Exposure to source-specific air pollution in residential areas and its association with dementia incidence: a cohort study in Northern Sweden.

The aim of this study was to investigate the relationship between source-specific ambient particulate air pollution concentrations and the incidence of dementia. The study encompassed 70,057 participants from the Västerbotten intervention program cohort in Northern Sweden with a median age of 40 years at baseline. High-resolution dispersion models were employed to estimate source-specific particulate matter (PM) concentrations, such as PM10 and PM2.5 from traffic, exhaust, and biomass (mainly wood) burning, at the residential addresses of each participant. Cox regression models, adjusted for potential confounding factors, were used for the assessment. Over 884,847 person-years of follow-up, 409 incident dementia cases, identified through national registers, were observed. The study population's average exposure to annual mean total PM10 and PM2.5 lag 1-5 years was 9.50 µg/m3 and 5.61 µg/m3, respectively. Increased risks were identified for PM10-Traffic (35% [95% CI 0-82%]) and PM2.5-Exhaust (33% [95% CI - 2 to 79%]) in the second exposure tertile for lag 1-5 years, although no such risks were observed in the third tertile. Interestingly, a negative association was observed between PM2.5-Wood burning and the risk of dementia. In summary, this register-based study did not conclusively establish a strong association between air pollution exposure and the incidence of dementia. While some evidence indicated elevated risks for PM10-Traffic and PM2.5-Exhaust, and conversely, a negative association for PM2.5-Wood burning, no clear exposure-response relationships were evident.

External exposome and all-cause mortality in European cohorts: the EXPANSE project.

Background: Many studies reported associations between long-term exposure to environmental factors and mortality; however, little is known on the combined effects of these factors and health. We aimed to evaluate the association between external exposome and all-cause mortality in large administrative and traditional adult cohorts in Europe. Methods: Data from six administrative cohorts (Catalonia, Greece, Rome, Sweden, Switzerland and the Netherlands, totaling 27,913,545 subjects) and three traditional adult cohorts (CEANS-Sweden, EPIC-NL-the Netherlands, KORA-Germany, totaling 57,653 participants) were included. Multiple exposures were assigned at the residential addresses, and were divided into three a priori defined domains: (1) air pollution [fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and warm-season Ozone (warm-O3)]; (2) land/built environment (Normalized Difference Vegetation Index-NDVI, impervious surfaces, and distance to water); (3) air temperature (cold- and warm-season mean and standard deviation). Each domain was synthesized through Principal Component Analysis (PCA), with the aim of explaining at least 80% of its variability. Cox proportional-hazards regression models were applied and the total risk of the external exposome was estimated through the Cumulative Risk Index (CRI). The estimates were adjusted for individual- and area-level covariates. Results: More than 205 million person-years at risk and more than 3.2 million deaths were analyzed. In single-component models, IQR increases of the first principal component of the air pollution domain were associated with higher mortality [HRs ranging from 1.011 (95% CI: 1.005-1.018) for the Rome cohort to 1.076 (1.071-1.081) for the Swedish cohort]. In contrast, lower levels of the first principal component of the land/built environment domain, pointing to reduced vegetation and higher percentage of impervious surfaces, were associated with higher risks. Finally, the CRI of external exposome increased mortality for almost all cohorts. The associations found in the traditional adult cohorts were generally consistent with the results from the administrative ones, albeit without reaching statistical significance. Discussion: Various components of the external exposome, analyzed individually or in combination, were associated with increased mortality across European cohorts. This sets the stage for future research on the connections between various exposure patterns and human health, aiding in the planning of healthier cities.

Long-term ambient air pollution and coronary atherosclerosis: Results from the Swedish SCAPIS study.

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 µm (PM2.5), <10 µm (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 µg/m3 (range 3.5-13.4 µg/m3). 51 % of participants were women and 51 % were never-smokers. None of the assessed pollutants were associated with a higher SIS or CACS. Exposure to PM2.5 was associated with NCP (adjusted OR 1.34, 95 % CI 1.13, 1.58, per 2.05 µg/m3). Associations with significant stenoses were inconsistent. 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.

Socioeconomic per-case costs of stroke, myocardial infarction, and preterm birth attributable to air pollution in Sweden.

BACKGROUND: Incident cases of stroke, myocardial infarction, and preterm birth have established exposure-response functions associated with air pollution. However, there are no studies reporting detailed costs per case for these health outcomes that are adapted to the cost-benefit tools that guide the regulation of air pollution. OBJECTIVES: The primary objective was to establish non-fatal per-case monetary estimates for stroke, myocardial infarction, and preterm birth attributable to air pollution in Sweden, and the secondary objective was to ease the economic evaluation process of air pollution morbidity effects and their inclusion in cost-benefit assessments. METHODS: Based on recommendations from the literature, the case-cost analysis considered direct and indirect medical costs, as well as production losses and informal costs relevant for the calculation of the net present value. A literature search was conducted to estimate the costs of each category for each incident case in Sweden. Informal costs were estimated using the quality-adjusted life-years approach and the corresponding willingness-to-pay in the Swedish population. The total average per-case cost was estimated based on specific health outcome durations and severity and was discounted by 3.5% per year. Sensitivity analysis included varying discount rates, severity of health outcome, and the range of societal willingness to pay for quality-adjusted life years. RESULTS: The average net present value cost estimate was €2016 460k (185k-1M) for non-fatal stroke, €2016 24k (16k-38k) for myocardial infarction, and €2016 34k (19k-57k) for late preterm birth. The main drivers of the per-case total cost estimates were health outcome severity and societal willingness to pay for risk reduction. Varying the discount rate had the largest effect on preterm birth, with costs changing by ±30% for the discount rates analysed. RECOMMENDATION: Because stroke, myocardial infarction, and preterm birth have established exposure-response functions linking these to air pollution, cost-benefit analyses should include the costs for these health outcomes in order to adequately guide future air pollution and climate change policies.

Increase in sick leave episodes from short-term fine particulate matter exposure: A case-crossover study in Stockholm, Sweden.

Air pollution's short-term effects on a wide range of health outcomes have been studied extensively, primarily focused on vulnerable groups (e.g., children and the elderly). However, the air pollution effects on the adult working population through sick leave have received little attention. This study aims to 1) estimate the associations between particulate matter ≤2.5 µm3 (PM2.5) and sick leave episodes and 2) calculate the attributable number of sick leave days and the consequential productivity loss in the City of Stockholm, Sweden. Individual level daily sick leave data was obtained from Statistics Sweden for the years 2011-2019. Daily average concentrations of PM2.5 were obtained from the main urban background monitoring station in Stockholm. A case-crossover study design was applied to estimate the association between short-term PM2.5 and onset of sick leave episodes. Conditional logistic regression was used to estimate the relative increase in odds of onset per 10 µg/m3 of PM2.5, adjusting for temperature, season, and pollen. A human capital method was applied to estimate the PM2.5 attributable productivity loss. In total, 1.5 million (M) individual sick leave occurrences were studied. The measured daily mean PM2.5 concentration was 4.2 µg/m3 (IQR 3.7 µg/m3). The odds of a sick leave episode was estimated to increase by 8.5% (95% CI: 7.8-9.3) per 10 µg/m3 average exposure 2-4 days before. Sub-group analysis showed that private sector and individuals 15-24 years old had a lower increase in odds of sick leave episodes in relation to PM2.5 exposure. In Stockholm, 4% of the sick leave episodes were attributable to PM2.5 exposure, corresponding to €17 M per year in productivity loss. Our study suggests a positive association between PM2.5 and sick leave episodes in a low exposure area.

A regional comparison of children's blood cadmium, lead, and mercury in rural, urban and industrial areas of six European countries, and China, Ecuador, and Morocco.

OBJECTIVES: The authors aimed to evaluate whether blood cadmium (B-Cd), lead (B-Pb) and mercury (B-Hg) in children differ regionally in 9 countries, and to identify factors correlating with exposure. MATERIAL AND METHODS: The authors performed a cross-sectional study of children aged 7-14 years, living in 2007-2008 in urban, rural, or potentially polluted ("hot spot") areas (ca. 50 children from each area, in total 1363 children) in 6 European and 3 non-European countries. The authors analyzed Cd, Pb, and total Hg in blood and collected information on potential determinants of exposure through questionnaires. Regional differences in exposure levels were assessed within each country. RESULTS: Children living near industrial "hot-spots" had B-Cd 1.6 (95% CI: 1.4-1.9) times higher in the Czech Republic and 2.1 (95% CI:1.6-2.8) times higher in Poland, as compared to urban children in the same countries (geometric means [GM]: 0.13 µg/l and 0.15 µg/l, respectively). Correspondingly, B-Pb in the "hot spot" areas was 1.8 (95% CI: 1.6-2.1) times higher than in urban areas in Slovakia and 2.3 (95% CI: 1.9-2.7) times higher in Poland (urban GM: 19.4 µg/l and 16.3 µg/l, respectively). In China and Morocco, rural children had significantly lower B-Pb than urban ones (urban GM: 64 µg/l and 71 µg/l, respectively), suggesting urban exposure from leaded petrol, water pipes and/or coal-burning. Hg "hot spot" areas in China had B-Hg 3.1 (95% CI: 2.7-3.5) times higher, and Ecuador 1.5 (95% CI: 1.2-1.9) times higher, as compared to urban areas (urban GM: 2.45 µg/l and 3.23 µg/l, respectively). Besides industrial exposure, traffic correlated with B-Cd; male sex, environmental tobacco smoke, and offal consumption with B-Pb; and fish consumption and amalgam fillings with B-Hg. However, these correlations could only marginally explain regional differences. CONCLUSIONS: These mainly European results indicate that some children experience about doubled exposures to toxic elements just because of where they live. These exposures are unsafe, identifiable, and preventable and therefore call for preventive actions. Int J Occup Med Environ Health. 2023;36(3):349-64.

Are doctors using more preventive medication for cardiovascular disease? A Swedish cross-sectional study.

BACKGROUND: Despite decreasing mortality from cardiovascular disease (CVD), there are persistent inequities in mortality between socioeconomic groups. Primary preventative medications reduce mortality in CVD; thus, inequitable treatments will contribute to unequal outcomes. Physicians might contribute to inequality by prescribing preventative medication for CVD to themselves in a biased manner. AIM: To determine whether primary medications for preventing CVD were prescribed inequitably between physicians and non-physicians. DESIGN AND SETTING: This retrospective study retrieved registry data on prescribed medications for all physicians in Sweden aged 45-74 years, during 2013, and for reference non-physician individuals, matched by sex, age, residence, and level of education. The outcome was any medication for preventing CVD, received at least once during 2013. METHOD: Age and the sex-specific prevalence of myocardial infarction (MI) among physicians and non-physicians were used as a proxy for the need for medication. Thereafter, to limit the analysis to preventative medication, we excluded individuals that were diagnosed with CVD or diabetes. To analyse differences in medication usage between physicians and matched non-physicians, we estimated odds ratios (ORs) with conditional logistic regression and adjusted for need and household income. RESULTS: MI prevalences were 5.7% for men and 2.3% for women, among physicians, and 5.4% for men and 1.8% for women, among non-physicians. We included 25,105 physicians and 44,366 non-physicians. The OR for physicians receiving any CVD preventative medication, compared to non-physicians, was 1.65 (95% confidence interval 1.59-1.72). CONCLUSION: We found an inequity in prescribed preventative CVD medications, which favoured physicians over non-physicians.

KEYPOINTSGroups with low socioeconomic status have lower rates of using medication that prevents cardiovascular disease, compared to groups with high socioeconomic status.Physicians are responsible for prescribing all medicines to prevent cardiovascular disease; thus, biased prescriptions could have effects on the equality of care in the population.Compared to individuals with equivalent education, physicians had higher rates of using medication that prevents cardiovascular disease.This study highlights the need for systematic population-based evaluation of CVD risk in order to promote equitable CVD outcomes.

Traffic noise in the bedroom in association with markers of obesity: a cross-sectional study and mediation analysis of the respiratory health in Northern Europe cohort.

BACKGROUND: Previous research suggests an association between road traffic noise and obesity, but current evidence is inconclusive. The aim of this study was to assess the association between nocturnal noise exposure and markers of obesity and to assess whether sleep disturbance might be a mediator in this association. 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 adjusted linear, and logistic regression models, evaluated effect modifications and conducted mediation analysis. RESULTS: Based on fully adjusted models we found that women, who reported very high traffic noise levels in bedroom, had 1.30 (95% CI 0.24-2.37) kg/m2 higher BMI and 3.30 (95% CI 0.39-6.20) 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 and have abdominal obesity with OR varying from 1.15 to 1.26 compared to women, who reported no traffic noise in the bedroom. For men, the associations were rather opposite, although mostly statistically insignificant. Furthermore, men, who reported much or very much traffic noise in the bedroom, had a statistically significantly lower risk of abdominal obesity. Sleep disturbance fully or partially mediated the association between noise in bedroom and obesity markers among women. CONCLUSION: Our results suggest that self-reported traffic noise in the bedroom may be associated to being overweight or obese trough sleep disturbance among women, but associations were inconclusive among men.

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.

Disentangling associations between multiple environmental exposures and all-cause mortality: an analysis of European administrative and traditional cohorts.

Background: We evaluated the independent and joint effects of air pollution, land/built environment characteristics, and ambient temperature on all-cause mortality as part of the EXPANSE project. Methods: We collected data from six administrative cohorts covering Catalonia, Greece, the Netherlands, Rome, Sweden, and Switzerland and three traditional cohorts in Sweden, the Netherlands, and Germany. Participants were linked to spatial exposure estimates derived from hybrid land use regression models and satellite data for: air pollution [fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3)], land/built environment [normalized difference vegetation index (NDVI), distance to water, impervious surfaces], and ambient temperature (the mean and standard deviation of warm and cool season temperature). We applied Cox proportional hazard models accounting for several cohort-specific individual and area-level variables. We evaluated the associations through single and multiexposure models, and interactions between exposures. The joint effects were estimated using the cumulative risk index (CRI). Cohort-specific hazard ratios (HR) were combined using random-effects meta-analyses. Results: We observed over 3.1 million deaths out of approximately 204 million person-years. In administrative cohorts, increased exposure to PM2.5, NO2, and BC was significantly associated with all-cause mortality (pooled HRs: 1.054, 1.033, and 1.032, respectively). We observed an adverse effect of increased impervious surface and mean season-specific temperature, and a protective effect of increased O3, NDVI, distance to water, and temperature variation on all-cause mortality. The effects of PM2.5 were higher in areas with lower (10th percentile) compared to higher (90th percentile) NDVI levels [pooled HRs: 1.054 (95% confidence interval (CI) 1.030-1.079) vs. 1.038 (95% CI 0.964-1.118)]. A similar pattern was observed for NO2. The CRI of air pollutants (PM2.5 or NO2) plus NDVI and mean warm season temperature resulted in a stronger effect compared to single-exposure HRs: [PM2.5 pooled HR: 1.061 (95% CI 1.021-1.102); NO2 pooled HR: 1.041 (95% CI 1.025-1.057)]. Non-significant effects of similar patterns were observed in traditional cohorts. Discussion: The findings of our study not only support the independent effects of long-term exposure to air pollution and greenness, but also highlight the increased effect when interplaying with other environmental exposures.

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.

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.

Overall health impacts of a potential increase in cycle commuting in Stockholm, Sweden.

AIMS: To estimate the overall health impact of transferring commuting trips from car to bicycle. METHODS: In this study registry information on the location of home and work for residents in Stockholm County was used to obtain the shortest travel route on a network of bicycle paths and roads. Current modes of travel to work were based on travel survey data. The relation between duration of cycling and distance cycled was established as a basis for selecting the number of individuals that normally would drive a car to work, but have a distance to work that they could bicycle within 30 minutes. The change in traffic flows was estimated by a transport model (LuTrans) and effects on road traffic injuries and fatalities were estimated by using national hospital injury data. Effects on air pollution concentrations were modelled using dispersion models. RESULTS: Within the scenario, 111,000 commuters would shift from car to bicycle. On average the increased physical activity reduced the one-year mortality risk by 12% among the additional bicyclists. Including the number of years lost due to morbidity, the total number of disability adjusted life-years gained was 696. The amount of disability adjusted life-years gained in the general population due to reduced air pollution exposure was 471. The number of disability adjusted life-years lost by traffic injuries was 176. Also including air pollution effects among bicyclists, the net benefit was 939 disability adjusted life-years per year. CONCLUSIONS: Large health benefits were estimated by transferring commuting by car to bicycle.

Symptoms and oxylipins in plasma before and after exposure to rooms in which individuals have both experienced and not experienced building-related symptoms - an exploratory study.

The aim of this study was to investigate if there are differences in symptom ratings and plasma concentrations of oxylipins as a measure of acute inflammation between individuals with building-related symptoms (BRS) and referents during exposure to rooms where people experienced BRS and rooms where they did not experience BRS. Medically examined individuals with BRS and healthy, age and sex matched referents working in the same building were exposed for 60 min. Ratings of symptoms and collection of blood to measure oxylipins in plasma were performed before and after each exposure. Individuals with BRS reported more symptoms (mostly mucosal) than the referents in the problem rooms and there was a tendency towards a difference between the groups in concentration of metabolites from the cyclooxygenase pathway (COX). The mean reported intensity of symptoms among all participants was also found to be positively correlated with both COX and lipoxygenase (LOX-15) oxylipins in problem rooms.

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 Residential Exposure to Particulate Matter and Its Components, Nitrogen Dioxide and Ozone-A Northern Sweden Cohort Study on Mortality.

This study aims to estimate the mortality risk associated with air pollution in a Swedish cohort with relatively low exposure. Air pollution models were used to estimate annual mean concentrations of particulate matter with aerodynamic diameter ≤ 2.5 µm (PM2.5), primary emitted carbonaceous particles (BC/pOC), sea salt, chemically formed particles grouped as secondary inorganic and organic aerosols (SIA and SOA) as well as ozone (O3) and nitrogen dioxide (NO2). The exposure, as a moving average was calculated based on home address for the time windows 1 year (lag 1), 1-5 years (lag 1-5) and 1-10 years (lag 1-10) preceding the death. During the study period, 1151 cases of natural mortality, 253 cases of cardiovascular disease (CVD) mortality and 113 cases of respiratory and lung cancer mortality were observed during 369,394 person-years of follow-up. Increased natural mortality was observed in association with NO2 (3% [95% CI -8-14%] per IQR) and PM2.5 (2% [95% CI -5-9%] for an IQR increase) and its components, except for SOA where a decreased risk was observed. Higher risk increases were observed for CVD mortality (e.g., 18% [95% CI 1-39%] per IQR for NO2). These findings at low exposure levels are relevant for future decisions concerning air quality policies.

Does Physical Activity Modify the Association between Air Pollution and Recurrence of Cardiovascular Disease?

We aimed to assess a possible interaction effect between physical activity and particulate air pollution exposure on recurrence of ischemic heart disease (IHD) and stroke. We followed 2221 adult participants comprising first time IHD (1403) and stroke (818) cases from the Västerbotten Intervention Program between 1 January 1990 to 31 December 2013. During mean follow-up times of 5.5 years, 428 and 156 participants developed IHD and stroke recurrence, respectively. PM2.5 concentrations above the median (5.48 µg/m3) were associated with increased risk of IHD and stroke recurrence by 13% (95% CI -17-45%) and 21% (95% CI -19-80%), respectively. These risk increases were however only observed among those that exercised at most once a week at 21% (95% CI -5-50%) and 25% (95% CI -19-90%) for IHD and stroke recurrence, respectively. Higher frequency of exercise at recruitment was positively associated with IHD and stroke recurrence but only the association with IHD recurrence among participants with low residential PM2.5 was statistically significant (96% increased risk (95%-CI 22-215%)). However, no interaction effect between physical activity and PM2.5 exposure was found. Our findings suggest that physical activity may reduce the air pollution exposure associated risk for recurrent cardiovascular disease, likely by reducing the inflammatory response.

Air pollution, physical activity and ischaemic heart disease: a prospective cohort study of interaction effects.

OBJECTIVE: To assess a possible interaction effect between physical activity and air pollution on first incidence of ischaemic heart disease (IHD). DESIGN: Prospective cohort study. SETTING: Umeå, Northern Sweden. PARTICIPANTS: We studied 34 748 adult participants of Västerbotten Intervention Programme cohort from 1990 to January 2014. Annual particulate matter concentrations (PM2.5 and PM10) at the participants' residential addresses were modelled and a questionnaire on frequency of exercise and active commuting was completed at baseline. Cox proportional hazards modelling was used to estimate (1) association with physical activity at different levels of air pollution and (2) the association with particulate matter at different levels of physical activity. OUTCOME: First incidence of IHD. RESULTS: Over a mean follow-up of 12.4 years, there were 1148 IHD cases. Overall, we observed an increased risk of IHD among individuals with higher concentrations of particles at their home address. Exercise at least twice a week was associated with a lower risk of IHD among participants with high residential PM2.5 (hazard ratio (HR) 0.60; 95% CI: 0.44 to 0.82) and PM10 (HR 0.55; 95% CI: 0.4 to 0.76). The same beneficial effect was not observed with low residential PM2.5 (HR 0.94; 95% CI: 0.72 to 1.22) and PM10 (HR 0.99; 95% CI: 0.76 to 1.29). An increased risk associated with higher long-term exposure to particles was only observed among participants that exercised in training clothes at most one a week and among those not performing any active commuting. However, only the interaction effect on HRs for exercise was statistically significant. CONCLUSION: Exercise was associated with a lower risk of first incidence of IHD among individuals with higher residential particle concentrations. An air pollution-associated risk was only observed among those who exercised less. The findings support the promotion of physical activity and a mitigation of air pollution.

Potential for reduced premature mortality by current and increased bicycle commuting: a health impact assessment using registry data on home and work addresses in Stockholm, Sweden.

OBJECTIVES: The study aims to make use of individual data to estimate the impact on premature mortality due to both existing commuter bicycling and the potential impact due to increased physical activity through shifting transport mode from car commuting to bicycling. METHODS: Using registry data on home and work addresses for the population of Stockholm County the shortest bicycling route on a network of bicycle paths and roads was retrieved. Travel survey data were used to establish current modes of commuting. The relation between duration of bicycling and distance bicycled within the general population in 2015 was established as a basis for identifying individuals that currently drive a car to work but were estimated to have the physical capacity to bicycle to work within 30 min. Within this mode-shift scenario from car-to-bike the duration of bicycling per week was estimated, both among current and potential bicycle commuters. The health impact assessment (HIA) on mortality due to bicycle commuting physical activity was estimated using the same relative risk as within the WHO Health Economic Assessment Tool. RESULTS: The current number of bicycle commuters were 53 000, and the scenario estimated an additional 111 000. Their mean bicycle distances were 4.5 and 3.4 km, respectively. On average these respective amounts of physical activity reduced the yearly mortality by 16% and 12%, resulting in 11.3 and 16.2 fewer preterm deaths per year. CONCLUSION: The HIA of transferring commuting by car to bicycle estimated large health benefits due to increased physical activity.

Potential Effects on Travelers' Air Pollution Exposure and Associated Mortality Estimated for a Mode Shift from Car to Bicycle Commuting.

This study aims to use dispersion-modeled concentrations of nitrogen oxides (NOx) and black carbon (BC) to estimate bicyclist exposures along a network of roads and bicycle paths. Such modeling was also performed in a scenario with increased bicycling. Accumulated concentrations between home and work were thereafter calculated for both bicyclists and drivers of cars. A transport model was used to estimate traffic volumes and current commuting preferences in Stockholm County. The study used individuals' home and work addresses, their age, sex, and an empirical model estimate of their expected physical capacity in order to establish realistic bicycle travel distances. If car commuters with estimated physical capacity to bicycle to their workplace within 30 min changed their mode of transport to bicycle, >110,000 additional bicyclists would be achieved. Time-weighted mean concentrations along paths were, among current bicyclists, reduced from 25.8 to 24.2 µg/m3 for NOx and 1.14 to 1.08 µg/m3 for BC. Among the additional bicyclists, the yearly mean NOx dose from commuting increased from 0.08 to 1.03 µg/m3. This would be expected to yearly cause 0.10 fewer deaths for current bicycling levels and 1.7 more deaths for additional bicycling. This increased air pollution impact is much smaller than the decrease in the total population.