathways related to inflammation, cellular development, and immune responses. These findings contribute in clarifying the pathways linking these exposures and age-related diseases but need further confirmation in the context of mediation analyses. https://doi.org/10.1289/EHP6174.

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., (Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2018. For permissions, please email: journals.permissions@oup.com.)

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., (© The Author 2017. Published by Oxford University Press on behalf of the International Epidemiological Association)

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. [ABSTRACT FROM AUTHOR]

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 ð57:6%exposedÞ=32:8 (8.0) dB; Ldenrail ð44:6% exposedÞ=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. [ABSTRACT FROM AUTHOR]

Abstract 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 [OR Lden : 1.90 (95% CI: 1.25, 2.89) per 10 dB; p-value of interaction (adult-onset vs. childhood-onset): 0.03; OR noise 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. Highlights • We studied association of noise level and annoyance with adult respiratory morbidity. • Noise annoyance was associated with respiratory symptoms and current asthma. • Noise level was only associated with respiratory symptoms in asthmatic participants. • Noise level and annoyance were not associated with the development of asthma. • The results highlight the potential importance of perceived noise and noise annoyance on respiratory health. [ABSTRACT FROM AUTHOR]

Abstract 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. Highlights • Long-term exposure to road traffic noise over time may increase the risk of obesity. • Cross-sectionally, it also relates to higher BMI, waist circumference and body fat. • Cross-sectionally, it also relates to general and central obesity and overweight. • Long-term exposure to railway noise might also relate to risk of overweight. [ABSTRACT FROM AUTHOR]

Noise annoyance (NA) might lead to behavioral patterns not captured by noise levels, which could reduce physical activity (PA) either directly or through impaired sleep and constitute a noise pathway towards cardiometabolic diseases. We investigated the association of long-term transportation NA and its main sources (aircraft, road, and railway) at home with PA levels. We assessed 3842 participants (aged 37–81) that attended the three examinations (SAP 1, 2, and 3 in years 1991, 2001 and 2011, respectively) of the population-based Swiss cohort on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA). Participants reported general 24-h transportation NA (in all examinations) and source-specific NA at night (only SAP 3) on an ICBEN-type 11-point scale. We assessed moderate, vigorous, and total PA from a short-questionnaire (SAP 3). The main outcome was moderate PA (active/inactive: cut-off ≥ 150 min/week). We used logistic regression including random effects by area and adjusting for age, sex, socioeconomic status, and lifestyles (main model) and evaluated potential effect modifiers. We analyzed associations with PA at SAP 3 a) cross-sectionally: for source-specific and transportation NA in the last year (SAP 3), and b) longitudinally: for 10-y transportation NA (mean of SAP 1 + 2), adjusting for prior PA (SAP 2) and changes in NA (SAP 3-2). Reported NA (score ≥ 5) was 16.4%, 7.5%, 3%, and 1.1% for 1-year transportation, road, aircraft, and railway at SAP 3, respectively. NA was greater in the past, reaching 28.5% for 10-y transportation NA (SAP 1 + 2). The 10-y transportation NA was associated with a 3.2% (95% CI: 6%–0.2%) decrease in moderate PA per 1-NA rating point and was related to road and aircraft NA at night in cross-sectional analyses. The longitudinal association was stronger for women, reported daytime sleepiness or chronic diseases and it was not explained by objectively modeled levels of road traffic noise at SAP 3. In conclusion, long-term NA (related to psychological noise appraisal) reduced PA and could represent another noise pathway towards cardiometabolic diseases. [ABSTRACT FROM AUTHOR]