In Europe, lack of consistent noise data has hampered large-scale epidemiological studies and disease burden assessments related to noise in Europe. This study addressed these limitations by developing and evaluating a Europe-wide noise model using CNOSSOS-EU, a standardized noise calculation framework in Europe.We implemented the CNOSSOS-EU model using harmonized input data, including traffic flow estimates for all roads. We compared our noise estimates with national estimates from three countries and one city in a agreement analysis. As a proof of concept, we estimated noise levels at the noisiest façade points of 102,560 randomly-selected buildings across Europe and 14 million buildings in the cohort study areas.Overall, plausible day-evening-night levels (Lden) were modelled at points with varying traffic flow on nearby roads. The Lden model estimates showed moderate correlations with national noise models in Switzerland, the Netherlands, and the United Kingdom (Pearson's cor = 0.52-0.77) but a lower correlation in Stockholm County (0.39). Most randomly-selected building façade points (62%) had traffic flows on nearby roads below the END modeling threshold, with substantial noise variability. Because the input traffic flow estimates on residential roads explained little variability, noise estimates should be applied with caution where residential roads dominate the noise exposure.While high-quality national models remain gold-standard and preferable for health analysis and impact assessments where available, our Europe-wide model offers standardized estimates across countries and expands beyond END maps. Both Europe-wide and national estimates should be considered in sensitivity analyses to assess potential differences in estimated health effects. The resulting noise estimates may further facilitate our understanding of noise-related health effects and disease burden at a broader scale in Europe for countries lacking national noise models.

Background: Urban residents are exposed to multiple environmental stressors, but robust evidence on inequities in environmental exposure and associated health and well-being outcomes remains limited. Aim: To assess inequities in residential exposure to air pollution (PM 2.5 , PM 10 , and NO 2 ), traffic noise (road, railway, and aircraft) and greenness (NDVI within 300 m), and to characterize associations with self-reported symptoms and annoyances. Methods: The study population comprised 46,282 adults (18–84 years) residing in Stockholm County, Sweden, who responded to the Swedish National Environmental Health Survey 2023. Residential exposure (dichotomized) was based on geocoded address coordinates and stratified by socioeconomic status (SES) and building type. Logistic regression estimated adjusted odds ratios (OR) with 95% confidence intervals (95% CI) and tested effect modification via interaction terms. Results: Apartment residents were more often exposed to air pollution and noise and had less surrounding greenness than house residents. SES-stratified analyses revealed exposure-specific patterns, but no consistent overall trends. Air pollution exposure was associated with perceived poor outdoor air quality (NO 2 : OR = 3.22; 95% CI = 2.75–3.79), traffic noise with, for example, high noise annoyance (road traffic: OR = 4.59; 95% CI = 4.02–5.26), and greenness, for example, with lower perceived indoor heat stress during summer (OR = 0.83; 95% CI = 0.79–0.88). Self-reported health and well-being varied by SES and building type. Conclusions: Our study reveals concentrated environmental stressors in dense residential areas and highlights multidimensional environmental inequities. Environmental exposure was associated with self-perceived health and well-being, underscoring the need for integrated, system-based policies, such as One Health, to promote sustainable urban well-being.

BACKGROUND:Environmental exposures have been associated with adiposity, but the evidence remains inconsistent. We examined associations of several environmental exposures with adiposity in young adulthood, and body mass index (BMI) trajectories from birth to 24 years. METHODS:In the Swedish birth cohort BAMSE, individual-level exposure to air pollutants, road traffic noise, and greenness was estimated using validated models. Time-weighted averages were calculated for early-life (first year) and recent exposure (five years prior to clinical assessment). At age 24, waist circumference and body composition (i.e., body/trunk fat percentage, fat mass index (FMI)) using bioimpedance were measured (n = 1612). BMI trajectories based on anthropometrics repeatedly measured up to 24 years were identified via latent class mixture modeling. Sex-specific associations were estimated via linear and multinomial logistic regression. RESULTS:One interquartile range increase in early-life fine particulate matter ≤2.5 μm (PM2.5) exposure (1.18 μg/m3) was associated with increased FMI in males (β = 0.30; 95% CI: 0.01-0.60), while in females, increase in recent PM2.5 exposure was linked to several adiposity markers. Similar patterns were observed for other air pollutants. Early-life PM2.5 exposure was also associated with an increased risk of being in the persistently high BMI trajectory group in females (OR = 2.39; 1.20-4.80). No consistent associations were observed with road traffic noise or greenness. CONCLUSION:Air pollution exposure was associated with adiposity markers in young adults in a time- and sex-specific manner. In females, exposure to air pollution at birth was linked to a higher likelihood of persistently elevated BMI from birth to age 24 years.

Importance:Air pollution exposure has been associated with an increased risk of neurodegenerative diseases; however, evidence is limited for motor neuron disease (MND), especially regarding disease progression. Objective:To determine whether long-term exposure to air pollution is associated with the risk and prognosis of MND. Design, Setting, and Participants:This population-based, nested case-control study used Swedish health register data of incident MND cases diagnosed between 2015 and 2023 with up to 8 years of follow-up. Participants included patients with MND, 5 age- and sex-matched population controls without MND per patient with MND, and full siblings of the patients with MND. Data were analyzed between November 6, 2024, and November 4, 2025. Exposures:Mean yearly concentrations of particulate matters of 2.5 µm or less, 10 µm or less, or 2.5 to 10 µm in diameter (PM2.5, PM10, PM2.5-10) and nitrogen dioxide (NO2) were assessed at the residential address using a spatiotemporal model to approximate accumulated air pollution exposure. Main Outcome and Measures:Association between air pollution and risk of MND was assessed by comparing cases to both population and sibling controls. Flexible parametric survival models estimated the association between air pollution exposure and the risk of mortality (or use of invasive ventilation) after MND diagnosis (case-only analyses). Based on the rate of decline in the ALS Functional Rating Scale-Revised (ALSFRS-R) score and its subscores after diagnosis, patients were classified into fast (upper 25th percentile) or slow (lower 75th percentile) progression. Logistic regression was used to assess air pollution exposure and the risk of fast progression. Results:The study included 1463 patients with MND, 7310 population controls, and 1768 sibling controls. The mean (SD) age for all patients with MND was 67.3 (11.7) years, and 814 (55.6) were male. In the population comparison, long-term air pollution was associated with an increased risk of MND; per IQR increase in the 10-year average level, the odds ratio was 1.21 (95% CI, 1.09-1.34) for PM2.5, 1.30 (95% CI, 1.19-1.42) for PM2.5-10, 1.29 (95% CI, 1.18-1.42) for PM10, and 1.20 (95% CI, 1.12-1.29) for NO2. A higher level of PM10 or NO2 was associated with a higher hazard of mortality, whereas a higher level of all PMs was associated with faster functional decline, particularly motor and respiratory functions, after MND diagnosis. Conclusions and Relevance:The findings of this case-control study suggest that air pollution, even at relatively low levels typical of Sweden, may contribute both to the risk of developing MND and disease prognosis after MND diagnosis.

Background:Urban residents are exposed to multiple environmental stressors, but robust evidence on inequities in environmental exposure and associated health and well-being outcomes remains limited. Aim:To assess inequities in residential exposure to air pollution (PM2.5, PM10, and NO2), traffic noise (road, railway, and aircraft) and greenness (NDVI within 300 m), and to characterize associations with self-reported symptoms and annoyances. Methods:The study population comprised 46,282 adults (18-84 years) residing in Stockholm County, Sweden, who responded to the Swedish National Environmental Health Survey 2023. Residential exposure (dichotomized) was based on geocoded address coordinates and stratified by socioeconomic status (SES) and building type. Logistic regression estimated adjusted odds ratios (OR) with 95% confidence intervals (95% CI) and tested effect modification via interaction terms. Results:Apartment residents were more often exposed to air pollution and noise and had less surrounding greenness than house residents. SES-stratified analyses revealed exposure-specific patterns, but no consistent overall trends. Air pollution exposure was associated with perceived poor outdoor air quality (NO2: OR = 3.22; 95% CI = 2.75-3.79), traffic noise with, for example, high noise annoyance (road traffic: OR = 4.59; 95% CI = 4.02-5.26), and greenness, for example, with lower perceived indoor heat stress during summer (OR = 0.83; 95% CI = 0.79-0.88). Self-reported health and well-being varied by SES and building type. Conclusions:Our study reveals concentrated environmental stressors in dense residential areas and highlights multidimensional environmental inequities. Environmental exposure was associated with self-perceived health and well-being, underscoring the need for integrated, system-based policies, such as One Health, to promote sustainable urban well-being.

Background: Increasing evidence suggests residential greenspace is beneficial for mental and cardiometabolic health. However, longitudinal studies on detailed residential greenspace and dementia incidence are yet limited, which this study examines, along with potential modifying effects of air pollution, road traffic noise, blue space, age, sex, and genetic risk profile in terms of carrying the APOE ε4 allele. Methods: Data were collected in the Swedish National Study of Aging and Care Kungsholmen and included 2993 dementia-free participants (mean age 73.1 years [±10.4 SD]) followed-up for 16 years, during which 477 (16%) developed clinically diagnosed dementia. Residential greenspace was assessed using satellite-derived Normalized Difference Vegetation Index (NDVI) within 100m, 250m, and 500m buffers. Hazard ratios (HR) and 95% confidence intervals (CI) of dementia incidence per interquartile range (IQR) increase in greenspace were estimated using Cox regression. Effect modifications of air pollution, blue space access, road traffic noise, age, sex and APOE-ε4 were tested through interaction terms (evaluated at p<0.1). Results: Per IQR (=0.18) increment in greenspace within a 100m buffer zone was associated with around 20% reduced hazard of dementia (HR 0.79 [CI 0.64, 0.96]). Associations were attenuated and statistically nonsignificant for larger buffers. The beneficial effect of greenspace on dementia incidence was stronger among female (HR 0.69 [CI 0.54, 0.89], p interaction=0.082) than male participants (HR 0.93 [CI 0.71, 1.24]). Other modifier interactions were statistically nonsignificant. Conclusions: Our findings suggest that greenspace in the close surrounding of the home may decrease the risk of developing dementia among older adults, especially women.

BACKGROUND:Residential greenness is linked to health, but its relationships with environmental exposures and lifestyle factors-often treated as confounders or mediators-are less clear. OBJECTIVE:We investigated the associations between residential greenness and air pollution, traffic noise and lifestyle factors (smoking, alcohol consumption, leisure-time physical activity) at six study sites in the Swedish CArdioPulmonary bioImage Study (SCAPIS), using waist circumference as an illustrative outcome. METHODS:Greenness assessment was based on the average 5-year pre-recruitment values of Normalized Difference Vegetation Index (NDVI) within 250 m buffers around participants' residences (n = 29,376; 50-65 years). We used linear regression to estimate associations between NDVI and fine particulate matter (PM2.5), respirable particulate matter (PM10), nitrogen dioxide (NO2) road traffic noise (Lden), and waist circumference; logistic regression to estimate associations between NDVI and smoking, alcohol consumption and sedentary lifestyle. RESULTS:NDVI (mean 0.47; range 0.08-0.79) varied across SCAPIS sites. Higher greenness was associated with lower air pollution and traffic noise and lower smoking and alcohol consumption, but not with sedentary lifestyle. Waist circumference (mean 89.4 cm in women; 99.7 cm in men) differed by site, but showed no independent association with greenness, after adjustment for urbanicity, site and socioeconomic variables. SCAPIS participants more often lived in urban, less green areas than the general population. SIGNIFICANCE:Greenness relates to environmental and lifestyle factors, partly in site-specific ways, underscoring the need to carefully consider what we adjust for in greenness epidemiology.

Background:This systematic review aimed to estimate relative risks for incident ischemic heart disease (IHD), myocardial infarction (MI), and stroke in relation to long-term road traffic noise exposure and to evaluate exposure-response functions. Methods:We systematically searched databases for longitudinal studies in humans on incident IHD, MI, and/or stroke, including quantitative estimates on individual exposure to residential road traffic noise based on validated models or measurements. Risk of bias was evaluated in each study based on predefined criteria. Pooled linear exposure-response functions were generated from random-effect models in meta-analyses of study-specific risk estimates. Restricted cubic spline models were used to capture potential nonlinear associations. Results:Twenty eligible studies were identified based on more than 8.4 million individuals, mostly from Europe, including between 160,000 and 240,000 cases for each of the outcomes. Pooled relative risk estimates were 1.017 (95% confidence interval [CI]: 0.990, 1.044) for IHD, 1.029 (95% CI: 1.011, 1.048) for MI, and 1.025 (95% CI: 1.009, 1.041) for stroke per 10 dB Lden in road traffic noise exposure. Risk estimates appeared higher in combined analyses of studies with a low risk of exposure assessment bias. Restricted cubic spline analyses of these studies showed clear risk increases with exposure for all three cardiovascular outcomes. Conclusions:The evidence indicates that long-term exposure to road traffic noise increases the incidence of IHD, including MI, and stroke. Given the abundant exposure, traffic noise is a cardiovascular risk factor of public health importance. High-quality assessment of noise exposure appears essential for the risk estimation.

INTRODUCTION:Ambient air pollution and road traffic noise are stroke risk factors, but evidence on their potential joint effects remains limited. This study investigated the independent and joint associations of air pollution and road traffic noise on stroke incidence using both multiplicative and additive scales. METHODS:We followed stroke incidence in ten cohorts in Sweden, Denmark, and Finland. We modelled annual average levels of outdoor particulate matter < 2.5 µm (PM2.5), nitrogen dioxide (NO2) and road traffic noise at residential addresses. We applied Cox proportional hazards regression to evaluate their single association. We assessed multiplicative interaction with interaction terms in Cox models and additive interaction using the Relative Excess Risk due to Interaction method. RESULTS:We followed 136,897 adults for 20 years, and 8.0 % experienced stroke incidence. PM2.5, NO2 and road traffic noise were associated with higher stroke risk in single-exposure models. Multiplicative models showed higher HRs between PM2.5 and stroke at higher levels of noise and vice versa: HRs per 5 μg/m3 of PM2.5 were 1.06 (95 % CI:0.94-1.21) at 40 dB and 1.11 (95 % CI:0.85-1.44) at 80 dB of road traffic noise; HRs per 12 dB of road traffic noise were 1.06 (95 % CI:1.01-1.11) at 4 μg/m3 and 1.17 (95 % CI:0.82-1.68) at 48 μg/m3 of PM2.5. Additive models showed that the combined association of PM2.5 and road traffic noise was 4 % (RERI = 0.04 (95 % CI:-0.05;1.12)) higher than the sum of their individual association. CONCLUSION:PM2.5 and road traffic noise showed a non-significant synergistic association on stroke incidence.

Road traffic noise exposure has been associated with multiple adverse outcomes in epidemiological studies. However, the underlying biological mechanisms remain unclear. The aim of this study was to investigate the association between road traffic noise exposure and cord blood and child blood DNA methylation (DNAm). Data from six European studies (BAMSE, Generation R, HELIX, INMA, LISA, PIAMA) were used to perform the discovery epigenome-wide meta-analysis. Prenatal, infancy, and recent road traffic noise exposure was assessed at the residential addresses. Blood DNAm was measured using the Illumina 450 K or EPIC arrays. To identify differentially methylated positions (DMPs), we fitted robust linear regression models for each cohort, and the results were subsequently meta-analyzed. Differentially methylated regions (DMRs) were identified using Comb-p and DMRcate. Findings were then looked-up in the independent ALSPAC cohort, in which noise was measured categorically. A total of 1477 newborns with DNAm data in cord blood, and 1129 and 2065 with DNAm in child blood (age 4-6 and age 8-10 years, respectively) were included in the discovery meta-analysis. We did not observe genome-wide significant (False Discovery Rate (FDR) < 0.05) DMPs associated with road traffic noise exposure. However, 46 DMPs reached suggestive significance (P < 1 × 10-5) across different time windows. One CpG site (cg09400092, annotated to SSTR1) associated with recent noise exposure at age 8-10 years was also significantly associated in the ALSPAC cohort (same direction of association with P = 0.00165). In addition, we identified a total of 93 FDR significant DMRs, of which 14 were nominally significant in the ALSPAC study. In conclusion, we observed suggestive evidence of an association between road traffic noise exposure and DNAm in child blood. This may indicate that differential DNAm plays a role in the biological mechanism underlying health effects of noise exposure.

Background and aims 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. Methods 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 mu m (PM2.5), <10 mu m (PM10), and nitrogen oxides (NOx) 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. Results Median 10-year average PM2.5 exposure was 6.2 mu g/m(3) (range 3.5-13.4 mu g/m(3)). 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 PM2.5 was associated with NCP (adjusted OR 1.34, 95 % CI 1.13, 1.58, per 2.05 mu g/m(3)). Associations with significant stenoses were inconsistent. Conclusions 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, PM2.5 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.

[This corrects the article DOI: 10.1016/j.lanepe.2024.101091.].

Background:Available evidence suggests a link between exposure to transportation noise and an increased risk of obesity. We aimed to assess exposure-response functions for long-term residential exposure to road traffic, railway and aircraft noise, and markers of obesity.Methods:Our cross-sectional study is based on pooled data from 11 Nordic cohorts, including up to 162,639 individuals with either measured (69.2%) or self-reported obesity data. Residential exposure to transportation noise was estimated as a time-weighted average Lden 5 years before recruitment. Adjusted linear and logistic regression models were fitted to assess beta coefficients and odds ratios (OR) with 95% confidence intervals (CI) for body mass index, overweight, and obesity, as well as for waist circumference and central obesity. Furthermore, natural splines were fitted to assess the shape of the exposure-response functions.Results:For road traffic noise, the OR for obesity was 1.06 (95% CI = 1.03, 1.08) and for central obesity 1.03 (95% CI = 1.01, 1.05) per 10 dB Lden. Thresholds were observed at around 50-55 and 55-60 dB Lden, respectively, above which there was an approximate 10% risk increase per 10 dB Lden increment for both outcomes. However, linear associations only occurred in participants with measured obesity markers and were strongly influenced by the largest cohort. Similar risk estimates as for road traffic noise were found for railway noise, with no clear thresholds. For aircraft noise, results were uncertain due to the low number of exposed participants.Conclusion:Our results support an association between road traffic and railway noise and obesity.

Background:Transportation noise has been linked with cardiometabolic outcomes, yet whether it is a risk factor for atrial fibrillation (AF) remains inconclusive. We aimed to assess whether transportation noise was associated with AF in a large, pooled Nordic cohort. Methods:We pooled data from 11 Nordic cohorts, totaling 161,115 participants. Based on address history from five years before baseline until end of follow-up, road, railway, and aircraft noise was estimated at a residential level. Incident AF was ascertained via linkage to nationwide patient registries. Cox proportional hazards models were utilized to estimate associations between running 5-year time-weighted mean transportation noise (Lden) and AF after adjusting for sociodemographics, lifestyle, and air pollution. Findings:We identified 18,939 incident AF cases over a median follow-up of 19.6 years. Road traffic noise was associated with AF, with a hazard ratio (HR) and 95% confidence interval (CI) of 1.02 (1.00-1.04) per 10-dB of 5-year mean time-weighted exposure, which changed to 1.03 (1.01-1.06) when implementing a 53-dB cut-off. In effect modification analyses, the association for road traffic noise and AF appeared strongest in women and overweight and obese participants. Compared to exposures ≤40 dB, aircraft noise of 40.1-50 and > 50 dB were associated with HRs of 1.04 (0.93-1.16) and 1.12 (0.98-1.27), respectively. Railway noise was not associated with AF. We found a HR of 1.19 (1.02-1.40) among people exposed to noise from road (≥45 dB), railway (>40 dB), and aircraft (>40 dB) combined. Interpretation:Road traffic noise, and possibly aircraft noise, may be associated with elevated risk of AF. Funding:NordForsk.

Background:Road-traffic noise may influence the development of cardiovascular events such as stroke and myocardial infarction, but etiological mechanisms remain unclear. This study aimed to assess the relationship between long-term road-traffic noise exposure and coronary atherosclerosis in Sweden. Methods:In the Swedish CArdioPulmonary bioImage Study (SCAPIS) cohort, including 30,154 subjects aged 50-65 years, recruited between 2013 and 2018, coronary atherosclerosis was measured based on computer tomography (CT) scans as coronary artery calcium score, segment involvement score (SIS), and non-calcified plaques (NCP) at enrollment. Based on modified Nordic model, road-traffic noise exposure was modeled for 2000, 2013, and 2018 with interpolation for intermediate years. We investigated the association between time-weighted long-term exposure to road-traffic noise (Lden) and the prevalence of atherosclerosis using ordinal logistic regression models adjusting for potential socioeconomic, behavioral, and environmental confounders, including air pollution. Results:No clear associations were found between road-traffic noise and coronary atherosclerosis. The odds ratio for coronary artery calcium score was 1.00 (95% confidence interval [CI] = 0.96, 1.04), SIS 0.99 (0.96, 1.03), and NCP 0.98 (0.90, 1.03) per interquartile range (9.4 dB Lden) for road-traffic noise exposure during 10 years before enrollment. No consistent associations were observed in site-specific analyses or using shorter exposure periods. Furthermore, exposure-response analyses revealed no clear trends, and there were no strong interactions between road-traffic noise and cardiovascular risk factors in relation to the atherosclerosis markers. Conclusions:Long-term exposure to road-traffic noise was not linked to coronary atherosclerosis or calcification in relatively healthy, middle-aged populations in Sweden.

BACKGROUND AND AIMS: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. METHODS: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. RESULTS: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 Lden; 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 Lden 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). CONCLUSIONS:Transportation noise was linked to cognitive impairment and faster cognitive decline among older adults. Future studies are warranted to confirm our results.

Abstract Background Previous research suggests an association between road traffic noise and obesity, but current evidence is inconclusive. We aimed to investigate associations between self-reported traffic noise in bedrooms and self-measured obesity markers. Methods We applied data from the Respiratory Health in Northern Europe (RHINE) cohort. We used self-measured waist circumference (WC) and body mass index (BMI) as outcome values. Noise exposure was assessed as perceived traffic noise in the bedroom and/or the bedroom window’s location towards the street. We applied linear, and logistic regression models and evaluated effect modifications by sex. Results Women, who reported very high traffic noise levels in bedroom, had 1.35 (95% CI 0.32–2.38) kg/m2 higher BMI and 4.66 (95% CI 1.83–7.48) cm higher WC compared to women, who reported no traffic noise in the bedroom. Women who reported higher exposure to road traffic noise had statistically significant higher odds of being overweight, obese or have abdominal obesity with OR varying from 1.16 to 1.67 compared to women, who reported no traffic noise in the bedroom. Among men we did not find any clear associations between noise pollution and obesity measures. Conclusion Our results suggest that self-reported traffic noise in the bedroom may be associated to being overweight or obese among women, but not among men.