Long-Term Exposure to Transportation Noise and Risk of Incident Stroke: A Pooled Study of Nine Scandinavian Cohorts.
Ontology highlight
ABSTRACT: Background
Transportation noise is increasingly acknowledged as a cardiovascular risk factor, but the evidence base for an association with stroke is sparse.Objective
We aimed to investigate the association between transportation noise and stroke incidence in a large Scandinavian population.Methods
We harmonized and pooled data from nine Scandinavian cohorts (seven Swedish, two Danish), totaling 135,951 participants. We identified residential address history and estimated road, railway, and aircraft noise for all addresses. Information on stroke incidence was acquired through linkage to national patient and mortality registries. We analyzed data using Cox proportional hazards models, including socioeconomic and lifestyle confounders, and air pollution.Results
During follow-up (median=19.5y), 11,056 stroke cases were identified. Road traffic noise (Lden) was associated with risk of stroke, with a hazard ratio (HR) of 1.06 [95% confidence interval (CI): 1.03, 1.08] per 10-dB higher 5-y mean time-weighted exposure in analyses adjusted for individual- and area-level socioeconomic covariates. The association was approximately linear and persisted after adjustment for air pollution [particulate matter (PM) with an aerodynamic diameter of ≤2.5μm (PM2.5) and NO2]. Stroke was associated with moderate levels of 5-y aircraft noise exposure (40-50 vs. ≤40 dB) (HR=1.12; 95% CI: 0.99, 1.27), but not with higher exposure (≥50 dB, HR=0.94; 95% CI: 0.79, 1.11). Railway noise was not associated with stroke.Discussion
In this pooled study, road traffic noise was associated with a higher risk of stroke. This finding supports road traffic noise as an important cardiovascular risk factor that should be included when estimating the burden of disease due to traffic noise. https://doi.org/10.1289/EHP8949.
SUBMITTER: Roswall N
PROVIDER: S-EPMC8489401 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description: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) ?g/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.
| S-EPMC5837207 | biostudies-literature
Project description:Exposure to transportation noise is widespread and has been associated with obesity in some studies. However, the evidence from longitudinal studies is limited and little is known about effects of combined exposure to different noise sources.The aim of this longitudinal study was to estimate the association between exposure to noise from road traffic, railways, or aircraft and the development of obesity markers.We assessed individual long-term exposure to road traffic, railway, and aircraft noise based on residential histories in a cohort of 5,184 men and women from Stockholm County. Noise levels were estimated at the most exposed façade of each dwelling. Waist circumference, weight, and height were measured at recruitment and after an average of 8.9 y of follow-up. Extensive information on potential confounders was available from repeated questionnaires and registers.Waist circumference increased 0.04 cm/y (95% CI: 0.02, 0.06) and 0.16 cm/y (95% CI: 0.14, 0.17) per 10 dB Lden in relation to road traffic and aircraft noise, respectively. No corresponding association was seen for railway noise. Weight gain was only related to aircraft noise exposure. A similar pattern occurred for incidence rate ratios (IRRs) of central obesity and overweight. The IRR of central obesity increased from 1.22 (95% CI: 1.08, 1.39) in those exposed to only one source of transportation noise to 2.26 (95% CI: 1.55, 3.29) among those exposed to all three sources.Our results link transportation noise exposure to development of obesity and suggest that combined exposure from different sources may be particularly harmful. https://doi.org/10.1289/EHP1910.
| S-EPMC5947937 | biostudies-literature
Project description:BackgroundRoad traffic noise at normal urban levels can lead to stress and sleep disturbances. Both excess of stress hormones and reduction in sleep quality and duration may lead to higher risk for type 2 diabetes.ObjectiveWe investigated whether long-term exposure to residential road traffic noise is associated with an increased risk of diabetes.MethodsIn the population-based Danish Diet, Cancer and Health cohort of 57,053 people 50-64 years of age at enrollment in 1993-1997, we identified 3,869 cases of incident diabetes in a national diabetes registry between enrollment and 2006. The mean follow-up time was 9.6 years. Present and historical residential addresses from 1988 through 2006 were identified using a national register, and exposure to road traffic noise was estimated for all addresses. Associations between exposure to road traffic noise and incident diabetes were analyzed in a Cox regression model.ResultsA 10-dB higher level of average road traffic noise at diagnosis and during the 5 years preceding diagnosis was associated with an increased risk of incident diabetes, with incidence rate ratios (IRR) of 1.08 (95% CI: 1.02, 1.14) and 1.11 (95% CI: 1.05, 1.18), respectively, after adjusting for potential confounders including age, body mass index, waist circumference, education, air pollution (nitrogen oxides), and lifestyle characteristics. After applying a stricter definition of diabetes (2,752 cases), we found IRRs of 1.11 (95% CI: 1.03, 1.19) and 1.14 (95% CI: 1.06, 1.22) per 10-dB increase in road traffic noise at diagnosis and during the 5 years preceding diagnosis, respectively.ConclusionExposure to residential road traffic noise was associated with a higher risk of diabetes. This study provides further evidence that urban noise may adversely influence population health.
| S-EPMC3569689 | biostudies-literature
Project description:BackgroundNoise has been related to several cardiovascular diseases (CVDs) such as coronary heart disease and to their risk factors such as hypertension, but associations with stroke remain under-researched, even if CVD likely share similar pathophysiologic mechanisms.AimThe objective of the study was to examine the association between long-term residential exposure to total environmental noise and stroke incidence in Montreal, Canada.Materials and methodsWe created an open cohort of adults aged ≥45years, free of stroke before entering the cohort for the years 2000 to 2014 with health administrative data. Residential total environmental noise levels were estimated with land use regression (LUR) models. Incident stroke was based on hospital admissions. Cox hazard models with age as the time axis and time-varying exposures were used to estimate associations, which were adjusted for material deprivation, year, nitrogen dioxide, stratified for sex, and indirectly adjusted for smoking.ResultsThere were 9,072,492 person-years of follow-up with 47% men; 26,741 developed stroke (21,402 ischemic; 4947 hemorrhagic; 392 had both). LUR total noise level acoustic equivalent for 24 hours (LAeq24h) ranged 44 to 79 dBA. The adjusted hazard ratio (HR) for stroke (all types), for a 10-dBA increase in LAeq24h, was 1.06 [95% confidence interval (CI): 1.03-1.09]. The LAeq24h was associated with ischemic (HR per 10 dBA: 1.08; 95% CI: 1.04-1.12) but not hemorrhagic stroke (HR per 10 dBA: 0.97; 95% CI: 0.90-1.04).ConclusionThe results suggest that total environmental noise is associated with incident stroke, which is consistent with studies on transportation noise and other CVD.
| S-EPMC9703819 | biostudies-literature
Project description:BackgroundEvidence of nonauditory health effects of road traffic noise exposure is growing. This prospective cohort study aimed to estimate the association between long-term exposure to road traffic noise above a threshold and incident myocardial infarction (MI) in Denmark.MethodsIn the Danish Nurse Cohort study, we used data of 22,378 women, at recruitment in 1993 and 1999, who reported information on MI risk factors. The participants' first hospital contact or out-of-hospital death due to MI were followed-up until 2014. We investigated a relationship between residential exposures to road traffic noise levels (Lden) up to 23 years and incident MI (overall, nonfatal, and fatal) using time-varying Cox regression models adjusting for potential confounders and air pollutants. We estimated thresholds of road traffic noise (53, 56, and 58 dB) associated with incident MI in a piece-wise linear regression model.ResultsOf the 22,378 participants, 633 developed MI, 502 of which were nonfatal. We observed a non-linear relationship between the 23-year running mean of Lden and incident MI with a threshold level of 56 dB, above which hazard ratios (95% confidence intervals) were 1.30 (0.97, 1.75) for overall and 1.46 (1.05, 2.03) for nonfatal MI per 10 dB. The association with nonfatal MI attenuated slightly to 1.34 (0.95, 1.90) after adjustment for fine particles.ConclusionsWe found that long-term exposure to road traffic noise above 56 dB may increase the risk of MI. The study findings suggest that road traffic noise above 56 dB may need regulation in addition to the regulation of ambient pollutants.
| S-EPMC8078417 | biostudies-literature
Project description:Various subtypes of breast cancer defined by estrogen receptor (ER), progesterone receptor (PR), and HER2 exhibit etiologic differences in reproductive factors, but associations with other risk factors are inconsistent. To clarify etiologic heterogeneity, we pooled data from nine cohort studies. Multivariable, joint Cox proportional hazards regression models were used to estimate HRs and 95% confidence intervals (CI) for molecular subtypes. Of 606,025 women, 11,741 invasive breast cancers with complete tissue markers developed during follow-up: 8,700 luminal A-like (ER+ or PR+/HER2-), 1,368 luminal B-like (ER+ or PR+/HER2+), 521 HER2-enriched (ER-/PR-/HER2+), and 1,152 triple-negative (ER-/PR-/HER2-) disease. Ever parous compared with never was associated with lower risk of luminal A-like (HR, 0.78; 95% CI, 0.73-0.83) and luminal B-like (HR, 0.74; 95% CI, 0.64-0.87) as well as a higher risk of triple-negative disease (HR, 1.23; 95% CI, 1.02-1.50; P value for overall tumor heterogeneity < 0.001). Direct associations with luminal-like, but not HER2-enriched or triple-negative, tumors were found for age at first birth, years between menarche and first birth, and age at menopause (P value for overall tumor heterogeneity < 0.001). Age-specific associations with baseline body mass index differed for risk of luminal A-like and triple-negative breast cancer (P value for tumor heterogeneity = 0.02). These results provide the strongest evidence for etiologic heterogeneity of breast cancer to date from prospective studies.Significance: These findings comprise the largest study of prospective data to date and contribute to the accumulating evidence that etiological heterogeneity exists in breast carcinogenesis. Cancer Res; 78(20); 6011-21. ©2018 AACR.
| S-EPMC6223627 | biostudies-literature
Project description:BackgroundEpidemiologic studies have linked transportation noise to increased morbidity and mortality, particularly for cardiovascular outcomes. However, studies investigating metabolic outcomes such as diabetes are limited and have focused only on noise exposures estimated for the loudest residential façade.ObjectivesWe aimed to examine the influence of long-term residential exposure to transportation noise at the loudest and quietest residential façades and the risk for type 2 diabetes.MethodsRoad traffic and railway noise exposures (Lden) at the most and least exposed façades were estimated for all dwellings in Denmark during 1990-2017. Aircraft noise was estimated in 5-dB categories. Ten-year time-weighted mean noise exposures were estimated for 3.56 million individuals ≥35 years of age. From 2000 to 2017, 233,912 incident cases of type 2 diabetes were identified using hospital and prescription registries, with a mean follow-up of 12.9 y. We used Cox proportional hazards models adjusting for individual- and area-level covariates and long-term residential air pollution. The population-attributable fraction (PAF) was also computed.ResultsHazard ratios (HRs) and 95% confidence intervals (CIs) for type 2 diabetes in association with 10-dB increases in 10-y mean road traffic noise at the most and least exposed façades, respectively, were 1.05 (95% CI: 1.04, 1.05) and 1.09 (95% CI: 1.08, 1.10). Following subsequent adjustment for fine particulate matter [particulate matter ≤2.5μm in aerodynamic diameter] (10-y mean), the HRs (CIs) were 1.03 (95% CI: 1.03, 1.04) and 1.08 (95% CI: 1.07, 1.09), respectively. For railway noise, the HRs per 10-dB increase in 10-y mean exposure were 1.03 (95% CI: 1.02, 1.04) and 1.02 (95% CI: 1.01, 1.04) for the most and least exposed façades, respectively. Categorical models supported a linear exposure-outcome relationship for road traffic noise and, to a lesser extent, for railway noise. Aircraft noise >45 dB was associated with a 1-4% higher likelihood of type 2 diabetes compared with those who were unexposed. We found road traffic and railway noise associated with a PAF of 8.5% and 1.4%, respectively, of the diabetes cases.DiscussionLong-term exposure to road, railway, and possibly aircraft traffic noise was associated with an increased risk of type 2 diabetes in a nationwide cohort of Danish adults. Our findings suggest that diabetes should be included when estimating the burden of disease due to transportation noise. https://doi.org/10.1289/EHP9146.
| S-EPMC8638828 | biostudies-literature
Project description:BackgroundRoad traffic noise has been linked to increased risk of ischemic heart disease, yet evidence on stroke shows mixed results. We examine the association between long-term exposure to road traffic noise and incidence of stroke, overall and by subtype (ischemic or hemorrhagic), after adjustment for air pollution.MethodsTwenty-five thousand six hundred and sixty female nurses from the Danish Nurse Cohort recruited in 1993 or 1999 were followed for stroke-related first-ever hospital contact until December 31st, 2014. Full residential address histories since 1970 were obtained and annual means of road traffic noise (Lden [dB]) and air pollutants (particulate matter with diameter < 2.5 μm and < 10 μm [PM2.5 and PM10], nitrogen dioxide [NO2], nitrogen oxides [NOx]) were determined using validated models. Time-varying Cox regression models were used to estimate hazard ratios (HR) (95% confidence intervals [CI]) for the associations of one-, three-, and 23-year running means of Lden preceding stroke (all, ischemic or hemorrhagic), adjusting for stroke risk factors and air pollutants. The World Health Organization and the Danish government's maximum exposure recommendations of 53 and 58 dB, respectively, were explored as potential Lden thresholds.ResultsOf 25,660 nurses, 1237 developed their first stroke (1089 ischemic, 148 hemorrhagic) during 16 years mean follow-up. For associations between a 1-year mean of Lden and overall stroke incidence, the estimated HR (95% CI) in the fully adjusted model was 1.06 (0.98-1.14) per 10 dB, which attenuated to 1.01 (0.93-1.09) and 1.00 (0.91-1.09) in models further adjusted for PM2.5 or NO2, respectively. Associations for other exposure periods or separately for ischemic or hemorrhagic stroke were similar. There was no evidence of a threshold association between Lden and stroke.ConclusionsLong-term exposure to road traffic noise was suggestively positively associated with the risk of overall stroke, although not after adjusting for air pollution.
| S-EPMC8571835 | biostudies-literature
Project description:BackgroundFew 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.ObjectiveWe performed mutually independent EWAS on transportation noise and air pollution exposures.MethodsWe 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 (NO2); and particulate matter (PM) with aerodynamic diameter <2.5μm (PM2.5). 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.ResultsWe 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; NO2; and PM2.5, 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 PM2.5), 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 (NO2) and decreased methylation in cg17629796 (PM2.5).ConclusionsMutually 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.
| S-EPMC7263738 | biostudies-literature
Project description:BackgroundAssociations between long-term exposure to air pollution and road traffic noise have been established for ischemic heart disease, but findings have been mixed for atrial fibrillation (AF).ObjectivesThe goal of the study was to examine associations of long-term exposure to road traffic noise and air pollution with AF.MethodsTime-varying Cox regression models were used to estimate associations of 1-, 3-, and 23-y mean road traffic noise and air pollution exposures with AF incidence in 23,528 women enrolled in the Danish Nurse Cohort (age >44y at baseline in 1993 or 1999). AF diagnoses were ascertained via the Danish National Patient Register. Annual mean weighted 24-h average road traffic noise levels (Lden) at the nurses' residences, since 1970, were estimated using the Nord2000 model, and annual mean levels of particulate matter with a diameter <2.5μm (PM2.5) and nitrogen dioxide (NO2) were estimated using the DEHM/UBM/AirGIS model.ResultsOf 23,528 nurses with no prior AF diagnosis at the cohort baseline, 1,522 developed AF during follow-up. In a fully adjusted model (including PM2.5), the estimated risk of AF was 18% higher [hazard ratio (HR); 95% confidence interval (CI): 1.18; 1.02, 1.36] in nurses with residential 3-y mean Lden levels >58 dB vs. <48 dB, with similar findings for 1-y mean exposures. A 3.9-μg/m3 increase in 3-y mean PM2.5 was associated with incident AF before and after adjustment for concurrent exposure to road traffic noise (HR 1.09; 95% CI: 1.00, 1.20 and 1.08; 95% CI: 0.97, 1.19, respectively). Associations with 1-y mean PM2.5 exposures were positive but closer to the null and not significant. Associations with NO2 were null for all time periods before and after adjustment for road traffic noise and inverse when adjusted for concurrent PM2.5.ConclusionOur analysis of prospective data from a cohort of Danish female nurses followed for up to 14 y provided suggestive evidence of independent associations between incident AF and 1- and 3-y exposures to road traffic noise and PM2.5. https://doi.org/10.1289/EHP8090.
| S-EPMC8327770 | biostudies-literature