Aircraft noise exposure and body mass index among female participants in two Nurses' Health Study prospective cohorts living around 90 airports in the United States.

OBJECTIVE: Aircraft noise exposure is linked to cardiovascular disease risk. One understudied candidate pathway is obesity. This study investigates the association between aircraft noise and obesity among female participants in two prospective Nurses' Health Study (NHS and NHSII) cohorts. METHODS: Aircraft day-night average sound levels (DNL) were estimated at participant residential addresses from modeled 1 dB (dB) noise contours above 44 dB for 90 United States (U.S.) airports in 5-year intervals 1995-2010. Biennial surveys (1994-2017) provided information on body mass index (BMI; dichotomized, categorical) and other individual characteristics. Change in BMI from age 18 (BMI18; tertiles) was also calculated. Aircraft noise exposures were dichotomized (45, 55 dB), categorized (<45, 45-54, ≥55 dB) or continuous for exposure ≥45 dB. Multivariable multinomial logistic regression using generalized estimating equations were adjusted for individual characteristics and neighborhood socioeconomic status, greenness, population density, and environmental noise. Effect modification was assessed by U.S. Census region, climate boundary, airline hub type, hearing loss, and smoking status. RESULTS: At baseline, the 74,848 female participants averaged 50.1 years old, with 83.0%, 14.8%, and 2.2% exposed to <45, 45-54, and ≥55 dB of aircraft noise, respectively. In fully adjusted models, exposure ≥55 dB was associated with 11% higher odds (95% confidence interval [95%CI]: -1%, 24%) of BMIs ≥30.0, and 15% higher odds (95%CI: 3%, 29%) of membership in the highest tertile of BMI18 (ΔBMI 6.7 to 71.6). Less-pronounced associations were observed for the 2nd tertile of BMI18 (ΔBMI 2.9 to 6.6) and BMI 25.0-29.9 as well as exposures ≥45 versus <45 dB. There was evidence of DNL-BMI trends (ptrends ≤ 0.02). Stronger associations were observed among participants living in the West, arid climate areas, and among former smokers. DISCUSSION: In two nationwide cohorts of female nurses, higher aircraft noise exposure was associated with higher BMI, adding evidence to an aircraft noise-obesity-disease pathway.

Health position paper and redox perspectives - Disease burden by transportation noise.

Transportation noise is a ubiquitous urban exposure. In 2018, the World Health Organization concluded that chronic exposure to road traffic noise is a risk factor for ischemic heart disease. In contrast, they concluded that the quality of evidence for a link to other diseases was very low to moderate. Since then, several studies on the impact of noise on various diseases have been published. Also, studies investigating the mechanistic pathways underlying noise-induced health effects are emerging. We review the current evidence regarding effects of noise on health and the related disease-mechanisms. Several high-quality cohort studies consistently found road traffic noise to be associated with a higher risk of ischemic heart disease, heart failure, diabetes, and all-cause mortality. Furthermore, recent studies have indicated that road traffic and railway noise may increase the risk of diseases not commonly investigated in an environmental noise context, including breast cancer, dementia, and tinnitus. The harmful effects of noise are related to activation of a physiological stress response and nighttime sleep disturbance. Oxidative stress and inflammation downstream of stress hormone signaling and dysregulated circadian rhythms are identified as major disease-relevant pathomechanistic drivers. We discuss the role of reactive oxygen species and present results from antioxidant interventions. Lastly, we provide an overview of oxidative stress markers and adverse redox processes reported for noise-exposed animals and humans. This position paper summarizes all available epidemiological, clinical, and preclinical evidence of transportation noise as an important environmental risk factor for public health and discusses its implications on the population level.

Contributions of residential traffic noise to depression and mental wellbeing in Hong Kong: A prospective cohort study.

Prior studies on the association between traffic noise and mental health have been mostly conducted in settings with lower population densities. However, evidence is lacking in high population-density settings where traffic noise is more pervasive and varies by topography and the vertical elevation of the residential unit. This study aimed to assess the mental health impact of residential traffic noise in one of the world's most urbanised populations. Data were analysed from 13,401 participants aged ≥15 years in a prospective cohort in Hong Kong from 2009 to 2014. Residential traffic noise level was estimated using 3D-geocoding and validated models that accounted for sound propagation in a highly vertical landscape. The 24-h day-night exposure to traffic noise, denoted as Ldn, was estimated with a 10-dB(A) penalty for night hours. Probable depression and mental wellbeing were assessed using the Patient Health Questionnaire-9 and the Short Form Health Questionnaire SF-12v2, respectively. Mixed effect regressions with random intercepts were used to examine the association between traffic noise and mental health outcomes. Residential road traffic noise (for each increment of 10 A-weighted decibels [dB(A)] 24-h average exposure) was associated with probable depression (odds ratio (OR) = 1.17, 95% CI: 1.05, 1.31), and poorer mental wellbeing (mean difference = -0.19, 95% CI: 0.31, -0.06), adjusting for sociodemographics, smoking, body mass index, self-reported health, proximity to green space, and neighbourhood characteristics (average household income, population density, and Gini coefficient). The results were robust to further adjustment for air pollution. In stratified analyses, residential traffic noise was associated with probable depression and poorer mental wellbeing among students and individuals aged 15-34 years. Residential traffic noise was associated with probable depression and poorer mental wellbeing in a highly urbanised setting. As traffic noise is increasing in urban settings, the public health impact of noise pollution could be substantial.

Aircraft noise exposure and risk for recurrent cardiovascular events after acute coronary syndrome: A prospective patient cohort study.

In several population based cohort studies associations between aircraft noise and various diagnoses of cardiovascular disease were observed. However, no study has yet addressed the risk of recurrences in relation to transportation noise in patients with acute coronary heart disease. We conducted a prospective patient cohort study of 737 individuals recruited from eleven cardiac centers in the Rhine-Main region in the vicinity of Frankfurt Airport. All patients had an angiographically confirmed acute coronary syndrome diagnosed between July 2013 and November 2018. Individual aircraft noise exposure at the place of residence was calculated using Soundplan software, and exposure to road traffic and railway noise was obtained from noise maps provided by the Hessian State Agency. Data was analyzed by means of Cox regression adjusted for relevant confounders. Recurrent event as non-fatal endpoint was defined as myocardial infarction, stroke, bypass surgery or percutaneous coronary intervention with stent implantation. In addition, all-cause mortality was evaluated. Follow-up data including socioeconomic and confounder information was obtained from 663 (90%) patients covering a mean follow-up period of 42 (range: 1-80) months. Mean Lden aircraft noise exposure was 48.1 dB. Adjusted hazard ratio (HR) for recurrence was 1.24 (95%-CI: 0.97-1.58) per 10 dB increase in Lden aircraft noise exposure. A combined analysis of recurrence and all-cause mortality yielded a HR of 1.31 (95%-CI: 1.03-1.66). Similar HRs were found for Lday and Lnight aircraft noise exposure. HRs for road traffic and railway noise were above unity but less pronounced and not significant. Observed exposure-response associations for aircraft noise were more pronounced than previously observed in population-based cohort studies suggesting that acute coronary heart disease patients are particularly vulnerable to effects from transportation noise. Measures to reduce environmental noise exposure may thus be helpful in improving clinical outcome of patients with coronary heart disease.

Exposure to long-term source-specific transportation noise and incident breast cancer: A pooled study of eight Nordic cohorts.

BACKGROUND: Environmental noise is an important environmental exposure that can affect health. An association between transportation noise and breast cancer incidence has been suggested, although current evidence is limited. We investigated the pooled association between long-term exposure to transportation noise and breast cancer incidence. METHODS: Pooled data from eight Nordic cohorts provided a study population of 111,492 women. Road, railway, and aircraft noise were modelled at residential addresses. Breast cancer incidence (all, estrogen receptor (ER) positive, and ER negative) was derived from cancer registries. Hazard ratios (HR) were estimated using Cox Proportional Hazards Models, adjusting main models for sociodemographic and lifestyle variables together with long-term exposure to air pollution. RESULTS: A total of 93,859 women were included in the analyses, of whom 5,875 developed breast cancer. The median (5th-95th percentile) 5-year residential road traffic noise was 54.8 (40.0-67.8) dB Lden, and among those exposed, the median railway noise was 51.0 (41.2-65.8) dB Lden. We observed a pooled HR for breast cancer (95 % confidence interval (CI)) of 1.03 (0.99-1.06) per 10 dB increase in 5-year mean exposure to road traffic noise, and 1.03 (95 % CI: 0.96-1.11) for railway noise, after adjustment for lifestyle and sociodemographic covariates. HRs remained unchanged in analyses with further adjustment for PM2.5 and attenuated when adjusted for NO2 (HRs from 1.02 to 1.01), in analyses using the same sample. For aircraft noise, no association was observed. The associations did not vary by ER status for any noise source. In analyses using <60 dB as a cutoff, we found HRs of 1.08 (0.99-1.18) for road traffic and 1.19 (0.95-1.49) for railway noise. CONCLUSIONS: We found weak associations between road and railway noise and breast cancer risk. More high-quality prospective studies are needed, particularly among those exposed to railway and aircraft noise before conclusions regarding noise as a risk factor for breast cancer can be made.

Mitigation of aircraft noise-induced vascular dysfunction and oxidative stress by exercise, fasting, and pharmacological α1AMPK activation: molecular proof of a protective key role of endothelial α1AMPK against environmental noise exposure.

AIMS: Environmental stressors such as traffic noise represent a global threat, accounting for 1.6 million healthy life years lost annually in Western Europe. Therefore, the noise-associated health side effects must be effectively prevented or mitigated. Non-pharmacological interventions such as physical activity or a balanced healthy diet are effective due to the activation of the adenosine monophosphate-activated protein kinase (α1AMPK). Here, we investigated for the first time in a murine model of aircraft noise-induced vascular dysfunction the potential protective role of α1AMPK activated via exercise, intermittent fasting, and pharmacological treatment. METHODS AND RESULTS: Wild-type (B6.Cg-Tg(Cdh5-cre)7Mlia/J) mice were exposed to aircraft noise [maximum sound pressure level of 85 dB(A), average sound pressure level of 72 dB(A)] for the last 4 days. The α1AMPK was stimulated by different protocols, including 5-aminoimidazole-4-carboxamide riboside application, voluntary exercise, and intermittent fasting. Four days of aircraft noise exposure produced significant endothelial dysfunction in wild-type mice aorta, mesenteric arteries, and retinal arterioles. This was associated with increased vascular oxidative stress and asymmetric dimethylarginine formation. The α1AMPK activation with all three approaches prevented endothelial dysfunction and vascular oxidative stress development, which was supported by RNA sequencing data. Endothelium-specific α1AMPK knockout markedly aggravated noise-induced vascular damage and caused a loss of mitigation effects by exercise or intermittent fasting. CONCLUSION: Our results demonstrate that endothelial-specific α1AMPK activation by pharmacological stimulation, exercise, and intermittent fasting effectively mitigates noise-induced cardiovascular damage. Future population-based studies need to clinically prove the concept of exercise/fasting-mediated mitigation of transportation noise-associated disease.

Traffic noise, e.g. from aircraft, significantly contributes to an increased risk of cardiovascular or metabolic diseases in the general population by brain-dependent stress reactions leading to higher levels of circulating stress hormones and vasoconstrictors, all of which cause hypertension, oxidative stress, and inflammation. With the present experimental studies, we provide for the first time molecular mechanisms responsible for successful noise mitigation: Physical exercise, intermittent fasting, and pharmacological activation of the adenosine monophosphate-activated protein kinase (AMPK), a metabolic master regulator protein, prevent cardiovascular damage caused by noise exposure, such as hypertension, endothelial dysfunction, and reactive oxygen species formation (e.g. free radicals) and inflammation.These beneficial mitigation manoeuvers are secondary to an activation of the endothelial AMPK, thereby mimicking the antidiabetic drug metformin.

Long-term exposure to residential transportation noise and mortality: A nationwide cohort study.

Studies have indicated that transportation noise is associated with higher cardiovascular mortality, whereas evidence of noise as a risk factor for respiratory and cancer mortality is scarce and inconclusive. Also, knowledge on effects of low-level noise on mortality is very limited. We aimed to investigate associations between road and railway noise and natural-cause and cause-specific mortality in the Danish population. We estimated address-specific road and railway noise at the most (LdenMax) and least (LdenMin) exposed façades for all residential addresses in Denmark from 1990 to 2017 using high-quality exposure models. Using these data, we calculated 10-year time-weighted mean noise exposure for 2.6 million Danes aged >50 years, of whom 600,492 died from natural causes during a mean follow-up of 11.7 years. We analyzed data using Cox proportional hazards models with adjustment for individual and area-level sociodemographic variables and air pollution (PM2.5 and NO2). We found that a 10-year mean exposure to road LdenMax and road LdenMin per 10 dB were associated with hazard ratios (95% confidence intervals) of, respectively, 1.09 (1.09; 1.10) and 1.10 (1.10; 1.11) for natural-cause mortality, 1.09 (1.08; 1.10) and 1.09 (1.08; 1.10) for cardiovascular mortality, 1.13 (1.12; 1.14) and 1.17 (1.16; 1.19) for respiratory mortality and 1.03 (1.02; 1.03) and 1.06 (1.05; 1.07) for cancer mortality. For LdenMax, the associations followed linear exposure-response relationships from 35 dB to 60-<65 dB, after which the function levelled off. For LdenMin, exposure-response relationships were linear from 35 dB and up, with some levelling off at high noise levels for natural-cause and cardiovascular mortality. Railway noise did not seem associated with higher mortality in an exposure-response dependent manner. In conclusion, road traffic noise was associated with higher mortality and the increase in risk started well below the current World Health Organization guideline limit for road traffic noise of 53 dB.

Association between exposure to multiple air pollutants, transportation noise and cause-specific mortality in adults in Switzerland.

BACKGROUND: Long-term exposure to air pollution and noise is detrimental to health; but studies that evaluated both remain limited. This study explores associations with natural and cause-specific mortality for a range of air pollutants and transportation noise. METHODS: Over 4 million adults in Switzerland were followed from 2000 to 2014. Exposure to PM2.5, PM2.5 components (Cu, Fe, S and Zn), NO2, black carbon (BC) and ozone (O3) from European models, and transportation noise from source-specific Swiss models, were assigned at baseline home addresses. Cox proportional hazards models, adjusted for individual and area-level covariates, were used to evaluate associations with each exposure and death from natural, cardiovascular (CVD) or non-malignant respiratory disease. Analyses included single and two exposure models, and subset analysis to study lower exposure ranges. RESULTS: During follow-up, 661,534 individuals died of natural causes (36.6% CVD, 6.6% respiratory). All exposures including the PM2.5 components were associated with natural mortality, with hazard ratios (95% confidence intervals) of 1.026 (1.015, 1.038) per 5 µg/m3 PM2.5, 1.050 (1.041, 1.059) per 10 µg/m3 NO2, 1.057 (1.048, 1.067) per 0.5 × 10-5/m BC and 1.045 (1.040, 1.049) per 10 dB Lden total transportation noise. NO2, BC, Cu, Fe and noise were consistently associated with CVD and respiratory mortality, whereas PM2.5 was only associated with CVD mortality. Natural mortality associations persisted < 20 µg/m3 for PM2.5 and NO2, < 1.5 10-5/m BC and < 53 dB Lden total transportation noise. The O3 association was inverse for all outcomes. Including noise attenuated all outcome associations, though many remained significant. Across outcomes, noise was robust to adjustment to air pollutants (e.g. natural mortality 1.037 (1.033, 1.042) per 10 dB Lden total transportation noise, after including BC). CONCLUSION: Long-term exposure to air pollution and transportation noise in Switzerland contribute to premature mortality. Considering co-exposures revealed the importance of local traffic-related pollutants such as NO2, BC and transportation noise.

Long-term exposure to traffic noise and risk of incident colon cancer: A pooled study of eleven Nordic cohorts.

Background Colon cancer incidence is rising globally, and factors pertaining to urbanization have been proposed involved in this development. Traffic noise may increase colon cancer risk by causing sleep disturbance and stress, thereby inducing known colon cancer risk-factors, e.g. obesity, diabetes, physical inactivity, and alcohol consumption, but few studies have examined this. Objectives The objective of this study was to investigate the association between traffic noise and colon cancer (all, proximal, distal) in a pooled population of 11 Nordic cohorts, totaling 155,203 persons. Methods We identified residential address history and estimated road, railway, and aircraft noise, as well as air pollution, for all addresses, using similar exposure models across cohorts. Colon cancer cases were identified through national registries. We analyzed data using Cox Proportional Hazards Models, adjusting main models for harmonized sociodemographic and lifestyle data. Results During follow-up (median 18.8 years), 2757 colon cancer cases developed. We found a hazard ratio (HR) of 1.05 (95% confidence interval (CI): 0.99-1.10) per 10-dB higher 5-year mean time-weighted road traffic noise. In sub-type analyses, the association seemed confined to distal colon cancer: HR 1.06 (95% CI: 0.98-1.14). Railway and aircraft noise was not associated with colon cancer, albeit there was some indication in sub-type analyses that railway noise may also be associated with distal colon cancer. In interaction-analyses, the association between road traffic noise and colon cancer was strongest among obese persons and those with high NO2-exposure. Discussion A prominent study strength is the large population with harmonized data across eleven cohorts, and the complete address-history during follow-up. However, each cohort estimated noise independently, and only at the most exposed façade, which may introduce exposure misclassification. Despite this, the results of this pooled study suggest that traffic noise may be a risk factor for colon cancer, especially of distal origin.

Long-term exposure to transportation noise and risk of type 2 diabetes: A cohort study.

BACKGROUND: Some studies have found transportation noise to be associated with higher diabetes risk. This includes studies based on millions of participants, relying entirely on register-based confounder adjustment, which raises concern about residual lifestyle confounding. We aimed to investigate associations between noise and type 2 diabetes (T2D), including investigation of effects of increasing confounder adjustment for register-data and lifestyle. METHODS: In a cohort of 286,151 participants randomly selected across Denmark in 2010-2013 and followed up until 2017, we identified 7574 incident T2D cases. Based on residential address-history for all participants linked with exposure assessment of high spatial resolution, we calculated 10-year time-weighted mean road and railway noise at the most (LdenMax) and least (LdenMin) exposed façades and air pollution (PM2.5). We used Cox models to calculate hazard ratios (HR) with increasing adjustment for individual- and area-level register-based sociodemographic covariates, self-reported lifestyle and air pollution. RESULTS: We found that a 10 dB increase in 10-year mean road LdenMin was associated with HRs (95% CI) of 1.06 (1.02-1.10) after adjustment for age, sex and year, 1.08 (1.04-1.13) after further adjustment for register-based sociodemographic covariates, 1.07 (1.03-1.12) after further lifestyle adjustment (e.g. smoking, diet and alcohol) and 1.06 (1.02-1.11) after further PM2.5 adjustment. For road LdenMax, the corresponding HRs were 1.07 (1.04-1.10), 1.05 (1.02-1.08), 1.04 (1.01-1.07) and 1.03 (1.00-1.06). Railway noise was associated with HRs of 1.04 (0.98-1.11) for LdenMax and 1.02 (0.92-1.12) for LdenMin after adjustment for sociodemographic and lifestyle covariates and PM2.5. CONCLUSIONS: Long-term exposure to road traffic noise was associated with T2D, which together with previous literature indicates that T2D should be considered when calculating health impacts of noise. After sociodemographic adjustment, further lifestyle adjustment only changed HRs slightly, suggesting that large register-based studies with adjustment for key sociodemographic covariates can produce reliable results.

The combined effect of air and transportation noise pollution on atherosclerotic inflammation and risk of cardiovascular disease events.

BACKGROUND: Air pollution and noise exposures individually associate with major adverse cardiovascular events (MACE) via a mechanism involving arterial inflammation (ArtI); however, their combined impact on ArtI and MACE remains unknown. We tested whether dual (vs. one or neither) exposure associates with greater ArtI and MACE risk and whether MACE risk is mediated via ArtI. METHODS: Individuals (N = 474) without active cancer or known cardiovascular disease with clinical 18F-FDG-PET/CT imaging were followed for 5 years for MACE. ArtI was measured. Average air pollution (particulate matter ≤ 2.5 µm, PM2.5) and transportation noise exposure were determined at individual residences. Higher exposures were defined as noise > 55 dBA (World Health Organization cutoff) and PM2.5 ≥ sample median. RESULTS: At baseline, 46%, 46%, and 8% were exposed to high levels of neither, one, or both pollutants; 39 experienced MACE over a median 4.1 years. Exposure to an increasing number of pollutants associated with higher ArtI (standardized ß [95% CI: .195 [.052, .339], P = .008) and MACE (HR [95% CI]: 2.897 [1.818-4.615], P < .001). In path analysis, ArtI partially mediated the relationship between pollutant exposures and MACE (P < .05). CONCLUSION: Air pollution and transportation noise exposures contribute incrementally to ArtI and MACE. The mechanism linking dual exposure to MACE involves ArtI.

Relationships between long-term residential exposure to total environmental noise and stroke incidence.

Background: Noise 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. Aim: The 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 Methods: We 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. Results: There 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). Conclusion: The results suggest that total environmental noise is associated with incident stroke, which is consistent with studies on transportation noise and other CVD.

Residential road traffic and railway noise and risk of childhood cancer: A nationwide register-based case-control study in Denmark.

BACKGROUND: The aetiology of most childhood cancers remains poorly understood. We conducted a nationwide register-based case-control study to assess the association between residential road traffic and railway noise exposure and risk of childhood cancers. METHODS: We identified all cases of first cancers diagnosed in children aged 0-19 years in 1985-2013 from the Danish Cancer Registry (N = 3962) and sampled four individually matched (by sex and date of birth) controls per case (N = 14,790) using the Central Population Register. We estimated time-weighted exposure averages of residential road traffic and railway noise at the most (Lden max) and least (Lden min) exposed façades from birth to index-date (for additional analysis: in utero period) based on the individual address history for the respective time windows. We fitted conditional logistic regression models to estimate odds ratios (OR) and their 95% confidence intervals (CI). RESULTS: ORs varied by noise estimate and cancer type, with generally wide CIs mostly including 1.00. We found a tendency of higher ORs with increasing railway and road traffic noise for Hodgkin lymphoma (ORs for railway and road Lden min were 1.63 (95% CI 1.00; 2.66) and 1.14 (95% CI 0.87; 1.48) per 10 dB), as well as a tendency of higher ORs with increasing railway noise for non-Hodgkin lymphoma. For embryonal CNS tumours and astrocytoma and other glioma we observed also some weak suggestions of a positive association. Analysing exposure to traffic noise in utero revealed similar patterns to those of the main analyses. CONCLUSIONS: This nationwide study with minimal risk of bias suggests no strong associations between traffic noise and risk of most childhood cancers. We found however some suggestive evidence for a positive association with Hodgkin lymphoma, non-Hodgkin lymphoma and some CNS tumours. Further research is warranted to confirm these associations in other populations and elucidate the underlying biological mechanisms.

Long-term exposure to road traffic noise and all-cause and cause-specific mortality: a Danish Nurse Cohort study.

BACKGROUND: Long-term road traffic noise exposure is linked to cardio-metabolic disease morbidity, whereas evidence on mortality remains limited. OBJECTIVES: We investigated association of long-term exposure to road traffic noise with all-cause and cause-specific mortality. METHODS: We linked 22,858 females from the Danish Nurse Cohort (DNC), recruited into the Danish Register of Causes of Death up to 2014. Road traffic noise levels since 1970 were modelled by Nord2000 as the annual mean of a weighted 24 h average (Lden). Cox regression models examined the associations between Lden (5-year and 23-year means) and all-cause and cause-specific mortalities, adjusting for lifestyle and exposure to PM2.5 (particulate matter with diameter < 2.5 µm) and NO2 (nitrogen dioxide). RESULTS: During follow-up (mean 17.4 years), 3902 nurses died: 1622 from cancer, 922 from CVDs (289 from stroke), 338 from respiratory diseases (186 from chronic obstructive pulmonary disease, 114 from lower respiratory tract infections [ALRIs]), 234 from dementia, 95 from psychiatric disorders, and 79 from diabetes. Hazard ratios (95% confidence intervals) for all-cause mortality from fully-adjusted models were 1.06 (1.01, 1.11) and 1.09 (1.03, 1.15) per 10 dB of 5-year and 23-year mean Lden, respectively, which attenuated slightly in our main model (fully-adjusted plus PM2.5: 1.04 [1.00, 1.10]; 1.08 [1.02, 1.13]). Main model estimates suggested the strongest associations between 5-year mean Lden and diabetes (1.14: 0.81, 1.61), ALRIs (1.13: 0.84, 1.54), dementia (1.12: 0.90, 1.38), and stroke (1.10: 0.91, 1.31), whereas associations with 23-year mean Lden were suggested for respiratory diseases (1.15: 0.95, 1.39), psychiatric disorders (1.11: 0.78, 1.59), and all cancers (1.08: 0.99, 1.17). DISCUSSION: Among the female nurses from the DNC, we observed that long-term exposure to road traffic noise led to premature mortality, independently of air pollution, and its adverse effects may extend well beyond those on the cardio-metabolic system to include respiratory diseases, cancer, neurodegenerative and psychiatric disorders.

Experimental Study on Vibration and Noise Characteristics of Steel-Concrete Railway Bridge.

The paper presents the results of vibroacoustic tests of a plate girder railway bridge consisting of two parallel dilated structures and a common ballast trough. The requirements currently set for railway bridges relate to, among others, vibrations considered as one of the criteria for traffic safety and to noise emissions that may pose a threat to the environment. In this article, the results of tests conducted on vibrations of elements of the analyzed structure are presented, and the level of these vibrations in terms of meeting the requirements of the European standards is assessed. Vibrating criteria of structure performance were checked, and safety was assessed. The results of noise measurements in the vicinity of the analyzed bridge are also presented, and the environmental impact of this structure is determined. The test results show that the bridge meets the requirements for vibration acceleration and noise. An increased acoustic emission in the analyzed case does not pose a significant threat, but if this type of structure was on high supports in an urbanized area, it would be a nuisance to the environment.

Transportation noise and risk for colorectal cancer: a nationwide study covering Denmark.

PURPOSE: Few studies have suggested that traffic noise is a risk factor for cancer, but evidence is inconclusive. We aimed to investigate whether road traffic and railway noise are associated with risk of colorectal cancer. METHODS: We obtained address history for all 3.5 million people above 40 years of age and living in Denmark for the period 1990-2017 and estimated road traffic and railway noise (Lden) at the most and least exposed facades of all addresses as well as air pollution (PM2.5). During follow-up (2000-2017), 35,881 persons developed colon cancer and 19,755 developed rectal cancer. Information on individual and area-level demographic and socioeconomic variables was collected from Danish registries. We analyzed data using Cox proportional hazards models, including traffic noise as time-varying 10-year average exposure. RESULTS: Exposure to road traffic noise at the most exposed façade was associated with an incidence rate ratio and 95% confidence interval for proximal colon cancer of 1.018 (0.999-1.038) per 10 dB higher noise. We observed no associations for road traffic noise at the least exposed façade or for railway noise in relation to proximal colon cancer. Also, we found no association between road traffic or railway noise and risk for distal colon cancer or rectal cancer. CONCLUSION: Traffic noise did not seem associated with higher risk for colorectal cancer, although the suggestion of a slightly higher risk of proximal colon cancer following exposure to road traffic noise warrants further research.

Effects of exposure to surrounding green, air pollution and traffic noise with non-accidental and cause-specific mortality in the Dutch national cohort.

BACKGROUND: Everyday people are exposed to multiple environmental factors, such as surrounding green, air pollution and traffic noise. These exposures are generally spatially correlated. Hence, when estimating associations of surrounding green, air pollution or traffic noise with health outcomes, the other exposures should be taken into account. The aim of this study was to evaluate associations of long-term residential exposure to surrounding green, air pollution and traffic noise with mortality. METHODS: We followed approximately 10.5 million adults (aged ≥ 30 years) living in the Netherlands from 1 January 2013 until 31 December 2018. We used Cox proportional hazard models to evaluate associations of residential surrounding green (including the average Normalized Difference Vegetation Index (NDVI) in buffers of 300 and 1000 m), annual average ambient air pollutant concentrations [including particulate matter (PM2.5), nitrogen dioxide (NO2)] and traffic noise with non-accidental and cause-specific mortality, adjusting for potential confounders. RESULTS: In single-exposure models, surrounding green was negatively associated with all mortality outcomes, while air pollution was positively associated with all outcomes. In two-exposure models, associations of surrounding green and air pollution attenuated but remained. For respiratory mortality, in a two-exposure model with NO2 and NDVI 300 m, the HR of NO2 was 1.040 (95%CI: 1.022, 1.059) per IQR increase (8.3 µg/m3) and the HR of NDVI 300 m was 0.964 (95%CI: 0.952, 0.976) per IQR increase (0.14). Road-traffic noise was positively associated with lung cancer mortality only, also after adjustment for air pollution or surrounding green. CONCLUSIONS: Lower surrounding green and higher air pollution were associated with a higher risk of non-accidental and cause-specific mortality. Studies including only one of these correlated exposures may overestimate the associations with mortality of that exposure.

Risk of cardiovascular mortality, stroke and coronary heart mortality associated with aircraft noise around Congonhas airport, São Paulo, Brazil: a small-area study.

BACKGROUND: Noise pollution is increasingly recognised as a public health hazard, yet limited evidence is available from low- and middle-income countries (LMIC), particularly for specific sources. Here, we investigated the association between day-night average (Ldn) aircraft noise and the risk of death due to cardiovascular disease (CVD), stroke and coronary heart disease (CHD) at small-area level around São Paulo's Congonhas airport, Brazil during the period 2011-2016. METHODS: We selected 3259 census tracts across 16 districts partially or entirely exposed to ≥50 dB aircraft noise levels around the Congonhas airport, using pre-modelled 5 dB Ldn noise  bands (≤50 dB to > 65 dB). We estimated the average noise exposure per census tract using area-weighting. Age, sex and calendar year-specific death counts for CVD, stroke and CHD were calculated by census tract, according to the residential address at time of death. We fitted Poisson regression models to quantify the risk associated with aircraft noise exposure, adjusting for age, sex, calendar year and area-level covariates including socioeconomic development, ethnicity, smoking and road traffic related noise and air pollution. RESULTS: After accounting for all covariates, areas exposed to the highest levels of noise (> 65 dB) showed a relative risk (RR) for CVD and CHD of 1.06 (95% CI: 0.94; 1.20) and 1.11 (95%CI: 0.96; 1.27), respectively, compared to those exposed to reference noise levels (≤50 dB). The RR for stroke ranged between 1.05 (95%CI: 0.95;1.16) and 0.91 (95%CI: 0.78;1.11) for all the noise levels assessed. We found a statistically significant positive trend for CVD and CHD mortality risk with increasing levels of noise (p = 0.043 and p = 0.005, respectively). No significant linear trend was found for stroke. Risk estimates were generally higher after excluding road traffic density, suggesting that road traffic air and noise pollution are potentially important confounders. CONCLUSIONS: This study provides some evidence that aircraft noise is associated with increased risk of CVD and CHD mortality in a middle-income setting. More research is needed to validate these results in other LMIC settings and to further explore the influence of residual confounding and ecological bias. Remarkably, 60% of the study population living near the Congonhas airport (~ 1.5 million) were exposed to aircraft noise levels > 50 dB, well above those recommended by the WHO (45 dB), highlighting the need for public health interventions.

Residential traffic noise exposure and headaches: Results from the population-based heinz nixdorf recall study.

CONTEXT AND AIM: The link between headaches and exposure to loud noise in occupational settings has been established. However, the effect of less intense but chronic residential traffic noise exposure on headache occurrence is less clear. SETTINGS AND DESIGN: We included 3,025 participants from the Heinz Nixdorf Recall study in Germany for this cross-sectional analysis. METHODS AND MATERIAL: Residential road traffic noise exposure at the 2006-2008 address was modelled in A-weighted decibels (dB(A)) according to the European Noise Directive (2002/49/EC) for 24-hour (Lden) and night-time noise (22-6 h, Lnight). Indoor traffic noise exposure was obtained by modifying Lden and Lnight based on residence orientation, window type, and personal window opening habits. Traffic noise exposure below 55, 45 dB(A), 35 and 25 dB(A) were set as the reference for Lden, Lnight, Lden,indoor and Lnight,indoor, respectively. Average number of days with headache per month over the past three months was ascertained during the follow-up (2011-2015) medical interview. STATISTICAL ANALYSIS USED: Prevalence Odds Ratios (POR) of having eight or more headaches per month per 5 dB(A) increase in traffic noise exposure were calculated using logistic regression, adjusting for age, sex, sport, number of chronic conditions, years of education and smoking status. RESULTS: The mean age of participants was 58.3. Mean Lden was 54 dB(A). Median monthly headache days was one. No association was seen between traffic noise exposure and having ≥8 headaches/month for all the examined traffic noise indicators. However, traffic noise was positively associated with traffic noise-annoyance and insomnia; and night-time traffic noise-annoyance and insomnia were positively associated with headache. CONCLUSION: In conclusion, our data did not provide any evidence for an association between chronic traffic noise exposure and prevalence of headaches at this population's exposure levels. This should be explored in different populations given that this is the first study of its type and that noise exposure was generally low in our population.

Road traffic noise and cardiovascular disease risk factors in UK Biobank.

AIMS: The aim of this study was to investigate the cross-sectional associations of modelled residential road traffic noise with cardiovascular disease risk factors [systolic (SBP) and diastolic blood pressure (DBP), C-reactive protein, triglycerides, glycated haemoglobin, and self-reported hypertension] in UK Biobank. METHODS AND RESULTS: The UK Biobank recruited 502 651 individuals aged 40-69 years across the UK during 2006-10. Road traffic noise (Lden and Lnight) exposure for 2009 was estimated at baseline address using a simplified version of the Common Noise Assessment Methods model. We used multivariable linear and logistic regression models, adjusting for age, sex, body mass index (BMI), smoking, alcohol intake, area- and individual-level deprivation, season of blood draw, length of time at residence, and nitrogen dioxide (main model), in an analytical sample size of over 370 000 participants. Exposure to road-traffic Lden >65 dB[A], as compared to ≤55 dB[A], was associated with 0.77% [95% confidence interval (CI) 0.60%, 0.95%], 0.49% (95% CI 0.32%, 0.65%), 0.79% (95% CI 0.11%, 1.47%), and 0.12% (95% CI -0.04%, 0.28%) higher SBP, DBP, triglycerides, and glycated haemoglobin, respectively. Removing BMI from the main model yielded significant positive associations with all five markers with elevated percent changes. The associations with SBP or DBP did not appear to be impacted by hypertension medication while a positive association with prevalent self-reported hypertension was seen in the non-medicated group who exposed to a Lden level of 60-65 dB[A] (odds ratio 1.07, 95% CI 1.00, 1.15). CONCLUSION: Exposure to road traffic noise >65 dB[A], independent of nitrogen dioxide, was associated with small but adverse changes in blood pressure and cardiovascular biochemistry.