The toxicity of particulate matter (PM) is dependent on particle physical and chemical properties and is commonly studied using in vivo and in vitro approaches. PM to be used for in vivo and in vitro studies is often collected on filters and then extracted from the filter surface using a solvent. During extraction and further PM sample handling, particle properties change, but this is often neglected in toxicology studies, with possible implications for health effect assessment. To address the current lack of knowledge and investigate changes in particle properties further, ambient PM with diameter less than 2.5 μm (PM2.5) was collected on filters at an urban site and extracted using a standard methanol protocol. After extraction, the PM was dried, dispersed in water and subsequently nebulized. The resulting aerosol properties were then compared to those of the ambient PM2.5. The number size distribution for the nebulized aerosol resembled the ambient in terms of the main mode diameter, and > 90 % of particle mass in the nebulized size distribution was still in the PM2.5 range. Black carbon made up a similar fraction of PM mass in nebulized as in ambient aerosol. The sulfate content in the nebulized aerosol seemed depleted and the chemical composition of the organic fraction was altered, but it remains unclear to what extent other non-refractory components were affected by the extraction process. Trace elements were not distributed equally across size fractions, neither in ambient nor nebulized PM. Change in chemical form was studied for zinc, copper and iron. The form did not appear to be different between the ambient and nebulized PM for iron and copper, but seemed altered for zinc. Although many of the studied properties were reasonably well preserved, it is clear that the PM2.5 collection and re-aerosolization process affects particles, and thus potentially also their health effects. Because of this, the effect of the particle collection and extraction process must be considered when evaluating cellular and physiological outcomes upon PM2.5 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.

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: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.

Ambient air pollution remains the major environmental cause of disease. Accurate assessment of population exposure and small-scale spatial exposure variations over long time periods is essential for epidemiological studies. We estimated annual exposure to fine and coarse particulate matter (PM 2.5 , PM 10 ), and nitrogen oxides (NO x , NO 2 ) with high spatial resolution to examine time trends 2000‒2018, compliance with the WHO Air Quality Guidelines, and assess the health impact. The modelling area covered six metropolitan areas in Sweden with a combined population of 5.5 million. Long-range transported air pollutants were modelled using a chemical transport model with bias correction, and locally emitted air pollutants using source-specific Gaussian-type dispersion models at resolutions up to 50 × 50 m. The modelled concentrations were validated using quality-controlled monitoring data. Lastly, we estimated the reduction in mortality associated with the decrease in population exposure. The validity of modelled air pollutant concentrations was good (R 2 for PM 2.5 0.84, PM 10 0.61, and NO x 0.87). Air pollution exposure decreased substantially, from a population weighted mean exposure to PM 2.5 of 12.2 µg m −3 in 2000 to 5.4 µg m −3 in 2018. We estimated that the decreased exposure was associated with a reduction of 2719 (95% CI 2046–3055) premature deaths annually. However, in 2018, 65%, 8%, and 42% of residents in the modelled areas were still exposed to PM 2.5 , PM 10 , or NO 2 levels, respectively, that exceeded the current WHO Air Quality Guidelines for annual average exposure. This emphasises the potential public health benefits of reductions in air pollution emissions.

Soot, or black carbon (BC), aerosol is a major climate forcer with severe health effects. The impacts depend strongly on particle number concentration, size and mixing state. This work reports on two field campaigns at nearby urban and rural sites, 65 km apart, in southern Sweden during late summer 2018. BC was measured using a single-particle soot photometer (SP2) and Aethalometers (AE33). Differences in BC concentrations between the sites are driven primarily by local traffic emissions. Equivalent and refractory BC mass concentrations at the urban site were on average a factor 2.2 and 2.5, with peaks during rush hour up to a factor similar to 4, higher than the rural background levels. The number fraction of particles containing a soot core was significantly higher in the city. BC particles at the urban site were on average smaller by mass and had less coating owing to fresh traffic emissions. The organic components of the fresh traffic plumes were similar in mass spectral signature to hydrocarbon-like organic aerosol (HOA), commonly associated with traffic. Despite the intense local traffic (similar to 30000 vehicles passing per day), PM1, including organic aerosol, was dominated by aged continental air masses even at the curbside site. The fraction of thickly coated particles at the urban site was highly correlated with the mass concentrations of all measured chemical species of PM1, consistent with aged, internally mixed aerosol. Trajectory analysis for the whole year showed that air masses arriving at the rural site from eastern Europe contained approximately double the amount of BC compared to air masses from western Europe. Furthermore, the largest regional emissions of BC transported to the rural site, from the Malmo-Copenhagen urban area, are discernible above background levels only when precipitation events are excluded. We show that continental Europe and not the Malmo-Copenhagen region is the major contributor to the background BC mass concentrations in southern Sweden.

BACKGROUND AND AIM: Despite firm evidence for an association between long-term air pollution exposure and cardiovascular events also at low exposure levels, previous epidemiological studies on the association with atherosclerosis have been inconsistent. The aim of this study was to investigate associations between long-term low-level air pollutant exposure and coronary atherosclerosis. METHOD: We performed a cross-sectional analysis in the large Swedish CardioPulmonary bioImaging Study (SCAPIS, n = 30 154). Men and women 50–64 years old were recruited from the general population of six Swedish cities 2013–2018. Outcomes were coronary atherosclerosis (segment involvement score, SIS), coronary artery calcium score (CACS), and non-calcified coronary plaque (NCP) prevalence. Hourly total and source-specific residential PM2.5, PM10, and NOx were modelled in dispersion models with high spatial resolution and averaged over 10 years before recruitment. Prevalence odds ratios (POR) were estimated with ordinal logistic regression models adjusted for site and known risk factors, based on a directed acyclical graph. RESULTS: Median PM2.5 exposure was 6.2 µg/m3; 44% of participants had detectable coronary atherosclerosis. PM2.5 was not associated with SIS or CACS, but with a higher NCP prevalence (POR 1.65, 95% CI 1.18, 2.31, per interquartile range [2.05 µg/m3] higher PM2.5) with a dose-response pattern (p = 0.034 for linear trend). Other pollutants and source-specific exposures did not demonstrate consistent positive associations with any of the outcomes. CONCLUSIONS: In this large, middle-aged general population sample at low exposure levels, PM2.5 exposure was not associated with estimates of general coronary atherosclerosis or calcification, yet appeared to be associated with non-calcified plaques, which may reflect an association with the early phase of atherosclerosis or more vulnerable forms of atherosclerosis. The main funder of SCAPIS is the Swedish Heart and Lung Foundation. Funding for this study was provided by the Swedish Research Council for Health, Working Life and Welfare (FORTE).

In this study, the long-term mortality effects associated with exposure to PM10 (particles with an aerodynamic diameter smaller than or equal to 10 µm), PM2.5 (particles with an aerodynamic diameter smaller than or equal to 2.5 µm), BC (black carbon), and NOx (nitrogen oxides) were analyzed in a cohort in southern Sweden during the period from 1991 to 2016. Participants (those residing in Malmö, Sweden, born between 1923 and 1950) were randomly recruited from 1991 to 1996. At enrollment, 30,438 participants underwent a health screening, which consisted of questionnaires about lifestyle and diet, a clinical examination, and blood sampling. Mortality data were retrieved from the Swedish National Cause of Death Register. The modeled concentrations of PM10, PM2.5, BC, and NOx at the cohort participants’ home addresses were used to assess air pollution exposure. Cox proportional hazard models were used to estimate the associations between long-term exposure to PM10, PM2.5, BC, and NOx and the time until death among the participants during the period from 1991 to 2016. The hazard ratios (HRs) associated with an interquartile range (IQR) increase in each air pollutant were calculated based on the exposure lag windows of the same year (lag0), 1–5 years (lag1–5), and 6–10 years (lag6–10). Three models were used with varying adjustments for possible confounders including both single-pollutant estimates and two-pollutant estimates. With adjustments for all covariates, the HRs for PM10, PM2.5, BC, and NOx in the single-pollutant models at lag1–5 were 1.06 (95% CI: 1.02–1.11), 1.01 (95% CI: 0.95–1.08), 1.07 (95% CI: 1.04–1.11), and 1.11 (95% CI: 1.07–1.16) per IQR increase, respectively. The HRs, in most cases, decreased with the inclusion of a larger number of covariates in the models. The most robust associations were shown for NOx, with statistically significant positive HRs in all the models. An overall conclusion is that road traffic-related pollutants had a significant association with mortality in the cohort.

In this study, long-term mortality effects associated with exposure to PM10, PM2.5, BC (black carbon), and NOx were analyzed in a cohort in southern Sweden during the period from 1991‒2016. Participants (those residing in Malmö, Sweden, born between 1923‒1950) were randomly recruited from 1991‒1996. At enrollment, 30,438 participants underwent a health screening, which consisted of questionnaires about lifestyle and diet, a clinical examination, and blood sampling. Mortality data were retrieved from the Swedish national cause of death register. The modeled concentrations of PM10 (particles with an aerodynamic diameter smaller than or equal to 10 µm), PM2.5 (particles with an aerodynamic diameter smaller than or equal to 2.5 µm), BC (black carbon), and NOx (nitrogen oxides) at the cohort participants' home addresses were used to assess air pollution exposure. Cox proportional hazard models were used to estimate the associations between long-term exposure to PM10, PM2.5, BC, and NOx and the time until death among the participants during the period from 1991‒2016. The hazard ratios (HRs) associated with an interquartile range (IQR) increase in each air pollutant were calculated based on the exposure lag windows of the same year (lag0), 1‒5 years (lag1‒5), and 6‒10 years (lag6‒10). Three models were used with varying adjustments for possible confounders including both single-pollutant estimates and two-pollutant estimates. With adjustments for all covariates, the HRs for PM10, PM2.5, BC, and NOx in the single-pollutant models at lag1‒5 were 1.06 (95% CI: 1.02‒1.11), 1.01 (95% CI: 0.95‒1.08), 1.07 (95% CI: 1.04‒1.11), and 1.11 (95% CI: 1.07‒1.16) per IQR increase, respectively. The HRs were in most cases decreased by the inclusion of a larger number of covariates in the models. The most robust associations were shown for NOx, with statistically significant positive HRs in all models. An overall conclusion is that road traffic-related pollutants had a significant association with mortality in the cohort.

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

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.

Air pollution is a major contributor to the global burden of disease and has been linked to several diseases and conditions, including cardiovascular disease. The biological mechanisms are related to inflammation and increased coagulability, factors that play an important role in the pathogenesis of venous thromboembolism (VTE, i.e., deep vein thrombosis or pulmonary embolism). This study investigates if long-term exposure to air pollution is associated with increased VTE incidence. The study followed 29 408 participants from the Malmo & BULL; Diet and Cancer (MDC) cohort, which consists of adults aged 44-74 recruited in Malmo & BULL;, Sweden between 1991 and 1996. For each participant, annual mean residential exposures to particulate matter <2.5 & mu;g (PM2.5) and <10 & mu;g (PM10), nitrogen oxides (NOx) and black carbon (BC) from 1990 up to 2016 were calculated. Associations with VTE were analysed using Cox proportional hazard models for air pollution in the year of the VTE event (lag0) and the mean of the prior 1-10 years (lag1-10). Annual air pollution exposures for the full follow-up period had the following means: 10.8 & mu;g/m3 for PM2.5, 15.8 & mu;g/m3 for PM10, 27.7 & mu;g/m3 for NOx, and 0.96 & mu;g/m3 for BC. The mean follow-up period was 19.5 years, with 1418 incident VTE events recorded during this period. Exposure to lag1-10 PM2.5 was associated with an increased risk of VTE (HR 1.17 (95%CI 1.01-1.37)) per interquartile range (IQR) of 1.2 & mu;g/m3 increase in PM2.5 exposure. No significant associations were found be-tween other pollutants or lag0 PM2.5 and incident VTE. When VTE was divided into specific diagnoses, associ-ations with lag1-10 PM2.5 exposure were similarly positive for deep vein thrombosis but not for pulmonary embolism. Results persisted in sensitivity analyses and in multi-pollutant models. Long-term exposure to mod-erate concentrations of ambient PM2.5 was associated with increased risks of VTE in the general population in Sweden.

Background: Air pollution is associated with cardiovascular morbidity and mortality, but its role in the development of congestive heart failure (CHF) and the role of different pollution sources in cardiovascular disease remain uncertain.Methods: Participants were enrolled in the Malmo spacing diaeresis Diet and Cancer cohort in 1991-1996 with information on lifestyle and clinical indicators of cardiovascular disease. The cohort participants were followed through registers until 2016. Annual total and local source-specific concentrations of particulate matter less than 10 mu m and 2.5 mu m (PM10 and PM2.5), black carbon (BC), and nitrogen oxides (NOx) from traffic, residential heating, and industry were assigned to each participant's address throughout the study period. Cox proportional hazards models adjusted for possible confounders was used to estimate associations between air pollution 1-5 years prior to outcomes of incident CHF, fatal myocardial infarction (MI), major adverse coronary events (MACE), and ischemic stroke.Results: Air pollution exposure levels (mean annual exposures to PM2.5 of 11 mu g/m(3) and NOx of 26 mu g/m(3)) within the cohort were moderate in terms of environmental standards. After adjusting for confounders, we observed statistically significant associations between NOx and CHF (hazard ratio [HR] 1.11, 95% confidence interval [CI] 1.01-1.22) and NOx and fatal MI (HR 1.10, 95%CI 1.01-1.20) per interquartile range (IQR) of 9.6 mu g/m(3). In fully adjusted models, the estimates were similar, but the precision worse. In stratified analyses, the associations were stronger in males, ever-smokers, older participants, and those with baseline carotid artery plaques. Locally emitted and traffic-related air pollutants generally showed positive associations with CHF and fatal MI. There were no associations between air pollution and MACE or stroke. Discussion/conclusion: In an area with low to moderate air pollution exposure, we observed significant associations of long-term residential NOx with increased risk of incident CHF and fatal MI, but not with coronary events and stroke.

Background: Air pollution is a major contributor to the global burden of disease and has been linked to several diseases and conditions. The mechanisms are related to inflammation and increased coagulability, factors that play an important role in the pathogenesis of venous thromboembolism (VTE). We investigated if long-term exposure to air pollution was associated with increased VTE incidence. Methods: The study followed 29,408 participants from the Malmö Diet and Cancer (MDC) cohort. The population-based cohort recruited adults aged 44-74 from Malmö, Sweden between 1991-1996. Participants were assigned annual mean residential exposure to particulate matter <2.5μg (PM2.5) and <10μg (PM10), nitrogen oxides (NOx) and black carbon (BC) from enrollment up to 2016. Those with previous VTE events or VTE occurring close to a malignancy diagnosis were excluded from main analysis. Analyses were done using Cox proportional hazard models for air pollution in the year of VTE event (lag0) and the mean of 1-10 years before VTE event (lag1-10). VTE was defined as deep vein thrombosis (DVT) of the legs and pulmonary embolism (PE). Results: The means of annual air pollution exposure during the observation period were 15.8μg/m3 for PM10, 10.8μg/m3 for PM2.5, 27.7μg/m3 for NOx, and 0.96μg/m3 for BC. The mean follow-up period was 19.5 years, with 1418 VTE events recorded during this period. Exposure to lag1-10 PM2.5 was associated with increased risk of VTE (HR 1.17(95%CI 1.01–1.37) per 0.75μg/m3(IQR) increase in PM2.5 exposure) when adjusting for likely confounders. No association was found with lag0 air pollution exposure. Similar results were found for DVT, but no association was observed with PE. Results persisted in sensitivity analyses. Conclusion: Long-term exposure to moderate levels of ambient air pollution was associated with increased risks of VTE in the general population in Sweden. Keywords: Air pollution, venous thromboembolism, survival analysis, deep vein thromboembolism.

BACKGROUND AND AIM: The Swedish CArdioPulmonary bioImage Study, SCAPIS, is a nationwide population-based cohort for the study of cardiovascular and pulmonary disease. A total of 31,265 men and women aged 50-64 years old were recruited and investigated including detailed imaging of the cardiovascular and pulmonary systems. The database currently covers over 1,300 different variables and is growing. METHODS: We modelled yearly PM2.5 levels in the six SCAPIS regions, including major source types, traffic exhaust, road wear and resuspension, residential heating, shipping, with a spatial resolution of 50 x 50 m and assigned participants exposure 2000, 2011, and 2018. These areas cover over 40% of the total population in Sweden. RESULTS: The time trend within the cohort showed a strong decrease in Long Range Transported (LRT) pollutants for the 2000s for all study regions, but for Stockholm Uppsala and Umeå the LRT exposure levels levelled out during the 2010s. There was a decreasing gradient of LRT concentrations from the highest levels in the south to the lowest levels in the north. The relative importance of the different local sources, and their respective temporal trends, were site dependent. Malmö was strongly influenced by the closeness to Copenhagen, especially in the beginning of the study period. Gothenburg had the strongest influence from shipping, and the relative importance of residential heating was strongest in Umeå in the north. Another general trend was that traffic exhaust particles decreased over time, while the particle concentrations from traffic road wear and resuspension instead increased, illustrating the tail pipe emission reduction and the traffic increase. CONCLUSIONS: Exposure to air pollution in Sweden have decreased in the last two decades, but the pattern varies for the different regions and sources.

Introduction Air pollution is associated with increased risk of cardiovascular disease, possibly through chronic systemic inflammation that promotes the progression of atherosclerosis and the risk of cardiovascular events. This study aimed to investigate the associations between air pollution and established biomarkers of inflammation and cardiovascular disease. Methods The Cardiovascular Subcohort of the Malmö Diet and Cancer cohort includes 6103 participants from the general population of Malmö, Sweden. The participants were recruited 1991–1994. Annual mean residential exposure to particulate matter < 2.5 and < 10 μm (PM 2.5 and PM 10 ), and nitrogen oxides (NO x ) at year of recruitment were assigned from dispersion models. Blood samples collected at recruitment, including blood cell counts, and biomarkers (lymphocyte- and neutrophil counts, C-reactive protein (CRP), soluble urokinase-type plasminogen activator receptor (suPAR), lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ), ceruloplasmin, orosomucoid, haptoglobin, complement-C3, and alpha-1-antitrypsin) were analyzed. Multiple linear regression models were used to investigate the cross-sectional associations between air pollutants and biomarkers. Results The mean annual exposure levels in the cohort were only slightly or moderately above the new WHO guidelines of 5 μg/m 3 PM 2.5 (10.5 μg/m 3 PM 2.5 ). Residential PM 2.5 exposure was associated with increased levels of ceruloplasmin, orosomucoid, C3, alpha-1-antitrypsin, haptoglobin, Lp-PLA 2 and the neutrophil-lymphocyte ratio. Ceruloplasmin, orosomucoid, C3 and alpha-1-antitrypsin were also positively associated with PM 10 . There were no associations between air pollutants and suPAR, leukocyte counts or CRP. The associations between particles and biomarkers were still significant after removing outliers and adjustment for CRP levels. The associations were more prominent in smokers. Conclusion Long-term residential exposure to moderate levels of particulate air pollution was associated with several biomarkers of inflammation and cardiovascular disease. This supports inflammation as a mechanism behind the association between air pollution and 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.

Abstract. Soot, or black carbon (BC), aerosol is a major climate forcer with severe health effects. The impacts depend strongly on particle number concentration, size and mixing state. This work reports on two field campaigns at nearby urban and rural sites, 65 km apart, in southern Sweden during late summer 2018. BC was measured using a single particle soot photometer (SP2) and Aethalometers (AE33). Differences in BC concentrations between the sites are driven primarily by local traffic emissions. Equivalent and refractory BC mass concentrations at the urban site were on average a factor 2.2 and 2.5 higher than at the rural site. Peaks in rush hour BC mass concentrations at the urban site were up to a factor ~4 higher than the background levels. The number fraction of particles containing a soot core was significantly higher in the city. BC particles at the urban site were on average smaller by mass and had less coating owing to fresh traffic emissions. The organic components of the fresh plumes were similar in mass spectral signature to “hydrocarbon-like organic aerosol” (HOA), commonly associated with traffic. Despite the intense local traffic (~30 000 vehicles passing per day), PM1, including organic aerosol, was dominated by aged continental air masses even at the curbside site. The fraction of thickly coated particles at the urban site was highly correlated with the mass concentrations of all measured chemical species of PM1, consistent with aged, internally mixed aerosol. Trajectory analysis for the whole year showed that air masses arriving at the rural site from eastern Europe contained approximately double the amount of BC compared to air masses from western Europe. Furthermore, BC from the largest region emissions in the Malmö/Copenhagen urban area transported to the rural site is discernable above background levels only when precipitation events are excluded.

On the use of "dual vaporizer" in the SP-AMS measurementsWhen engaging the laser there is a small increase in the "Organic" signal due to vaporization of non-refractory components.Additionally, all species signals increase ~10% due to increased sensitivity with dual vaporizers.

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.