Long-term residential exposure to source-specific particulate matter and incidence of diabetes mellitus - A cohort study in northern Sweden.

Diabetes mellitus (DM) incidence have been assessed in connection with air pollution exposure in several studies; however, few have investigated associations with source-specific local emissions. This study aims to estimate the risk of DM incidence associated with source-specific air pollution in a Swedish cohort with relatively low exposure. Individuals in the Västerbotten intervention programme cohort were followed until either a DM diagnosis or initiation of treatment with glucose-lowering medication occurred. Dispersion models with high spatial resolution were used to estimate annual mean concentrations of particulate matter (PM) with aerodynamic diameter ≤10 µm (PM10) and ≤2.5 µm (PM2.5) at individual addresses. Hazard ratios were estimated using Cox regression models in relation to moving averages 1-5 years preceding the outcome. During the study period, 1479 incident cases of DM were observed during 261,703 person-years of follow-up. Increased incidence of DM was observed in association with PM10 (4% [95% CI: -54-137%] per 10 µg/m3), PM10-traffic (2% [95% CI: -6-11%] per 1 µg/m3) and PM2.5-exhaust (11% [95% CI: -39-103%] per 1 µg/m3). A negative association was found for both PM2.5 (-18% [95% CI: -99-66%] per 5 µg/m3), but only in the 2nd exposure tertile (-10% [95% CI: -25-9%] compared to the first tertile), and PM2.5-woodburning (-30% [95% CI: -49-4%] per 1 µg/m3). In two-pollutant models including PM2.5-woodburning, there was an 11% [95% CI: -11-38%], 6% [95% CI: -16-34%], 13% [95% CI: -7-36%] and 17% [95% CI: 4-41%] higher risk in the 3rd tertile of PM10, PM2.5, PM10-traffic and PM2.5-exhaust, respectively, compared to the 1st. Although the results lacked in precision they are generally in line with the current evidence detailing particulate matter air pollution from traffic as an environmental risk factor for DM.

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 particulate air pollution and presence and progression of carotid artery plaques - A northern Sweden VIPVIZA cohort study.

AIMS: To estimate the association between long-term exposure to particulate air pollution and sub-clinical atherosclerosis based on the existence of plaque and the carotid intima-media thickness (cIMT). METHODS: Visualization of asymptomatic atherosclerotic disease for optimum cardiovascular prevention (VIPVIZA) is a randomised controlled trial integrated within the Västerbotten Intervention Programme, an ongoing population-based cardiovascular disease (CVD) prevention programme in northern Sweden. Individuals aged 40, 50, or 60 years with one or more conventional CVD risk factors in Umeå municipality were eligible to participate. The 1425 participants underwent an ultrasound assessment of cIMT and plaque formation during the period 2013-2016 and at 3-year follow-up. Source-specific annual mean concentrations of particulate matter with aerodynamic diameter ≤10 µm (PM10) and ≤2.5 µm (PM2.5), and black carbon (BC) at the individual's residential address were modelled for the calendar years 1990, 2001 and 2011. Poisson regression was used to estimate prevalence ratios for presence of carotid artery plaques, and linear regression for cIMT. RESULTS: The plaque prevalence was 43% at baseline and 47% at follow-up. An interquartile range (IQR) increase in PM10 (range in year 2011: 7.1-13.5 µg/m3) was associated with a prevalence ratio at baseline ultrasound of 1.11 (95% CI 0.99-1.25), 1.08 (95% CI 0.99-1.17), and 1.00 (95% CI 0.93-1.08) for lag 23, 12 and 2 years, and at follow-up 1.04 (95% CI 0.95-1.14), 1.08 (95% CI 1.00-1.16), and 1.01 (95% CI 0.95-1.08). Similar prevalence ratios per IQR were found for PM2.5 and BC, but with somewhat lower precision for the later. Particle concentrations were however not associated with the progression of plaque. No cross-sectional or longitudinal associations of change were found for cIMT. CONCLUSIONS: This study of individuals with low/moderate risk for CVD give some additional support for an effect of long-term air pollution in early subclinical atherosclerosis.

Long-term exposure to air pollution, coronary artery calcification, and carotid artery plaques in the population-based Swedish SCAPIS Gothenburg cohort.

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 (PM2.5, PM10, PMcoarse, NOx, and exhaust-specific PM2.5 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 PM2.5 was low by international standards (8.5 µg/m3). There were no consistent associations between long-term total PM2.5 exposure and CAC score or presence of carotid artery plaques, but an association between total PM2.5 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.

Health impacts of PM2.5 originating from residential wood combustion in four nordic cities.

BACKGROUND: Residential wood combustion (RWC) is one of the largest sources of fine particles (PM2.5) in the Nordic cities. The current study aims to calculate the related health effects in four studied city areas in Sweden, Finland, Norway, and Denmark. METHODS: Health impact assessment (HIA) was employed as the methodology to quantify the health burden. Firstly, the RWC induced annual average PM2.5 concentrations from local sources were estimated with air pollution dispersion modelling. Secondly, the baseline mortality rates were retrieved from the national health registers. Thirdly, the concentration-response function from a previous epidemiological study was applied. For the health impact calculations, the WHO-developed tool AirQ + was used. RESULTS: Amongst the studied city areas, the local RWC induced PM2.5 concentration was lowest in the Helsinki Metropolitan Area (population-weighted annual average concentration 0.46 µg m- 3) and highest in Oslo (2.77 µg m- 3). Each year, particulate matter attributed to RWC caused around 19 premature deaths in Umeå (95% CI: 8-29), 85 in the Helsinki Metropolitan Area (95% CI: 35-129), 78 in Copenhagen (95% CI: 33-118), and 232 premature deaths in Oslo (95% CI: 97-346). The average loss of life years per premature death case was approximately ten years; however, in the whole population, this reflects on average a decrease in life expectancy by 0.25 (0.10-0.36) years. In terms of the relative contributions in cities, life expectancy will be decreased by 0.10 (95% CI: 0.05-0.16), 0.18 (95% CI: 0.07-0.28), 0.22 (95% CI: 0.09-0.33) and 0.63 (95% CI: 0.26-0.96) years in the Helsinki Metropolitan Area, Umeå, Copenhagen and Oslo respectively. The number of years of life lost was lowest in Umeå (172, 95% CI: 71-260) and highest in Oslo (2458, 95% CI: 1033-3669). CONCLUSIONS: All four Nordic city areas have a substantial amount of domestic heating, and RWC is one of the most significant sources of PM2.5. This implicates a substantial predicted impact on public health in terms of premature mortality. Thus, several public health measures are needed to reduce the RWC emissions.

Road traffic noise, air pollution and cardiovascular events in a Swedish cohort.

Urbanization and increasing road traffic cause exposure to both noise and air pollution. While the levels of air pollutants such as nitrogen oxides (NOx) 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 NOx. 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.

Long-term effects of total and source-specific particulate air pollution on incident cardiovascular disease in Gothenburg, Sweden.

BACKGROUND AND AIMS: Long-term exposure to air pollution increases cardiopulmonary morbidity and mortality, but it is not clear which components of air pollution are the most harmful, nor which time window of exposure is most relevant. Further studies at low exposure levels have also been called for. We analyzed two Swedish cohorts to investigate the effects of total and source-specific particulate matter (PM) on incident cardiovascular disease for different time windows of exposure. METHODS: Two cohorts initially recruited to study predictors of cardiovascular disease (the PPS cohort and the GOT-MONICA cohort) were followed from 1990 to 2011. We collected data on residential addresses and assigned each individual yearly total and source-specific PM and Nitrogen Oxides (NOx) exposures based on dispersion models. Using multivariable Cox regression models with time-dependent exposure, we studied the association between three different time windows (lag 0, lag 1-5, and exposure at study start) of residential PM and NOx exposure, and incidence of ischemic heart disease, stroke, heart failure and atrial fibrillation. RESULTS AND DISCUSSION: During the study period, there were 2266 new-onset cases of ischemic heart disease, 1391 of stroke, 925 of heart failure and 1712 of atrial fibrillation. The majority of cases were in the PPS cohort, where participants were older. Exposure levels during the study period were moderate (median: 13µg/m3 for PM10 and 9µg/m3 for PM2.5), and similar in both cohorts. Road traffic and residential heating were the largest local sources of PM air pollution, and long distance transportation the largest PM source in total. In the PPS cohort, there were positive associations between PM in the last five years and both ischemic heart disease (HR: 1.24 [95% CI: 0.98-1.59] per 10µg/m3 of PM10, and HR: 1.38 [95% CI: 1.08-1.77] per 5µg/m3 of PM2.5) and heart failure. In the GOT-MONICA cohort, there were positive but generally non-significant associations between PM and stroke (HR: 1.48 [95% CI: 0.88-2.49] per 10µg/m3 of PM10, and HR: 1.50 [95% CI: 0.90-2.51] per 5µg/m3 of PM2.5, in the last five years). Effect estimates were stronger for women, non-smokers, and higher socioeconomic classes. Exposure in the last five years seemed to be more strongly associated with outcomes than other exposure time windows. Associations between source-specific PM air pollution and outcomes were mixed and generally weak. High correlations between the main pollutants limited the use of multi-pollutant models. CONCLUSIONS: The main PM air pollutants were associated with ischemic heart disease and stroke (in women) at the relatively low exposure levels in Gothenburg, Sweden. The associations tended to be stronger for women than for men, for non-smokers than for smokers, and for higher socioeconomic classes than for lower. The associations could not be attributed to a specific PM source or type, and differed somewhat between the two cohorts. The results of this study confirm that further efforts to reduce air pollution exposure should be undertaken in Sweden to reduce the negative health effects in the general population.

PM2.5 and Dementia in a Low Exposure Setting: The Influence of Odor Identification Ability and APOE.

BACKGROUND: Growing evidence show that long term exposure to air pollution increases the risk of dementia. OBJECTIVE: The aim of this study was to investigate associations between PM2.5 exposure and dementia in a low exposure area, and to investigate the role of olfaction and the APOE ɛ4 allele in these associations. METHODS: Data were drawn from the Betula project, a longitudinal study on aging, memory, and dementia in Sweden. Odor identification ability was assessed using the Scandinavian Odor Identification Test (SOIT). Annual mean PM2.5 concentrations were obtained from a dispersion-model and matched at the participants' residential address. Proportional hazard regression was used to calculate hazard ratios. RESULTS: Of 1,846 participants, 348 developed dementia during the 21-year follow-up period. The average annual mean PM2.5 exposure at baseline was 6.77µg/m3, which is 1.77µg/m3 above the WHO definition of clean air. In a fully adjusted model (adjusted for age, sex, APOE, SOIT, cardiovascular diseases and risk factors, and education) each 1µg/m3 difference in annual mean PM2.5-concentration was associated with a hazard ratio of 1.23 for dementia (95% CI: 1.01-1.50). Analyses stratified by APOE status (ɛ4 carriers versus non-carriers), and odor identification ability (high versus low), showed associations only for ɛ4 carriers, and for low performance on odor identification ability. CONCLUSION: PM2.5 was associated with an increased risk of dementia in this low pollution setting. The associations between PM2.5 and dementia seemed stronger in APOE carriers and those with below average odor identification ability.

Association between exposure to combustion-related air pollution and multiple sclerosis risk.

BACKGROUND: Smoking and occupational pulmonary irritants contribute to multiple sclerosis (MS) development. We aimed to study the association between ambient air pollution and MS risk and potential interaction with the human leukocyte antigen (HLA)-DRB1*15:01 allele. METHODS: Exposure to combustion-related air pollution was estimated as outdoor levels of nitrogen oxides (NOx) at the participants' residence locations, by spatially resolved dispersion modelling for the years 1990-18. Using two population-based case-control studies (6635 cases, 8880 controls), NOx levels were associated with MS risk by calculating odds ratios (OR) with 95% confidence intervals (CI) using logistic regression models. Interaction between high NOx levels and the HLA-DRB1*15:01 allele regarding MS risk was calculated by the attributable proportion due to interaction (AP). In addition, a register study was performed comprising all MS cases in Sweden who had received their diagnosis between 1993 and 2018 (n = 22 173), with 10 controls per case randomly selected from the National Population register. RESULTS: Residential air pollution was associated with MS risk. NOx levels (3-year average) exceeding the 90th percentile (24.6 µg/m3) were associated with an OR of 1.37 (95% CI 1.10-1.76) compared with levels below the 25th percentile (5.9 µg/m3), with a trend of increasing risk of MS with increasing levels of NOx (P <0.0001). A synergistic effect was observed between high NOx levels (exceeding the lower quartile among controls) and the HLA-DRB1*15:01 allele regarding MS risk (AP 0.26, 95% CI 0.13-0.29). CONCLUSIONS: Our findings indicate that moderate levels of combustion-related ambient air pollution may play a role in MS development.

Long-Term Exposure to Transportation Noise and Ischemic Heart Disease: A Pooled Analysis of Nine Scandinavian Cohorts.

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. https://doi.org/10.1289/EHP10745.

Using Distributed Lag Non-Linear Models to Estimate Exposure Lag-Response Associations between Long-Term Air Pollution Exposure and Incidence of Cardiovascular Disease.

Long-term air pollution exposure increases the risk for cardiovascular disease, but little is known about the temporal relationships between exposure and health outcomes. This study aims to estimate the exposure-lag response between air pollution exposure and risk for ischemic heart disease (IHD) and stroke incidence by applying distributed lag non-linear models (DLNMs). Annual mean concentrations of particles with aerodynamic diameter less than 2.5 µm (PM2.5) and black carbon (BC) were estimated for participants in five Swedish cohorts using dispersion models. Simultaneous estimates of exposure lags 1-10 years using DLNMs were compared with separate year specific (single lag) estimates and estimates for lag 1-5- and 6-10-years using moving average exposure. The DLNM estimated no exposure lag-response between PM2.5 total, BC, and IHD. However, for PM2.5 from local sources, a 20% risk increase per 1 µg/m3 for 1-year lag was estimated. A risk increase for stroke was suggested in relation to lags 2-4-year PM2.5 and BC, and also lags 8-9-years BC. No associations were shown in single lag models. Increased risk estimates for stroke in relation to lag 1-5- and 6-10-years BC moving averages were observed. Estimates generally supported a greater contribution to increased risk from exposure windows closer in time to incident IHD and incident stroke.

Near-Source Risk Functions for Particulate Matter Are Critical When Assessing the Health Benefits of Local Abatement Strategies.

When mortality or other health outcomes attributable to fine particulate matter (PM2.5) are estimated, the same exposure-response function (ERF) is usually assumed regardless of the source and composition of the particles, and independently of the spatial resolution applied in the exposure model. While several recent publications indicate that ERFs based on exposure models resolving within-city gradients are steeper per concentration unit (µgm-3), the ERF for PM2.5 recommended by the World Health Organization does not reflect this observation and is heavily influenced by studies based on between-city exposure estimates. We evaluated the potential health benefits of three air pollution abatement strategies: electrification of light vehicles, reduced use of studded tires, and introduction of congestion charges in Stockholm and Gothenburg, using different ERFs. We demonstrated that using a single ERF for PM2.5 likely results in an underestimation of the effect of local measures and may be misleading when evaluating abatement strategies. We also suggest applying ERFs that distinguish between near-source and regional contributions of exposure to PM2.5. If separate ERFs are applied for near-source and regional PM2.5, congestion charges as well as a reduction of studded tire use are estimated to be associated with a significant reduction in the mortality burden in both Gothenburg and Stockholm. In some scenarios the number of premature deaths is more than 10 times higher using separate ERFs in comparison to using a single ERF irrespective of sources as recommended by the WHO. For electrification, the net change in attributable deaths is small or within the uncertainty range depending on the choice of ERF.

Local Contrasts in Concentration of Ambient Particulate Air Pollution (PM2.5) and Incidence of Alzheimer's Disease and Dementia: Results from the Betula Cohort in Northern Sweden.

Exposure to fine particulate air pollution (PM2.5) is emerging as a risk factor for Alzheimer's disease (AD), but existing studies are still limited and heterogeneous. We have previously studied the association between dementia (AD and vascular dementia) and PM2.5 stemming from vehicle exhaust and wood-smoke in the Betula cohort in Northern Sweden. The aim of this commentary is to estimate the association between total PM2.5 and dementia in the Betula cohort, which is more relevant to include in future meta-estimates than the source-specific estimates. The hazard ratio for incident dementia associated with a 1µg/m3 increase in local PM2.5 was 1.38 (95% confidence interval: 0.99 -1.92). The interpretation of our results is that they indicate an association between local contrasts in concentration of PM2.5 at the residential address and incidence of dementia in a low-level setting.

Long-term exposure to particulate air pollution and black carbon in relation to natural and cause-specific mortality: a multicohort study in Sweden.

OBJECTIVES: To estimate concentration-response relationships for particulate matter (PM) and black carbon (BC) in relation to mortality in cohorts from three Swedish cities with comparatively low pollutant levels. SETTING: Cohorts from Gothenburg, Stockholm and Umeå, Sweden. DESIGN: High-resolution dispersion models were used to estimate annual mean concentrations of PM with aerodynamic diameter ≤10 µm (PM10) and ≤2.5 µm (PM2.5), and BC, at individual addresses during each year of follow-up, 1990-2011. Moving averages were calculated for the time windows 1-5 years (lag1-5) and 6-10 years (lag6-10) preceding the outcome. Cause-specific mortality data were obtained from the national cause of death registry. Cohort-specific HRs were estimated using Cox regression models and then meta-analysed including a random effect of cohort. PARTICIPANTS: During the study period, 7 340 cases of natural mortality, 2 755 cases of cardiovascular disease (CVD) mortality and 817 cases of respiratory and lung cancer mortality were observed among in total 68 679 individuals and 689 813 person-years of follow-up. RESULTS: Both PM10 (range: 6.3-41.9 µg/m3) and BC (range: 0.2-6.8 µg/m3) were associated with natural mortality showing 17% (95% CI 6% to 31%) and 9% (95% CI 0% to 18%) increased risks per 10 µg/m3 and 1 µg/m3 of lag1-5 exposure, respectively. For PM2.5 (range: 4.0-22.4 µg/m3), the estimated increase was 13% per 5 µg/m3, but less precise (95% CI -9% to 40%). Estimates for CVD mortality appeared higher for both PM10 and PM2.5. No association was observed with respiratory mortality. CONCLUSION: The results support an effect of long-term air pollution on natural mortality and mortality in CVD with high relative risks also at low exposure levels. These findings are relevant for future decisions concerning air quality policies.

Long-Term Exposure to Transportation Noise and Risk of Incident Stroke: A Pooled Study of Nine Scandinavian Cohorts.

BACKGROUND: Transportation noise is increasingly acknowledged as a cardiovascular risk factor, but the evidence base for an association with stroke is sparse. OBJECTIVE: We aimed to investigate the association between transportation noise and stroke incidence in a large Scandinavian population. METHODS: We harmonized and pooled data from nine Scandinavian cohorts (seven Swedish, two Danish), totaling 135,951 participants. We identified residential address history and estimated road, railway, and aircraft noise for all addresses. Information on stroke incidence was acquired through linkage to national patient and mortality registries. We analyzed data using Cox proportional hazards models, including socioeconomic and lifestyle confounders, and air pollution. RESULTS: During follow-up (median=19.5y), 11,056 stroke cases were identified. Road traffic noise (Lden) was associated with risk of stroke, with a hazard ratio (HR) of 1.06 [95% confidence interval (CI): 1.03, 1.08] per 10-dB higher 5-y mean time-weighted exposure in analyses adjusted for individual- and area-level socioeconomic covariates. The association was approximately linear and persisted after adjustment for air pollution [particulate matter (PM) with an aerodynamic diameter of ≤2.5µm (PM2.5) and NO2]. Stroke was associated with moderate levels of 5-y aircraft noise exposure (40-50 vs. ≤40 dB) (HR=1.12; 95% CI: 0.99, 1.27), but not with higher exposure (≥50 dB, HR=0.94; 95% CI: 0.79, 1.11). Railway noise was not associated with stroke. DISCUSSION: In this pooled study, road traffic noise was associated with a higher risk of stroke. This finding supports road traffic noise as an important cardiovascular risk factor that should be included when estimating the burden of disease due to traffic noise. https://doi.org/10.1289/EHP8949.

Exposure to traffic-related particle matter and effects on lung function and potential interactions in a cross-sectional analysis of a cohort study in west Sweden.

OBJECTIVES: To investigate the long-term effects of source-specific particle matter (PM) on lung function, effects of Surfactant Protein A (SP-A) and glutathione S-transferase (GST) genes GSTP1 and GSTT1 gene variants and effect modification by single-nucleotide polymorphism (SNP) genotype. DESIGN: Cohort study with address-based annual PM exposure assigned from annual estimates of size (PM10, PM2.5 and PMBC) and source-specific (traffic, industry, marine traffic and wood burning) dispersion modelling. SETTING: Gothenburg, Sweden. PARTICIPANTS: The ADult-Onset asthma and NItric oXide Study had 6685 participants recruited from the general population, of which 5216 (78%) were included in the current study with information on all variables of interest. Mean age at the time of enrolment was 51.4 years (range 24-76) and 2427 (46.5%) were men. PRIMARY AND SECONDARY OUTCOME MEASURES: The primary outcome was forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1). Secondary outcome measures were effects and gene-environment interactions of SP-A and GSTT1 and GSTP1 genotypes. RESULTS: Exposure to traffic-related PM10 and PM2.5 was associated with decreases in percent-predicted (% predicted) FEV1 by -0.48% (95% CI -0.89% to -0.07%) and -0.47% (95% CI -0.88% to -0.07%) per IQR 3.05 and 2.47 µg/m3, respectively, and with decreases in % predicted FVC by -0.46% (95% CI -0.83% to -0.08%) and -0.47% (95% CI -0.83% to -0.10%). Total and traffic-related PMBC was strongly associated with both FEV1 and FVC by -0.53 (95% CI -0.94 to -0.13%) and -0.43% (95% CI -0.77 to -0.09%) per IQR, respectively, for FVC, and similarly for FEV1. Minor allele carrier status for two GSTP1 SNPs and the GSTT1 null genotype were associated with decreases in % predicted lung function. Three SP-A SNPs showed effect modification with exposure to PM2.5 from industry and marine traffic. CONCLUSIONS: PM exposure, specifically traffic related, was associated with FVC and FEV1 reductions and not modified by genotype. Genetic effect modification was suggested for industry and marine traffic PM2.5.

Modelling urban cyclists' exposure to black carbon particles using high spatiotemporal data: A statistical approach.

This is a pioneering work in South America to model the exposure of cyclists to black carbon (BC) while riding in an urban area with high spatiotemporal variability of BC concentrations. We report on mobile BC concentrations sampled on 10 biking sessions in the city of Curitiba (Brazil), during rush hours of weekdays, covering four routes and totaling 178 km. Moreover, simultaneous BC measurements were conducted within a street canyon (street and rooftop levels) and at a site located 13 km from the city center. We used two statistical approaches to model the BC concentrations: multiple linear regression (MLR) and a machine-learning technique called random forests (RF). A pool of 25 candidate variables was created, including pollution measurements, traffic characteristics, street geometry and meteorology. The aggregated mean BC concentration within 30-m buffers along the four routes was 7.09 µg m-3, with large spatial variability (5th and 95th percentiles of 1.75 and 16.83 µg m-3, respectively). On average, the concentrations at the street canyon façade (5 m height) were lower than the mobile data but higher than the urban background levels. The MLR model explained a low percentage of variance (24%), but was within the values found in the literature for on-road BC mobile data. RF explained a larger variance (54%) with the additional advantage of having lower requirements for the target and predictor variables. The most impactful predictor for both models was the traffic rate of heavy-duty vehicles. Thus, to reduce the BC exposure of cyclists and residents living close to busy streets, we emphasize the importance of renewing and/or retrofitting the diesel-powered fleet, particularly public buses with old vehicle technologies. Urban planners could also use this valuable information to project bicycle lanes with greater separation from the circulation of heavy-duty diesel vehicles.

Long-Term Exposure to Particulate Air Pollution, Black Carbon, and Their Source Components in Relation to Ischemic Heart Disease and Stroke.

BACKGROUND: Long-term exposure to particulate matter (PM) in ambient air has been associated with cardiovascular mortality, but few studies have considered incident disease in relation to PM from different sources. OBJECTIVES: We aimed to study associations between long-term exposure to different types of PM and sources, and incident ischemic heart disease (IHD) and stroke in three Swedish cities. METHODS: Based on detailed emission databases, monitoring data, and high-resolution dispersion models, we calculated source contributions to PM with aerodynamic diameter ≤10µm (PM10), PM with aerodynamic diameter ≤2.5µm (PM2.5), and black carbon (BC) from road wear, traffic exhaust, residential heating, and other sources in Gothenburg, Stockholm, and Umeå. Registry data for participants from four cohorts were used to obtain incidence of IHD and stroke for first hospitalization or death. We constructed time windows of exposure for same-year, 1- to 5-y, and 6- to 10-y averages preceding incidence from annual averages at residential addresses. Risk estimates were based on random effects meta-analyses of cohort-specific Cox proportional hazard models. RESULTS: We observed 5,166 and 3,119 incident IHD and stroke cases, respectively, in 114,758 participants. Overall, few consistent associations were observed between the different air pollution measures and IHD or stroke incidence. However, same-year levels of ambient locally emitted BC (range: 0.01-4.6 µg/m3) were associated with a 4.0% higher risk of incident stroke per interquartile range (IQR), 0.30 µg/m3 [95% confidence interval (CI): 0.04, 7.8]. This association was primarily related to BC from traffic exhaust. PM10 (range: 4.4-52 µg/m3) and PM2.5 (range: 2.9-22 µg/m3) were not associated with stroke. Associations with incident IHD were observed only for PM2.5 exposure from residential heating. DISCUSSION: Few consistent associations were observed between different particulate components and IHD or stroke. However, long-term residential exposure to locally emitted BC from traffic exhaust was associated with stroke incidence. The comparatively low exposure levels may have contributed to the paucity of associations. https://doi.org/10.1289/EHP4757.

Association between air pollution from residential wood burning and dementia incidence in a longitudinal study in Northern Sweden.

OBJECTIVES: There is highly suggestive evidence for an effect of air pollution exposure on dementia-related outcomes, but evidence is not yet present to clearly pinpoint which pollutants are the probable causal agents. The aims of this study was to assess the longitudinal association between exposures of fine ambient particulate matter (PM2.5) from residential wood burning, and vehicle exhaust, with dementia. METHOD: We used data from the Betula study, a longitudinal study of dementia in Umeå, Northern Sweden. The study size was 1 806 and the participants were followed from study entry (1993-1995) to 2010. Modelled levels of source-specific fine particulate matter at the residential address were combined with information on wood stoves or wood boilers, and with validated data on dementia diagnosis and individual-level characteristics from the Betula study. Cox proportional hazards models were used to estimate Hazard Ratios (HRs) and their 95% CIs for dementia incidence (vascular dementia and Alzheimer's disease), adjusted for individual-level characteristics. RESULTS: The emission of PM2.5 from local residential wood burning was associated with dementia incidence with a hazard ratio of 1.55 for a 1 µg/m3 increase in PM2.5 (95% Confidence Interval (CI): 1.00-2.41, p-value 0.05). Study participants with an address in an area with the highest quartile of PM2.5 from residential wood burning and who also had a wood-burning stove were more likely to develop dementia than those in the lower three quartiles without a wood-burning stove with hazard ratios of 1.74 (CI: 1.10-2.75, p-value 0.018). Particulate matter from traffic exhaust seemed to be associated with dementia incidence with hazard ratios of 1.66, (CI: 1.16-2.39), p-value 0.006, and 1.41 (CI: 0.97-2.23), p-value 0.07, in the third and fourth quartiles, respectively. CONCLUSIONS: If the associations we observed are causal, then air pollution from residential wood burning, and air pollution from traffic, might be independent important risk factors for dementia.

Health Impact of PM10, PM2.5 and Black Carbon Exposure Due to Different Source Sectors in Stockholm, Gothenburg and Umea, Sweden.

The most important anthropogenic sources of primary particulate matter (PM) in ambient air in Europe are exhaust and non-exhaust emissions from road traffic and combustion of solid biomass. There is convincing evidence that PM, almost regardless of source, has detrimental health effects. An important issue in health impact assessments is what metric, indicator and exposure-response function to use for different types of PM. The aim of this study is to describe sectorial contributions to PM exposure and related premature mortality for three Swedish cities: Gothenburg, Stockholm and Umea. Exposure is calculated with high spatial resolution using atmospheric dispersion models. Attributed premature mortality is calculated separately for the main local sources and the contribution from long-range transport (LRT), applying different relative risks. In general, the main part of the exposure is due to LRT, while for black carbon, the local sources are equally or more important. The major part of the premature deaths is in our assessment related to local emissions, with road traffic and residential wood combustion having the largest impact. This emphasizes the importance to resolve within-city concentration gradients when assessing exposure. It also implies that control actions on local PM emissions have a strong potential in abatement strategies.