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Objective: To examine the effect of work-related stress and road noise exposure on self-rated sleep and potential additive interaction effects. Methods: Sleep and predictor variables were surveyed within two subsamples with 2191 and 1764 working women in a cross-sectional study. Sleep was assessed using a single question on general sleep quality and four questions on specific sleep problems and subsequently dichotomized (poor sleep vs. no poor sleep). Work-related stress was operationalized by job strain and effort-reward imbalance. Nocturnal exposure to road traffic noise was assessed as (a) the orientation of the bedroom window to a quiet façade vs. a low-, medium- or high-trafficked street and (b) energy-equivalent sound pressure levels for night-time modelled at the most exposed façade (Lnight). We distinguished between low (< 45 dB(A)), medium (45–50 dB(A)) and high exposure (> 50 dB(A)). Results: Poor sleep was associated with job strain and effort-reward imbalance. The prevalence of poor sleep did not increase with increasing Lnight, but bedroom window orientation showed a non-significant trend. A quiet façade had a protective effect on sleep in each Lnight category. We found a non-significant trend for an additive interaction between bedroom window orientation and job strain. Conclusion: Noise levels modelled for the most exposed façade likely overestimate the actual exposure and thus may not be a precise predictor of poor sleep. Bedroom window orientation seems more relevant. Potential additive interaction effects between bedroom window orientation and job strain should be considered when interpreting epidemiological study results on noise-induced sleep disturbances. [ABSTRACT FROM AUTHOR]

Exposure to high levels of road traffic noise at the most exposed building facade is increasing, both due to urbanization and due to overall traffic increase. This study investigated how different noise reduction measures would influence the noise exposure on a city-wide scale in Gothenburg, a city in Sweden with approximately 550,000 inhabitants. Noise exposure was estimated under several different scenarios for the period 2015–2035, using the standardized Nordic noise prediction method together with traffic flow measurements and population statistics. The scenarios were based on reducing speed limits, reducing traffic flows, introducing more electrically powered vehicles and introducing low-noise tires and pavements. The most effective measures were introducing low-noise tires or pavements, which in comparison to business as usual produced between 13% and 29% reduction in the number of inhabitants exposed above 55 dB equivalent level. [ABSTRACT FROM AUTHOR]

Traffic noise exposure within a city varies over time and space. In this study, we developed a modified noise calculation method and used this method together with population and traffic data to estimate the time trend of noise exposure for the population in Gothenburg, Sweden, from 1975 to 2010. The noise calculation method was based on the standard Nordic method for road traffic noise with modifications using area-level statistics for population and building structures instead of precise geocoding of each inhabitant. Noise emission per vehicle was assumed to be constant over the period. The results show an increase in noise exposure over time. The number of inhabitants exposed at an equivalent level above 55 dB increased from 93000 to 146000 inhabitants between 1975 and 2010, and the percentage of the population exposed at this level increased from 22% to 29% over the same period. Traffic increase (1.4% per year) and population increase/concentration (0.50% per year) were approximately equally important factors behind this increase in exposure. [ABSTRACT FROM AUTHOR]

Internationally accepted exposure-response relationships show that railway noise causes less annoyance than road traffic and aircraft noise. Railway transport, both passenger and freight transport, is increasing, and new railway lines are planned for environmental reasons. The combination of more frequent railway traffic and faster and heavier trains will, most probably, lead to more disturbances from railway traffic in the near future. To effectively plan for mitigations against noise and vibration from railway traffic, new studies are needed to obtain a better basis of knowledge. The main objectives of the present study was to investigate how the relationship between noise levels from railway traffic and general annoyance is influenced by (i) number of trains, (ii) the presence of ground borne vibrations, and (iii) building situational factors, such as orientation of balcony/patio and bedroom window. Socio-acoustic field studies were executed in residential areas; (1) with relatively intense railway traffic; (2) with strong vibrations, and; (3) with the most intense railway traffic in the country. Data was obtained for 1695 respondents exposed to sound levels ranging from L Aeq,24h 45 to 65 dB. Both number of trains and presence of ground-borne vibrations, and not just the noise level per se, are of relevance for how annoying railway noise is perceived. The results imply that, for the proportion annoyed to be equal, a 5 - 7 dB lower noise level is needed in areas where the railway traffic causes strong ground-borne vibrations and in areas with a very large number of trains. General noise annoyance was twice as high among residents in dwellings with balcony / patio oriented towards the railway and about 1.5 times higher among residents with bedroom windows facing the railway. [ABSTRACT FROM AUTHOR]

One way of mitigating the negative effects of noise from road traffic is to include the external cost of noise in a road charging system. This study shows how standardized calculation methods for road traffic noise can be used together with monetary estimates of the social cost of noise exposure to calculate charges based on the social marginal cost. Using Swedish data on traffic volume and individuals exposed to road noise, together with official Swedish monetary values for noise exposure, we estimate road-noise charges for cars and heavy vehicles. [ABSTRACT FROM AUTHOR]

Abstract: In order to mitigate the negative effects of transportation and to achieve a competitive transport sector, infrastructure charges in the European Union should be based on short-run marginal costs. This paper shows that railway-noise charges can be estimated using already obtained knowledge of monetary and acoustical noise evaluation. Most European countries have standardized calculation methods for total noise level, which can be used to estimate the marginal acoustical effect. [Copyright &y& Elsevier]

Abstract: Prediction of noise levels at shielded positions in urban areas is more difficult than on exposed positions. At shielded positions, the predictions method must include multiple reflections, and many sources must be taken into account. Using numerical methods that solve the wave equation is possible, but very computationally heavy. Here two methods have been used, a very simplified ray model and a statistical model. The results show that concentrating the traffic and introducing absorption onto building façades will give lower levels at shielded positions. [Copyright &y& Elsevier]

The sound propagation into a courtyard shielded from direct exposure is predicted using an equivalent sources approach. The problem is simplified into that of a two-dimensional city canyon. A set of equivalent sources are used to couple the free half-space above the canyon to the cavity inside the canyon. Atmospheric turbulence causes an increase in the expected value of the sound pressure level compared to a homogeneous case. The level increase is estimated using a von Ka´rma´n turbulence model and the mutual coherences of all equivalent sources' contributions. For low frequencies the increase is negligible, but at 1.6 kHz it reaches 2–5 dB for the geometries and turbulence parameters used here. A comparison with a ray-based model shows reasonably good agreement. [Copyright &y& Elsevier]

The prediction of road traffic noise levels in areas not directly exposed, such as areas behind buildings and courtyards, is difficult using standardised methods. This is mainly due to the fact that traditionally only one or a few sources are included. Here a simple model that assumes a flat city on rigid ground is used to demonstrate that sources from a large area are important. Calculations are compared to measurements for four cases, and the proposed method predicts levels 6–10 dB too high for the equivalent level at all measurement positions. If a correction is applied for this over-estimation, the results agree well. [Copyright &y& Elsevier]

BACKGROUND: Transportation noise may induce cardiovascular disease, but the public health implications are unclear. OBJECTIVES: The study aimed to assess exposure–response relationships for different transportation noise sources and ischemic heart disease (IHD), including subtypes. METHODS: 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. RESULTS: 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 Lden 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 Lden 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 Lden was suggested in the exposure-response relation for road traffic noise and IHD. DISCUSSION: 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. [ABSTRACT FROM AUTHOR]

• Rail traffic is increasing following policy recommendations for sustainability. • People living close to rail tracks are exposed to both vibration and noise. • We show strong dose–response relationships for modelled vibration and annoyance. • The associations are strongest for freight trains. • Important to consider railway noise in the investigation of vibration annoyance. Rail traffic is increasing following policy recommendations for a sustainable transportation model. However, the health effects of rail traffic vibration on residents living close to railways remain underexplored. We aimed to investigate the relationships between rail traffic vibration and vibration annoyance from different types of trains and to explore the influence of railway noise on these relationships. The study population (N = 7280) was randomly selected from adults living within 1 km of a trafficked railway in Sweden. Survey data were combined with modelled rail traffic vibration and noise. A cross-sectional design and logistic regression analysis were used. Results support a dose–response relationship between vibration and annoyance (stronger for freight trains and weaker for passenger trains). In the adjusted analysis, we observe a robust association between vibration and annoyance from all types of trains, accounting for socioeconomic factors. Furthermore, railway noise appears to modulate the vibration annoyance response. [ABSTRACT FROM AUTHOR]

Urbanization and increasing road traffic cause exposure to both noise and air pollution. While the levels of air pollutants such as nitrogen oxides (NO x) have decreased in Sweden during the past decades, exposure to traffic noise has increased. The association with cardiovascular morbidity is less well established for noise than for air pollution, and most studies have only studied one of the two highly spatially correlated exposures. The Swedish Primary Prevention Study cohort consists of men aged 47 to 55 when first examined in 1970–1973. The cohort members were linked to the Swedish patient registry through their personal identity number and followed until first cardiovascular event 1970–2011. The address history during the entire study period was used to assign annual modelled residential exposure to road traffic noise and NO x. The Cox proportional hazards model with age on the time axis and time-varying exposures were used in the analysis. The results for 6304 men showed a non-significant increased risk of cardiovascular disease for long-term road traffic noise at the home address, after adjusting for air pollution. The hazard ratios were 1.08 (95% CI 0.90–1.28) for cardiovascular mortality, 1.14 (95% CI 0.96–1.36) for ischemic heart disease incidence and 1.07 (95% CI 0.85–1.36) for stroke incidence, for noise above 60 dB, compared to below 50 dB. This study found some support for cardiovascular health effects of long-term exposure to road traffic noise above 60 dB, after having accounted for exposure to air pollution. • Association between residential noise and cardiovascular disease in a Swedish cohort. • Average exposure (1970–2011) to residential road traffic noise was 55 dB L AEq24h. • Indications of increased risk of cardiovascular disease above 60 dB L AEq24h. • Most risk estimates only marginally affected when adjusting for air pollution. [ABSTRACT FROM AUTHOR]

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=19.5 y), 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 =2.5 μm (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. [ABSTRACT FROM AUTHOR]

Abstract This paper describes a method to synthesise wind turbine sounds to be used in sleep studies using a parameter-based synthesis. The parameter values were determined using recordings of several types of operating wind turbines, thorough investigations of the recorded sounds, previous reports on wind turbine sound characteristics, and acoustic knowledge on how sound properties change from source to an outdoor receiver. The different wind turbine types are shown in the paper to have characteristic amplitude modulation (AM) spectra, with different AM strengths in different 1/3 octave bands. The statistical levels of the AM are evaluated and the correlation between A-weighted AM and AM in individual 1/3 octave bands is evaluated using linear regression. Method tests of the proposed synthesis technique show that it performs well and that wind turbine sound signals that include arbitrary AM spectra can be created. The work was part of the research project WiTNES (Wind Turbine Noise Effects on Sleep). [ABSTRACT FROM AUTHOR]

This paper evaluates the relative contribution of vibration and noise from railway on physiological sleep outcomes. Vibration from railway freight often accompanies airborne noise, yet is almost totally absent in the existing literature. In an experimental investigation, 23 participants, each sleeping for six nights in the laboratory, were exposed to 36 simulated railway freight pass-bys per night with vibration alone (aWd,max=0.0204 ms-2), noise alone (LAF,max=49.8 dB), or both vibration and noise simultaneously. A fourth exposure night involved 52 pass-bys with concurrent vibration and noise. Sleep was measured with polysomnography. Cardiac activity was measured with electrocardiography. The probability of cortical arousals or awakenings was greater following all exposures, including vibration alone, than spontaneous reaction probability (p<0.05). The effects of vibration exposure and noise exposure on changes of sleep stage and arousals were directly additive. Vibration and noise exposure both induced heart rate acceleration above spontaneously expected fluctuations at baseline. The results indicate that vibration and noise are processed in the brain separately yet in parallel, with both contributing towards the likelihood of sleep disruption. The findings show that vibration is of importance when considering the impact of railway freight on sleep. [ABSTRACT FROM AUTHOR]

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 NO 2 -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. • Few studies have examined an association between traffic noise and colon cancer. • This is the first international study on the association; pooling 11 cohorts. • This large study suggested that traffic noise is a risk factor for colon cancer. • The association was strongest for distal tumors and among obese people. • Our findings contributes largely to the evidence-base for an association. [ABSTRACT FROM AUTHOR]

Despite firm evidence for an association between long-term ambient air pollution exposure and cardiovascular morbidity and mortality, results from epidemiological studies on the association between air pollution exposure and atherosclerosis have not been consistent. We investigated associations between long-term low-level air pollution exposure and coronary atherosclerosis. We performed a cross-sectional analysis in the large Swedish CArdioPulmonary bioImaging Study (SCAPIS, n = 30 154), a random general population sample. Concentrations of total and locally emitted particulate matter <2.5 μm (PM 2.5), <10 μm (PM 10), and nitrogen oxides (NO x) at the residential address were modelled using high-resolution dispersion models. We estimated associations between air pollution exposures and segment involvement score (SIS), coronary artery calcification score (CACS), number of non-calcified plaques (NCP), and number of significant stenoses, using ordinal regression models extensively adjusted for potential confounders. Median 10-year average PM 2.5 exposure was 6.2 μg/m3 (range 3.5–13.4 μg/m3). 51 % of participants were women and 51 % were never-smokers. None of the assessed pollutants were associated with a higher SIS or CACS. Exposure to PM 2.5 was associated with NCP (adjusted OR 1.34, 95 % CI 1.13, 1.58, per 2.05 μg/m3). Associations with significant stenoses were inconsistent. In this large, middle-aged general population sample with low exposure levels, air pollution was not associated with measures of total burden of coronary atherosclerosis. However, PM 2.5 appeared to be associated with a higher prevalence of non-calcified plaques. The results suggest that increased risk of early-stage atherosclerosis or rupture, but not increased total atherosclerotic burden, may be a pathway for long-term air pollution effects on cardiovascular disease. [Display omitted] • Firm evidence shows that air pollution is a risk factor for cardiovascular disease. • However, studies of the association with atherosclerosis remain inconclusive. • We assessed air pollution and atherosclerosis in a large Swedish multi-city study. • Air pollution was associated with non-calcified plaques but not total plaque burden. • Our results may indicate an association with early or vulnerable atherosclerosis. [ABSTRACT FROM AUTHOR]

Background: A substantial increase in transportation of goods on railway may be hindered by public fear of increased vibration and noise leading to annoyance and sleep disturbance. As the majority of freight trains run during night time, the impact upon sleep is expected to be the most serious adverse effect. The impact of nocturnal vibration on sleep is an area currently lacking in knowledge. We experimentally investigated sleep disturbance with the aim to ascertain the impact of increasing vibration amplitude. Methodology/Principal Findings: The impacts of various amplitudes of horizontal vibrations on sleep disturbance and heart rate were investigated in a laboratory study. Cardiac accelerations were assessed using a combination of polysomnography and ECG recordings. Sleep was assessed subjectively using questionnaires. Twelve young, healthy subjects slept for six nights in the sleep laboratory, with one habituation night, one control night and four nights with a variation of vibration exposures whilst maintaining the same noise exposure. With increasing vibration amplitude, we found a decrease in latency and increase in amplitude of heart rate as well as a reduction in sleep quality and increase in sleep disturbance. Conclusions/Significance: We concluded that nocturnal vibration has a negative impact on sleep and that the impact increases with greater vibration amplitude. Sleep disturbance has short- and long-term health consequences. Therefore, it is necessary to define levels that protect residents against sleep disruptive vibrations that may arise from night time railway freight traffic. [ABSTRACT FROM AUTHOR]

Increasing evidence indicates aggravation of immune-mediated diseases due to physiological and psychological stress. Noise is a stressor, however, little is known about its effects on children's respiratory health. This study investigates the association between pre- or postnatal road traffic or occupational noise exposure and asthma as well as related symptoms from infancy to adolescence. The study was conducted in the Swedish birth cohort BAMSE, including over 4000 participants followed with repeated questionnaires and clinical tests until 16 years of age. Pre- and postnatal residential road traffic noise was assessed by estimating time-weighted average noise levels at the most exposed façade. Maternal occupational noise exposure during pregnancy was evaluated using a job-exposure-matrix. The associations between noise exposure and asthma-related outcomes were explored using logistic regression and generalised estimating equations. We observed non-significant associations for asthma ever up to 16 years with residential road traffic noise exposure in infancy ≥55 dB Lden (adjusted OR = 1.22; 95% CI 0.90–1.65), as well as prenatal occupational noise exposure ≥80 dB LAeq,8h (1.18, 0.85–1.62). In longitudinal analyses, however, no clear associations between pre- or postnatal exposure to residential road traffic noise, or average exposure to noise since birth, were detected in relation to asthma or wheeze until 16 years. We did not find a clear overall association between exposure to noise during different time periods and asthma or wheeze up to adolescence. • Evidence between respiratory health effects and environmental noise exposure is only sparsely available, particularly in children. • The present study is the first to investigate time aspects of long-term exposure to environmental noise in the context of childhood airway disease. • We found no consistent association between exposure to noise during different time periods and asthma or wheeze up to adolescence. [ABSTRACT FROM AUTHOR]

[Display omitted] • Higher level of aircraft noise was associated with faster cognitive decline. • Aircraft and railway noise increased the hazard of cognitive impairment. • Exposure to more noise sources increased the risk of cognitive impairment. Transportation noise is an environmental exposure with mounting evidence of adverse health effects. Besides the increased risk of cardiovascular and metabolic diseases, recent studies suggest that long-term noise exposure might accelerate cognitive decline in older age. We examined the association between transportation noise and cognitive function in a cohort of older adults. The present study is based on 2594 dementia-free participants aged 60 + years from the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). Global cognition score and CIND (cognitive impairment, no dementia) were assessed with a comprehensive neuropsychological battery at baseline and up to 16 years. Residential transportation noise resulting from road traffic, railway, and aircraft were estimated at the most exposed façade and the time-weighted average exposure was assessed. Linear mixed-effect models were used to assess the effect of long-term traffic noise exposure on the rate of change in global cognition score. Hazard ratios (HRs) and 95 % confidence intervals (CIs) of CIND by transportation noise exposure were obtained with Cox proportional hazard models. Global cognition score decreased at an average rate of −0.041 (95 %CI −0.043, −0.039) per year. Aircraft noise was associated with a 0.007 (per 10 dB L den ; 95 %CI −0.012, −0.001) faster annual rate of decline. Global cognition score seems to be not affected by road traffic and railway noise. During the follow-up, 422 (21 %) participants developed CIND. A 10-dB L den difference in exposure to aircraft and railway noise was associated with a 16 % (HR 1.16, 95 %CI 0.91, 1.49) and 26 % (HR 1.26, 95 %CI 1.01, 1.56) increased hazard of CIND in the multi-pollutant model, respectively. No association was found for road traffic (HR 1.00, 95 %CI 0.83, 1.21). Transportation noise was linked to cognitive impairment and faster cognitive decline among older adults. Future studies are warranted to confirm our results. [ABSTRACT FROM AUTHOR]

Background: Exposure to traffic noise has been associated with hypertension in adults but the evidence in adolescents is limited. We investigated long-term road traffic noise exposure, maternal occupational noise during pregnancy and other factors in relation to blood pressure and prehypertension at 16 years of age.Methods: Systolic and diastolic blood pressure were measured in 2597 adolescents from the Swedish BAMSE birth cohort. Levels of road traffic noise were estimated at home addresses during lifetime and for the mother during pregnancy as well as maternal occupational noise exposure during pregnancy. Exposure to NOx from local sources was also assessed. Associations between noise or NOx exposure and blood pressure or prehypertension were analysed using linear and logistic regression.Results: The prevalence of prehypertension was higher among males and in those with overweight, low physical activity or overweight mothers. No strong or consistent associations were observed between pre- or postnatal exposure to road traffic noise and blood pressure at 16 years of age. However, inverse associations were suggested for systolic or diastolic blood pressure and prehypertension, which reached statistical significance among males (OR 0.80 per 10 dB Lden, 95% CI 0.65-0.99) and those with maternal occupational noise exposure ≥ 70 dB LAeq8h (OR 0.60, 95% CI 0.41-0.87). On the other hand, occupational noise exposure during pregnancy tended to increase systolic blood pressure and prehypertension risk in adolescence. No associations were seen for NOx exposure.Conclusion: No conclusive associations were observed between pre- or postnatal noise exposure and blood pressure or prehypertension in adolescents. [ABSTRACT FROM AUTHOR]

Abstract Background There is growing evidence that traffic noise exposure is associated with adiposity among adults but data in children are limited. Objective This longitudinal study examined whether pre- and postnatal noise exposure is associated with body mass index (BMI) between birth and adolescence or with adverse birth outcomes. Methods The study was conducted using data from the BAMSE birth cohort, which included 4089 children born in Stockholm County, Sweden. Data on BMI from birth to adolescence were collected via questionnaires, clinical examinations and health care records. A national register provided information on birth outcomes. Road traffic noise levels at the most exposed façade were estimated for all residences of the children during follow-up, as well as of their mothers during pregnancy, and time-weighted average exposure was calculated for different time windows. Maternal occupational noise exposure was obtained from a job-exposure-matrix. Logistic- and quantile regression models were used to estimate associations between noise exposure and health outcomes. Results We found residential road traffic noise exposure to be associated with increases in BMI from school age to adolescence, but not at earlier ages. In the age groups 8–11 years and 12–16 years the BMI increments were 0.11 kg/m2 per 10 dB L den (95% CI 0.08–0.13) and 0.20 kg/m2 per 10 dB L den (95% CI 0.17–0.22), respectively. Maternal noise exposure during pregnancy was generally unrelated to adverse birth outcomes and BMI from birth to adolescence in the children, however, traffic noise exposure was associated with a decreased risk of preterm birth Conclusion Residential road traffic noise exposure was associated with BMI increases from school age to adolescence, but not at earlier ages. Maternal occupational noise exposure or exposure from road traffic during pregnancy were not consistently related to birth outcomes or BMI from birth to adolescence. Highlights • Evidence links traffic noise exposure to adiposity among adults but data in children are limited. • We saw increases in body mass from school age to adolescence related to road traffic noise exposure. • Maternal noise exposure in pregnancy was not associated with body mass development in children. • Adverse birth outcomes were generally unrelated to maternal noise exposure during pregnancy. • Our results support an environmental influence on body mass during school age and adolescence. [ABSTRACT FROM AUTHOR]

Background: The evidence on exposure to transportation noise and development of hypertension is inconclusive, mostly because of a lack of high quality studies of longitudinal design.Objectives: This cohort study aimed at investigating the association between exposure to road traffic, railway or aircraft noise and incidence of hypertension. We also assessed effects of varying lengths of exposure as well as of multiple sources of exposure.Methods: Based on the residential histories of a cohort of 4854 men and women from Stockholm County, we estimated the residential exposure to road traffic, railway and aircraft noise in 1, 5 and 10 year time-periods. Hypertension was assessed by blood pressure measurements, information from questionnaires and hospital diagnoses. Extensive information on potential confounders was available from repeated questionnaires and registers. Hazard Ratios (HR) and 95% confidence intervals (CI) of hypertension related to noise exposure was computed from Cox regression models.Results: We observed a positive association between aircraft noise exposure and incidence of hypertension with a HR of 1.16 (95% CI 1.08-1.24) per 10 dB Lden 5 years preceding the event. No clear differences in risk were indicated between the three exposure time windows. Road traffic and railway noise were not associated with incidence of hypertension during any of the exposure periods. There appeared to be a particularly high risk of hypertension among persons exposed to both aircraft and road traffic noise ≥45 dB Lden with an HR of 1.39 (95% CI 1.14-1.70).Conclusions: Exposure to aircraft noise may result in increased risk of hypertension. [ABSTRACT FROM AUTHOR]

Objectives: The understanding of determinants for saliva cortisol levels in adolescents is limited. This study investigated the role of road traffic noise exposure, noise annoyance and various other factors for saliva cortisol levels.Methods: We collected morning and evening saliva samples from 1751 adolescents from the BAMSE birth cohort based in Stockholm County. Façade noise levels from road traffic were estimated at the residences of the study subjects and repeated questionnaires and medical examinations provided extensive information on various exposures and conditions, including annoyance to noise from different sources. Cortisol was measured using radioimmunoassay. Associations between determinants and saliva cortisol levels were analysed using linear regression.Results: Morning saliva cortisol levels were significantly higher in females than in males (geometric mean 42.4 and 35.0 nmol/l, respectively) as well as in subjects with allergy related diseases. Height and age were related to saliva cortisol levels as well as sampling season. Road traffic noise exposure was not associated with saliva cortisol, however, annoyance to noise tended to increase the levels. Saliva cortisol levels appeared particularly high among those who were highly annoyed and exposed to road traffic noise levels ≥ 55 dB Lden (50.5 nmol/l, p = 0.02).Conclusion: Our findings suggest that individual perception of noise may be of importance for saliva cortisol levels. The results also point to the complexity of using saliva cortisol as a marker of noise exposure in adolescents. [ABSTRACT FROM AUTHOR]

To increase the understanding of wind turbine noise on sleep, human physiological reactions need to be studied in a controlled laboratory setting. The paper presents an outdoor–indoor noise level difference as a function of frequency, applicable to creating wind turbine indoor sounds with the outdoor sounds as input. For this, a combination of measurement data and modeling results has been used. The suggested data are provided in a table. [ABSTRACT FROM AUTHOR]

The combined health impact of concurrent railway noise and railway vibration exposure is not yet well understood. This systematic review gives an overview of epidemiological studies on health effects from railway vibration, aiming to quantify this association with exposure-effect curves. Moreover, the combined health effects of vibration and concurrent noise were investigated. We converted the vibration metric to an equivalent noise level and calculated an overall noise level by energetically summing the equivalent and railway noise level. The combined health effect was determined by using published evidence-based exposure-effect formulas. Studies included in this systematic review predominately investigated annoyance and self-reported sleep disturbances; no studies on manifest diseases were identified. For the combined effects of vibration and noise on "total" annoyance, the results based on the pooled analysis of CargoVibes project are recommended as conservative approach. Converting railway vibration into equivalent noise levels in dB may offer a pragmatic approach to assess the combined health effects of railway noise and railway vibration exposure. Future studies should include cardiovascular and mental diseases in addition to vibration-induced annoyance and sleep disturbances. Furthermore, future studies should include in-depth investigations of the interaction between railway noise and railway vibration to allow for a more accurate assessment of the railway-induced burden of disease. [ABSTRACT FROM AUTHOR]

Environmental noise is of increasing concern for public health. Quantification of associated health impacts is important for regulation and preventive strategies. To estimate the burden of disease (BoD) due to road traffic and railway noise in four Nordic countries and their capitals, in terms of DALYs (Disability-Adjusted Life Years), using comparable input data across countries. Road traffic and railway noise exposure was obtained from the noise mapping conducted according to the Environmental Noise Directive (END) as well as nationwide noise exposure assessments for Denmark and Norway. Noise annoyance, sleep disturbance and ischaemic heart disease were included as the main health outcomes, using exposure-response functions from the WHO, 2018 systematic reviews. Additional analyses included stroke and type 2 diabetes. Country-specific DALY rates from the Global Burden of Disease (GBD) study were used as health input data. Comparable exposure data were not available on a national level for the Nordic countries, only for capital cities. The DALY rates for the capitals ranged from 329 to 485 DALYs/100,000 for road traffic noise and 44 to 146 DALY/100,000 for railway noise. Moreover, the DALY estimates for road traffic noise increased with up to 17% upon inclusion of stroke and diabetes. DALY estimates based on nationwide noise data were 51 and 133% higher than the END-based estimates, for Norway and Denmark, respectively. Further harmonization of noise exposure data is required for between-country comparisons. Moreover, nationwide noise models indicate that DALY estimates based on END considerably underestimate national BoD due to transportation noise. The health-related burden of traffic noise was comparable to that of air pollution, an established risk factor for disease in the GBD framework. Inclusion of environmental noise as a risk factor in the GBD is strongly encouraged. • Transportation noise contributes with a considerable burden in the Nordic capitals. • END based BoD assessment underestimate the disease burden at the country level. • BoD due to traffic noise was of similar size as reported for PM 2.5 air pollution. • Fair comparison of BoD across countries requires further noise data harmonization. [ABSTRACT FROM AUTHOR]

BACKGROUND: 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. OBJECTIVES: 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. METHODS: 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. RESULTS: 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. CONCLUSION: Our results link transportation noise exposure to development of obesity and suggest that combined exposure from different sources may be particularly harmful. [ABSTRACT FROM AUTHOR]

Long-term exposure to air pollution is associated with cardiovascular events. A main suggested mechanism is that air pollution accelerates the progression of atherosclerosis, yet current evidence is inconsistent regarding the association between air pollution and coronary artery and carotid artery atherosclerosis, which are well-established causes of myocardial infarction and stroke. We studied associations between low levels of long-term air pollution, coronary artery calcium (CAC) score, and the prevalence and area of carotid artery plaques, in a middle-aged population-based cohort. The Swedish CArdioPulmonary bioImage Study (SCAPIS) Gothenburg cohort was recruited during 2013–2017 and thoroughly examined for cardiovascular risk factors, including computed tomography of the heart and ultrasonography of the carotid arteries. In 5070 participants (age 50–64 years), yearly residential exposures to air pollution (PM 2.5 , PM 10 , PM coarse , NO x , and exhaust-specific PM 2.5 1990–2015) were estimated using high-resolution dispersion models. We used Poisson regression to examine associations between long-term (26 years' mean) exposure to air pollutants and CAC score, and prevalence of carotid artery plaques, adjusted for potential confounders. Among participants with carotid artery plaques, we also examined the association with plaque area using linear regression. Mean exposure to PM 2.5 was low by international standards (8.5 μg/m3). There were no consistent associations between long-term total PM 2.5 exposure and CAC score or presence of carotid artery plaques, but an association between total PM 2.5 and larger plaque area in participants with carotid plaques. Associations with traffic-related air pollutants were consistently positive for both a high CAC score and bilateral carotid artery plaques. These associations were independent of road traffic noise. We found stronger associations among men and participants with cardiovascular risk factors. The results lend some support to atherosclerosis as a main modifiable pathway between low levels of traffic-related ambient air pollution and cardiovascular disease, especially in vulnerable individuals. • Long-term PM 2.5 was not associated with coronary calcification or carotid plaques. • Traffic-related air pollutants were consistently associated with atherosclerosis. • Associations were stronger in men and in participants with some risk factors. • There was no indication of confounding by road traffic noise. [ABSTRACT FROM AUTHOR]

Long-term exposure to air pollution is associated with cardiovascular events. A main suggested mechanism is that air pollution accelerates the progression of atherosclerosis, yet current evidence is inconsistent regarding the association between air pollution and coronary artery and carotid artery atherosclerosis, which are well-established causes of myocardial infarction and stroke. We studied associations between low levels of long-term air pollution, coronary artery calcium (CAC) score, and the prevalence and area of carotid artery plaques, in a middle-aged population-based cohort. The Swedish CArdioPulmonary bioImage Study (SCAPIS) Gothenburg cohort was recruited during 2013–2017 and thoroughly examined for cardiovascular risk factors, including computed tomography of the heart and ultrasonography of the carotid arteries. In 5070 participants (age 50–64 years), yearly residential exposures to air pollution (PM 2.5 , PM 10 , PM coarse , NO x , and exhaust-specific PM 2.5 1990–2015) were estimated using high-resolution dispersion models. We used Poisson regression to examine associations between long-term (26 years' mean) exposure to air pollutants and CAC score, and prevalence of carotid artery plaques, adjusted for potential confounders. Among participants with carotid artery plaques, we also examined the association with plaque area using linear regression. Mean exposure to PM 2.5 was low by international standards (8.5 μg/m3). There were no consistent associations between long-term total PM 2.5 exposure and CAC score or presence of carotid artery plaques, but an association between total PM 2.5 and larger plaque area in participants with carotid plaques. Associations with traffic-related air pollutants were consistently positive for both a high CAC score and bilateral carotid artery plaques. These associations were independent of road traffic noise. We found stronger associations among men and participants with cardiovascular risk factors. The results lend some support to atherosclerosis as a main modifiable pathway between low levels of traffic-related ambient air pollution and cardiovascular disease, especially in vulnerable individuals. • Long-term PM 2.5 was not associated with coronary calcification or carotid plaques. • Traffic-related air pollutants were consistently associated with atherosclerosis. • Associations were stronger in men and in participants with some risk factors. • There was no indication of confounding by road traffic noise. [ABSTRACT FROM AUTHOR]