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Nighttime noise carries a significant disease burden. The World Health Organization (WHO) recently published guidelines for the regulation of environmental noise based on a review of evidence published up to the year 2015 on the effects of environmental noise on sleep. This systematic review and meta-analysis will update the WHO evidence review on the effects of environmental noise on sleep disturbance to include more recent studies. Investigations of self-reported sleep among residents exposed to environmental traffic noise at home were identified using Scopus, PubMed, Embase, and PsycINFO. Awakenings, falling asleep, and sleep disturbance were the three outcomes included. Extracted data were used to derive exposure-response relationships for the probability of being highly sleep disturbed by nighttime noise [average outdoor A-weighted noise level ( ) 2300-0700 hours] for aircraft, road, and rail traffic noise, individually. The overall quality of evidence was assessed using Grading of Recommendations, Assessment, Development, and Evaluations (GRADE) criteria. Eleven studies ( responses) were included in addition to 25 studies ( responses) from the original WHO analysis. When sleep disturbance questions specifically mentioned noise as the source of disturbance, there was moderate quality of evidence for the probability of being highly sleep disturbed per 10-dB increase in for aircraft [ ; 95% confidence interval (CI): 2.01, 2.36], road ( ; 95% CI: 2.28, 2.79), and railway ( ; 95% CI: 2.57, 3.43) noise. When noise was not mentioned, there was low to very low quality of evidence for being sleep disturbed per 10-dB increase in for aircraft ( ; 95% CI: 1.20, 1.93), road ( ; 95% CI: 1.08, 1.21), and railway ( ; 95% CI: 0.91, 1.49) noise. Compared with the original WHO review, the exposure-response relationships closely agreed at low (40 dB ) levels for all traffic types but indicated greater disturbance by aircraft traffic at high noise levels. Sleep disturbance was not significantly different between European and non-European studies. Available evidence suggests that transportation noise is negatively associated with self-reported sleep. Sleep disturbance in this updated meta-analysis was comparable to the original WHO review at low nighttime noise levels. These low levels correspond to the recent WHO noise limit recommendations for nighttime noise, and so these findings do not suggest these WHO recommendations need revisiting. Deviations from the WHO review in this updated analysis suggest that populations exposed to high levels of aircraft noise may be at greater risk of sleep disturbance than determined previously. https://doi.org/10.1289/EHP10197.

Epidemiologic 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. We 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. Road 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 individuals 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. Hazard 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 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 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. Long-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.

To evaluate the quality of available evidence on the effects of environmental noise exposure on sleep a systematic review was conducted. The databases PSYCINFO, PubMed, Science Direct, Scopus, Web of Science and the TNO Repository were searched for non-laboratory studies on the effects of environmental noise on sleep with measured or predicted noise levels and published in or after the year 2000. The quality of the evidence was assessed using GRADE criteria. Seventy four studies predominately conducted between 2000 and 2015 were included in the review. A meta-analysis of surveys linking road, rail, and aircraft noise exposure to self-reports of sleep disturbance was conducted. The odds ratio for the percent highly sleep disturbed for a 10 dB increase in Lnight was significant for aircraft (1.94; 95% CI 1.61–2.3), road (2.13; 95% CI 1.82–2.48), and rail (3.06; 95% CI 2.38–3.93) noise when the question referred to noise, but non-significant for aircraft (1.17; 95% CI 0.54–2.53), road (1.09; 95% CI 0.94–1.27), and rail (1.27; 95% CI 0.89–1.81) noise when the question did not refer to noise. A pooled analysis of polysomnographic studies on the acute effects of transportation noise on sleep was also conducted and the unadjusted odds ratio for the probability of awakening for a 10 dBA increase in the indoor Lmax was significant for aircraft (1.35; 95% CI 1.22–1.50), road (1.36; 95% CI 1.19–1.55), and rail (1.35; 95% CI 1.21–1.52) noise. Due to a limited number of studies and the use of different outcome measures, a narrative review only was conducted for motility, cardiac and blood pressure outcomes, and for children’s sleep. The effect of wind turbine and hospital noise on sleep was also assessed. Based on the available evidence, transportation noise affects objectively measured sleep physiology and subjectively assessed sleep disturbance in adults. For other outcome measures and noise sources the examined evidence was conflicting or only emerging. According to GRADE criteria, the quality of the evidence was moderate for cortical awakenings and self-reported sleep disturbance (for questions that referred to noise) induced by traffic noise, low for motility measures of traffic noise induced sleep disturbance, and very low for all other noise sources and investigated sleep outcomes.

Nocturnal train noise exposure has been associated with hypertension and myocardial infarction. It remains unclear whether acute nighttime train exposure may induce subclinical atherosclerosis, such as endothelial dysfunction and other functional and/or biochemical changes. Thus, we aimed to expose healthy subjects to nocturnal train noise and to assess endothelial function, changes in plasma protein levels and clinical parameters. In a randomized crossover study, we exposed 70 healthy volunteers to either background or two different simulated train noise scenarios in their homes during three nights. After each night, participants visited the study center for measurement of vascular function and assessment of other biomedical and biochemical parameters. The three nighttime noise scenarios were exposure to either background noise (control), 30 or 60 train noise events (Noise30 or Noise60), with average sound pressure levels of 33, 52 and 54 dB(A), respectively. Flow-mediated dilation (FMD) of the brachial artery was 11.23 ± 4.68% for control, compared to 8.71 ± 3.83% for Noise30 and 8.47 ± 3.73% for Noise60 (p < 0.001 vs. control). Sleep quality was impaired after both Noise30 and Noise60 nights (p < 0.001 vs. control). Targeted proteomic analysis showed substantial changes of plasma proteins after the Noise60 night, mainly centered on redox, pro-thrombotic and proinflammatory pathways. Exposure to simulated nocturnal train noise impaired endothelial function. The proteomic changes point toward a proinflammatory and pro-thrombotic phenotype in response to nocturnal train noise and provide a molecular basis to explain the increased cardiovascular risk observed in epidemiological noise studies.

Transportation noise may induce cardiovascular disease, but the public health implications are unclear. The study aimed to assess exposure-response relationships for different transportation noise sources and ischemic heart disease (IHD), including subtypes. Pooled analyses were performed of nine cohorts from Denmark and Sweden, together including 132,801 subjects. Time-weighted long-term exposure to road, railway, and aircraft noise, as well as air pollution, was estimated based on residential histories. Hazard ratios (HRs) were calculated using Cox proportional hazards models following adjustment for lifestyle and socioeconomic risk factors. A total of 22,459 incident cases of IHD were identified during follow-up from national patient and mortality registers, including 7,682 cases of myocardial infarction. The adjusted HR for IHD was 1.03 [95% confidence interval (CI) 1.00, 1.05] per 10 dB for both road and railway noise exposure during 5 y prior to the event. Higher risks were indicated for IHD excluding angina pectoris cases, with HRs of 1.06 (95% CI: 1.03, 1.08) and 1.05 (95% CI: 1.01, 1.08) per 10 dB for road and railway noise, respectively. Corresponding HRs for myocardial infarction were 1.02 (95% CI: 0.99, 1.05) and 1.04 (95% CI: 0.99, 1.08). Increased risks were observed for aircraft noise but without clear exposure-response relations. A threshold at around 55 dB was suggested in the exposure-response relation for road traffic noise and IHD. Exposure to road, railway, and aircraft noise in the prior 5 y was associated with an increased risk of IHD, particularly after exclusion of angina pectoris cases, which are less well identified in the registries. https://doi.org/10.1289/EHP10745.

Transportation noise is increasingly acknowledged as a cardiovascular risk factor, but the evidence base for an association with stroke is sparse. We aimed to investigate the association between transportation noise and stroke incidence in a large Scandinavian population. 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. During follow-up ( ), 11,056 stroke cases were identified. Road traffic noise ( ) 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 ( ) and ]. Stroke was associated with moderate levels of 5-y aircraft noise exposure (40-50 vs. ) ( ; 95% CI: 0.99, 1.27), but not with higher exposure ( , ; 95% CI: 0.79, 1.11). Railway noise was not associated with stroke. 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.

ObjectivesA series of human field studies demonstrated that acute exposure to simulated nocturnal traffic noise is associated with cardiovascular complications and sleep disturbance, including endothelial dysfunction, increased blood pressure, and impaired sleep quality. A pooled analysis of these results remains to be established and is of tremendous interest to consolidate scientific knowledge.MethodsWe analyzed data from four randomized crossover studies (published between 2013 to 2021 and conducted at the University Medical Center Mainz, Germany). A total of 275 subjects (40.4% women, mean age 43.03 years) were each exposed to one control scenario (regular background noise) and at least to one traffic noise scenario (60 aircraft or train noise events) in their homes during nighttime. After each night, the subjects visited the study center for comprehensive cardiovascular function assessment, including the measurement of endothelial function and hemodynamic and biochemical parameters, as well as sleep-related variables.ResultsThe pooled analysis revealed a significantly impaired endothelial function when comparing the two different noise sequences (0–60 vs. 60–0 simulated noise events, mean difference in flow-mediated dilation −2.00%, 95% CI −2.32; −1.68, p < 0.0001). In concordance, mean arterial pressure was significantly increased after traffic noise exposure (mean difference 2.50 mmHg, 95% CI 0.54; 4.45, p = 0.013). Self-reported sleep quality, the restfulness of sleep, and feeling in the morning were significantly impaired after traffic noise exposure (all p < 0.0001).DiscussionAcute exposure to simulated nocturnal traffic noise is associated with endothelial dysfunction, increased mean arterial pressure, and sleep disturbance.

AbstractObjectiveTo investigate associations between long term residential exposure to road traffic noise and particulate matter with a diameter <2.5 µm (PM2.5) and infertility in men and women.DesignNationwide prospective cohort study.SettingDenmark.Participants526 056 men and 377 850 women aged 30-45 years, with fewer than two children, cohabiting or married, and residing in Denmark between 2000 and 2017.Main outcome measureIncident infertility in men and women during follow-up in the Danish National Patient Register.ResultsInfertility was diagnosed in 16 172 men and 22 672 women during a mean follow-up of 4.3 years and 4.2 years, respectively. Mean exposure to PM2.5 over five years was strongly associated with risk of infertility in men, with hazard ratios of 1.24 (95% confidence interval 1.18 to 1.30) among men aged 30-36.9 years and 1.24 (1.15 to 1.33) among men aged 37-45 years for each interquartile (2.9 µg/m3) higher PM2.5 after adjustment for sociodemographic variables and road traffic noise. PM2.5 was not associated with infertility in women. Road traffic noise (Lden, most exposed facade of residence) was associated with a higher risk of infertility among women aged 35-45 years, with a hazard ratio of 1.14 (1.10 to 1.18) for each interquartile (10.2 dB) higher five year mean exposure. Noise was not associated with infertility among younger women (30-34.9 years). In men, road traffic noise was associated with higher risk of infertility in the 37-45 age group (1.06, 1.02 to 1.11), but not among those aged 30-36.9 years (0.93, 0.91 to 0.96).ConclusionsPM2.5 was associated with a higher risk of an infertility diagnosis in men, whereas road traffic noise was associated with a higher risk of an infertility diagnosis in women older than 35 years, and potentially in men older than 37 years. If these results are confirmed in future studies, higher fertility could be added to the list of health benefits from regulating noise and air pollution.

Evidence for an association between transportation noise and cardiovascular disease has increased; however, few studies have examined metabolic outcomes such as diabetes or accounted for environmental coexposures such as air pollution, greenness, or walkability. Because diabetes prevalence is increasing and may be on the causal pathway between noise and cardiovascular disease, we examined the influence of long-term residential transportation noise exposure and traffic-related air pollution on the incidence of diabetes using a population-based cohort in British Columbia, Canada. We examined the influence of transportation noise exposure over a 5-y period (1994-1998) on incident diabetes cases in a population-based prospective cohort study (n=380,738) of metropolitan Vancouver (BC) residents who were 45-85 y old, with 4-y of follow-up (1999-2002). Annual average transportation noise (Lden), air pollution [black carbon, particulate matter with aerodynamic diameter <2.5μm (PM ), nitrogen oxides], greenness [Normalized Difference Vegetation Index (NDVI)], and neighborhood walkability at each participant's residence were modeled. Incident diabetes cases were identified using administrative health records. Transportation noise was associated with the incidence of diabetes [interquartile range (IQR) increase, 6.8 A-weighted decibels (dBA); OR=1.08 (95% CI: 1.05, 1.10)]. This association remained after adjustment for environmental coexposures including traffic-related air pollutants, greenness, and neighborhood walkability. After adjustment for coexposure to noise, traffic-related air pollutants were not associated with the incidence of diabetes, whereas greenness was protective. We found a positive association between residential transportation noise and diabetes, adding to the growing body of evidence that noise pollution exposure may be independently linked to metabolic health and should be considered when developing public health interventions. https://doi.org/10.1289/EHP1279.