Short-Term Ambient Air Pollution Exposure and Risk of Out-of-Hospital Cardiac Arrest in Sweden: A Nationwide Case-Crossover Study.

Background Air pollution is one of the main risk factors for cardiovascular disease globally, but its association with out-of-hospital cardiac arrest at low air pollution levels is unclear. This nationwide study in Sweden aims to investigate if air pollution is associated with a higher risk of out-of-hospital cardiac arrest in an area with relatively low air pollution levels. Methods and Results This study was a nationwide time-stratified case-crossover study investigating the association between short-term air pollution exposures and out-of-hospital cardiac arrest using data from the SRCR (Swedish Registry for Cardiopulmonary Resuscitation) between 2009 and 2019. Daily air pollution levels were estimated in 1×1-km grids for all of Sweden using a satellite-based machine learning model. The association between daily air pollutant levels and out-of-hospital cardiac arrest was quantified using conditional logistic regression adjusted for daily air temperature. Particulate matter <2.5 µm exposure was associated with a higher risk of out-of-hospital cardiac arrest among a total of 29 604 cases. In a multipollutant model, the association was most pronounced for intermediate daily lags, with an increased relative risk of 6.2% (95% CI, 1.0-11.8) per 10 µg/m3 increase of particulate matter <2.5 µm 4 days before the event. A similar pattern of association was observed for particulate matter <10 µm. No clear association was observed for O3 and NO2. Conclusions Short-term exposure to air pollution was associated with higher risk of out-of-hospital cardiac arrest. The findings add to the evidence of an adverse effect of particulate matter on out-of-hospital cardiac arrest, even at very low levels below current regulatory standards.

Changes in lifestyle, adiposity, and cardiometabolic markers among young adults in Sweden during the COVID-19 pandemic.

BACKGROUND: The COVID-19 pandemic has impacted on public health in several ways. The aim of the study was to investigate changes in lifestyle, adiposity, and cardiometabolic markers among young adults in Sweden during the COVID-19 pandemic and their determinants. METHODS: The study included 1 004 participants from the population-based birth cohort BAMSE. Anthropometrics, body composition (bioelectric impedance analyses), pulse, and blood pressure were measured before (December 2016-May 2019; mean age 22.6 years) and during (October 2020-June 2021; mean age 25.7 years) the COVID-19 pandemic. Lifestyle changes during the pandemic were assessed through a questionnaire. RESULTS: All measures of adiposity (weight, BMI, body fat percentage, trunk fat percentage) and cardiometabolic markers (blood pressure, pulse) increased during the study period (e.g., body fat percentage by a median of + 0.8% in females, p < 0.001, and + 1.5% in males, p < 0.001). Male sex, non-Scandinavian ethnicity, BMI status (underweight and obesity), and changes in lifestyle factors, e.g., decreased physical activity during the pandemic, were associated with higher increase in BMI and/or adiposity. CONCLUSION: Lifestyle factors, adiposity and cardiometabolic markers may have been adversely affected among young adults in Sweden during the COVID-19 pandemic compared with the preceding years. Targeted public health measures to reduce obesity and improve healthy lifestyle are important to prevent future non-communicable diseases.

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.

Breast Cancer Incidence in Relation to Long-Term Low-Level Exposure to Air Pollution in the ELAPSE Pooled Cohort.

BACKGROUND: Established risk factors for breast cancer include genetic disposition, reproductive factors, hormone therapy, and lifestyle-related factors such as alcohol consumption, physical inactivity, smoking, and obesity. More recently a role of environmental exposures, including air pollution, has also been suggested. The aim of this study, was to investigate the relationship between long-term air pollution exposure and breast cancer incidence. METHODS: We conducted a pooled analysis among six European cohorts (n = 199,719) on the association between long-term residential levels of ambient nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), and ozone in the warm season (O3) and breast cancer incidence in women. The selected cohorts represented the lower range of air pollutant concentrations in Europe. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. RESULTS: During 3,592,885 person-years of follow-up, we observed a total of 9,659 incident breast cancer cases. The results of the fully adjusted linear analyses showed a HR (95% confidence interval) of 1.03 (1.00-1.06) per 10 µg/m³ NO2, 1.06 (1.01-1.11) per 5 µg/m³ PM2.5, 1.03 (0.99-1.06) per 0.5 10-5 m-1 BC, and 0.98 (0.94-1.01) per 10 µg/m³ O3. The effect estimates were most pronounced in the group of middle-aged women (50-54 years) and among never smokers. CONCLUSIONS: The results were in support of an association between especially PM2.5 and breast cancer. IMPACT: The findings of this study suggest a role of exposure to NO2, PM2.5, and BC in development of breast cancer.

Short-term ambient air pollution exposure and risk of atrial fibrillation in patients with intracardiac devices.

Atrial fibrillation (AF) is the most common cardiac arrhythmia and is associated with substantial morbidity and mortality. Short-term exposure to fine particulate matter (PM2.5) has been causally linked to higher risk of cardiovascular disease, but the association with atrial fibrillation (AF) is less clear. Methods: We conducted a time-stratified case-crossover study to estimate the association between short-term air pollution levels and risk of AF episodes. The episodes were identified among patients with paroxysmal AF and an intracardiac devices able to register and store AF episodes. We obtained air pollution and temperature data from fixed monitoring stations and used conditional logistic regression to quantify the association of PM2.5, particulate matter (PM10), nitrogen dioxide (NO2) and ozone (O3) with onset of AF episodes, adjusting for temperature and public holidays.". Results: We analyzed 584 episodes of AF from 91 participants and observed increased risk of AF episodes with PM2.5 levels for the 48-72 hours lag (OR 1.05; CI [1.01,1.09] per IQR)] and 72-96 hours (OR 1.05 CI [1.00,1.10] per IQR). Our results were suggestive of an association between O3 levels and AF episodes during the warm season. We did not observe any statistically significant associations for PM10 nor NO2. Conclusion: Short-term increases in PM2.5 in a low-pollution level environment were associated with increased risk of AF episodes in a population with intracardiac devices. Our findings add to the evidence of a potential triggering of AF by short-term increases in air pollution levels, well below the new WHO air quality guidelines.

Occupational noise exposure and risk of incident stroke: a pooled study of five Scandinavian cohorts.

OBJECTIVES: To investigate the association between occupational noise exposure and stroke incidence in a pooled study of five Scandinavian cohorts (NordSOUND). METHODS: We pooled and harmonised data from five Scandinavian cohorts resulting in 78 389 participants. We obtained job data from national registries or questionnaires and recoded these to match a job-exposure matrix developed in Sweden, which specified the annual average daily noise exposure in five exposure classes (LAeq8h): <70, 70-74, 75-79, 80-84, ≥85 dB(A). We identified residential address history and estimated 1-year average road traffic noise at baseline. Using national patient and mortality registers, we identified 7777 stroke cases with a median follow-up of 20.2 years. Analyses were conducted using Cox proportional hazards models adjusting for individual and area-level potential confounders. RESULTS: Exposure to occupational noise at baseline was not associated with overall stroke in the fully adjusted models. For ischaemic stroke, occupational noise was associated with HRs (95% CI) of 1.08 (0.98 to 1.20), 1.09 (0.97 to 1.24) and 1.06 (0.92 to 1.21) in the 75-79, 80-84 and ≥85 dB(A) exposure groups, compared with <70 dB(A), respectively. In subanalyses using time-varying occupational noise exposure, we observed an indication of higher stroke risk among the most exposed (≥85 dB(A)), particularly when restricting analyses to people exposed to occupational noise within the last year (HR: 1.27; 95% CI: 0.99 to 1.63). CONCLUSIONS: We found no association between occupational noise and risk of overall stroke after adjustment for confounders. However, the non-significantly increased risk of ischaemic stroke warrants further investigation.

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 low ambient air pollution concentrations and mortality among 28 million people: results from seven large European cohorts within the ELAPSE project.

BACKGROUND: Long-term exposure to ambient air pollution has been associated with premature mortality, but associations at concentrations lower than current annual limit values are uncertain. We analysed associations between low-level air pollution and mortality within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE). METHODS: In this multicentre longitudinal study, we analysed seven population-based cohorts of adults (age ≥30 years) within ELAPSE, from Belgium, Denmark, England, the Netherlands, Norway, Rome (Italy), and Switzerland (enrolled in 2000-11; follow-up until 2011-17). Mortality registries were used to extract the underlying cause of death for deceased individuals. Annual average concentrations of fine particulate matter (PM2·5), nitrogen dioxide (NO2), black carbon, and tropospheric warm-season ozone (O3) from Europe-wide land use regression models at 100 m spatial resolution were assigned to baseline residential addresses. We applied cohort-specific Cox proportional hazard models with adjustment for area-level and individual-level covariates to evaluate associations with non-accidental mortality, as the main outcome, and with cardiovascular, non-malignant respiratory, and lung cancer mortality. Subset analyses of participants living at low pollutant concentrations (as per predefined values) and natural splines were used to investigate the concentration-response function. Cohort-specific effect estimates were pooled in a random-effects meta-analysis. FINDINGS: We analysed 28 153 138 participants contributing 257 859 621 person-years of observation, during which 3 593 741 deaths from non-accidental causes occurred. We found significant positive associations between non-accidental mortality and PM2·5, NO2, and black carbon, with a hazard ratio (HR) of 1·053 (95% CI 1·021-1·085) per 5 µg/m3 increment in PM2·5, 1·044 (1·019-1·069) per 10 µg/m3 NO2, and 1·039 (1·018-1·059) per 0·5 × 10-5/m black carbon. Associations with PM2·5, NO2, and black carbon were slightly weaker for cardiovascular mortality, similar for non-malignant respiratory mortality, and stronger for lung cancer mortality. Warm-season O3 was negatively associated with both non-accidental and cause-specific mortality. Associations were stronger at low concentrations: HRs for non-accidental mortality at concentrations lower than the WHO 2005 air quality guideline values for PM2·5 (10 µg/m3) and NO2 (40 µg/m3) were 1·078 (1·046-1·111) per 5 µg/m3 PM2·5 and 1·049 (1·024-1·075) per 10 µg/m3 NO2. Similarly, the association between black carbon and non-accidental mortality was highest at low concentrations, with a HR of 1·061 (1·032-1·092) for exposure lower than 1·5× 10-5/m, and 1·081 (0·966-1·210) for exposure lower than 1·0× 10-5/m. INTERPRETATION: Long-term exposure to concentrations of PM2·5 and NO2 lower than current annual limit values was associated with non-accidental, cardiovascular, non-malignant respiratory, and lung cancer mortality in seven large European cohorts. Continuing research on the effects of low concentrations of air pollutants is expected to further inform the process of setting air quality standards in Europe and other global regions. FUNDING: Health Effects Institute.

Long-term exposure to low-level ambient air pollution and incidence of stroke and coronary heart disease: a pooled analysis of six European cohorts within the ELAPSE project.

BACKGROUND: Long-term exposure to outdoor air pollution increases the risk of cardiovascular disease, but evidence is unclear on the health effects of exposure to pollutant concentrations lower than current EU and US standards and WHO guideline limits. Within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we investigated the associations of long-term exposures to fine particulate matter (PM2·5), nitrogen dioxide (NO2), black carbon, and warm-season ozone (O3) with the incidence of stroke and acute coronary heart disease. METHODS: We did a pooled analysis of individual data from six population-based cohort studies within ELAPSE, from Sweden, Denmark, the Netherlands, and Germany (recruited 1992-2004), and harmonised individual and area-level variables between cohorts. Participants (all adults) were followed up until migration from the study area, death, or incident stroke or coronary heart disease, or end of follow-up (2011-15). Mean 2010 air pollution concentrations from centrally developed European-wide land use regression models were assigned to participants' baseline residential addresses. We used Cox proportional hazards models with increasing levels of covariate adjustment to investigate the association of air pollution exposure with incidence of stroke and coronary heart disease. We assessed the shape of the concentration-response function and did subset analyses of participants living at pollutant concentrations lower than predefined values. FINDINGS: From the pooled ELAPSE cohorts, data on 137 148 participants were analysed in our fully adjusted model. During a median follow-up of 17·2 years (IQR 13·8-19·5), we observed 6950 incident events of stroke and 10 071 incident events of coronary heart disease. Incidence of stroke was associated with PM2·5 (hazard ratio 1·10 [95% CI 1·01-1·21] per 5 µg/m3 increase), NO2 (1·08 [1·04-1·12] per 10 µg/m3 increase), and black carbon (1·06 [1·02-1·10] per 0·5 10-5/m increase), whereas coronary heart disease incidence was only associated with NO2 (1·04 [1·01-1·07]). Warm-season O3 was not associated with an increase in either outcome. Concentration-response curves indicated no evidence of a threshold below which air pollutant concentrations are not harmful for cardiovascular health. Effect estimates for PM2·5 and NO2 remained elevated even when restricting analyses to participants exposed to pollutant concentrations lower than the EU limit values of 25 µg/m3 for PM2·5 and 40 µg/m3 for NO2. INTERPRETATION: Long-term air pollution exposure was associated with incidence of stroke and coronary heart disease, even at pollutant concentrations lower than current limit values. FUNDING: Health Effects Institute.

Long-Term Exposure to PM2.5 and Cognitive Decline: A Longitudinal Population-Based Study.

BACKGROUND: A growing but contrasting evidence relates air pollution to cognitive decline. The role of cerebrovascular diseases in amplifying this risk is unclear. OBJECTIVES: 1) Investigate the association between long-term exposure to air pollution and cognitive decline; 2) Test whether cerebrovascular diseases amplify this association. METHODS: We examined 2,253 participants of the Swedish National study on Aging and Care in Kungsholmen (SNAC-K). One major air pollutant (particulate matter ≤2.5µm, PM2.5) was assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses. The speed of cognitive decline (Mini-Mental State Examination, MMSE) was estimated as the rate of MMSE decline (linear mixed models) and further dichotomized into the upper (25%fastest cognitive decline), versus the three lower quartiles. The cognitive scores were used to calculate the odds of fast cognitive decline per levels of PM2.5 using regression models and considering linear and restricted cubic splines of 10 years exposure before the baseline. The potential modifier effect of cerebrovascular diseases was tested by adding an interaction term in the model. RESULTS: We observed an inverted U-shape relationship between PM2.5 and cognitive decline. The multi-adjusted piecewise regression model showed an increased OR of fast cognitive decline of 81%(95%CI = 1.2-3.2) per interquartile range difference up to mean PM2.5 level (8.6µg/m3) for individuals older than 80. Above such level we observed no further risk increase (OR = 0.89;95%CI = 0.74-1.06). The presence of cerebrovascular diseases further increased such risk by 6%. CONCLUSION: Low to mean PM2.5 levels were associated with higher risk of accelerated cognitive decline. Cerebrovascular diseases further amplified such risk.

Long-term exposure to fine particle elemental components and lung cancer incidence in the ELAPSE pooled cohort.

BACKGROUND: An association between long-term exposure to fine particulate matter (PM2.5) and lung cancer has been established in previous studies. PM2.5 is a complex mixture of chemical components from various sources and little is known about whether certain components contribute specifically to the associated lung cancer risk. The present study builds on recent findings from the "Effects of Low-level Air Pollution: A Study in Europe" (ELAPSE) collaboration and addresses the potential association between specific elemental components of PM2.5 and lung cancer incidence. METHODS: We pooled seven cohorts from across Europe and assigned exposure estimates for eight components of PM2.5 representing non-tail pipe emissions (copper (Cu), iron (Fe), and zinc (Zn)), long-range transport (sulfur (S)), oil burning/industry emissions (nickel (Ni), vanadium (V)), crustal material (silicon (Si)), and biomass burning (potassium (K)) to cohort participants' baseline residential address based on 100 m by 100 m grids from newly developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status). RESULTS: The pooled study population comprised 306,550 individuals with 3916 incident lung cancer events during 5,541,672 person-years of follow-up. We observed a positive association between exposure to all eight components and lung cancer incidence, with adjusted HRs of 1.10 (95% CI 1.05, 1.16) per 50 ng/m3 PM2.5 K, 1.09 (95% CI 1.02, 1.15) per 1 ng/m3 PM2.5 Ni, 1.22 (95% CI 1.11, 1.35) per 200 ng/m3 PM2.5 S, and 1.07 (95% CI 1.02, 1.12) per 200 ng/m3 PM2.5 V. Effect estimates were largely unaffected by adjustment for nitrogen dioxide (NO2). After adjustment for PM2.5 mass, effect estimates of K, Ni, S, and V were slightly attenuated, whereas effect estimates of Cu, Si, Fe, and Zn became null or negative. CONCLUSIONS: Our results point towards an increased risk of lung cancer in connection with sources of combustion particles from oil and biomass burning and secondary inorganic aerosols rather than non-exhaust traffic emissions. Specific limit values or guidelines targeting these specific PM2.5 components may prove helpful in future lung cancer prevention strategies.

Long-term low-level ambient air pollution exposure and risk of lung cancer - A pooled analysis of 7 European cohorts.

BACKGROUND/AIM: Ambient air pollution has been associated with lung cancer, but the shape of the exposure-response function - especially at low exposure levels - is not well described. The aim of this study was to address the relationship between long-term low-level air pollution exposure and lung cancer incidence. METHODS: The "Effects of Low-level Air Pollution: a Study in Europe" (ELAPSE) collaboration pools seven cohorts from across Europe. We developed hybrid models combining air pollution monitoring, land use data, satellite observations, and dispersion model estimates for nitrogen dioxide (NO2), fine particulate matter (PM2.5), black carbon (BC), and ozone (O3) to assign exposure to cohort participants' residential addresses in 100 m by 100 m grids. We applied stratified Cox proportional hazards models, adjusting for potential confounders (age, sex, calendar year, marital status, smoking, body mass index, employment status, and neighborhood-level socio-economic status). We fitted linear models, linear models in subsets, Shape-Constrained Health Impact Functions (SCHIF), and natural cubic spline models to assess the shape of the association between air pollution and lung cancer at concentrations below existing standards and guidelines. RESULTS: The analyses included 307,550 cohort participants. During a mean follow-up of 18.1 years, 3956 incident lung cancer cases occurred. Median (Q1, Q3) annual (2010) exposure levels of NO2, PM2.5, BC and O3 (warm season) were 24.2 µg/m3 (19.5, 29.7), 15.4 µg/m3 (12.8, 17.3), 1.6 10-5m-1 (1.3, 1.8), and 86.6 µg/m3 (78.5, 92.9), respectively. We observed a higher risk for lung cancer with higher exposure to PM2.5 (HR: 1.13, 95% CI: 1.05, 1.23 per 5 µg/m3). This association was robust to adjustment for other pollutants. The SCHIF, spline and subset analyses suggested a linear or supra-linear association with no evidence of a threshold. In subset analyses, risk estimates were clearly elevated for the subset of subjects with exposure below the EU limit value of 25 µg/m3. We did not observe associations between NO2, BC or O3 and lung cancer incidence. CONCLUSIONS: Long-term ambient PM2.5 exposure is associated with lung cancer incidence even at concentrations below current EU limit values and possibly WHO Air Quality Guidelines.

Building capacity for air pollution epidemiology in India.

Air pollution represents a major public health threat in India affecting 19% of the world's population at extreme levels. Despite this, research in India lags behind in large part due to a lack of comprehensive air pollution exposure assessment that can be used in conjunction with health data to investigate health effects. Our vision is to provide a consortium to rapidly expand the evidence base of the multiple effects of ambient air pollution. We intend to leapfrog current limitations of exposure assessment by developing a machine-learned satellite-informed spatiotemporal model to estimate daily levels of ambient fine particulate matter measuring less than 2.5 µm (PM2.5) at a fine spatial scale across all of India. To catalyze health effects research on an unprecedented scale, we will make the output from this model publicly available. In addition, we will also apply these PM2.5 estimates to study the health outcomes of greatest public health importance in India, including cardiovascular diseases, chronic obstructive pulmonary disease, pregnancy (and birth) outcomes, and cognitive development and/or decline. Thus, our efforts will directly generate actionable new evidence on the myriad effects of air pollution on health that can inform policy decisions, while providing a comprehensive and publicly available resource for future studies on both exposure and health effects. In this commentary, we discuss the motivation, rationale, and vision for our consortium and a path forward for reducing the enormous burden of disease from air pollution in India.

Association Between Cardiovascular Disease and Long-term Exposure to Air Pollution With the Risk of Dementia.

Importance: Emerging yet contrasting evidence associates air pollution with incident dementia, and the potential role of cardiovascular disease (CVD) in this association is unclear. Objective: To investigate the association between long-term exposure to air pollution and dementia and to assess the role of CVD in that association. Design, Setting, and Participants: Data for this cohort study were extracted from the ongoing Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), a longitudinal population-based study with baseline assessments from March 21, 2001, through August 30, 2004. Of the 5111 randomly selected residents in the Kungsholmen district of Stockholm 60 years or older and living at home or in institutions, 521 were not eligible (eg, due to death before the start of the study or no contact information). Among the remaining 4590 individuals, 3363 (73.3%) were assessed. For the current analysis, 2927 participants who did not have dementia at baseline were examined, with follow-up to 2013 (mean [SD] follow-up time, 6.01 [2.56] years). Follow-up was completed February 18, 2013, and data were analyzed from June 26, 2018, through June 20, 2019. Exposures: Two major air pollutants (particulate matter ≤2.5 µm [PM2.5] and nitrogen oxide [NOx]) were assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses. Main Outcomes and Measures: The hazard of dementia was estimated using Cox proportional hazards regression models. The potential of CVD (ie, atrial fibrillation, ischemic heart disease, heart failure, and stroke) to modify and mediate the association between long-term exposure to air pollution and dementia was tested using stratified analyses and generalized structural equation modeling. Results: At baseline, the mean (SD) age of the 2927 participants was 74.1 (10.7) years, and 1845 (63.0%) were female. Three hundred sixty-four participants with incident dementia were identified. The hazard of dementia increased by as much as 50% per interquartile range difference in mean pollutant levels during the previous 5 years at the residential address (hazard ratio [HR] for difference of 0.88 µg/m3 PM2.5, 1.54 [95% CI, 1.33-1.78]; HR for difference of 8.35 µg/m3 NOx, 1.14 [95% CI, 1.01-1.29]). Heart failure (HR for PM2.5, 1.93 [95% CI, 1.54-2.43]; HR for NOx, 1.43 [95% CI, 1.17-1.75]) and ischemic heart disease (HR for PM2.5, 1.67 [95% CI, 1.32-2.12]; HR for NOx, 1.36 [95% CI, 1.07-1.71]) enhanced the dementia risk, whereas stroke appeared to be the most important intermediate condition, explaining 49.4% of air pollution-related dementia cases. Conclusions and Relevance: This study found that long-term exposure to air pollution was associated with a higher risk of dementia. Heart failure and ischemic heart disease appeared to enhance the association between air pollution and dementia, whereas stroke seemed to be an important intermediate condition between the association of air pollution exposure with dementia.

Association Between Hospital Bed Occupancy and Outcomes in Emergency Care: A Cohort Study in Stockholm Region, Sweden, 2012 to 2016.

STUDY OBJECTIVE: We evaluate the importance of hospital bed occupancy for 30-day mortality, inhospital mortality, readmission for inpatient care within 30 days, and revisits to the emergency department (ED) within 7 days among all adult patients visiting the ED. METHODS: This was an observational cohort study including all adult patients visiting 6 EDs in Stockholm Region, Sweden. ED visits from 2012 to 2016 were categorized into groups by hospital bed occupancy in 5% intervals between 85% and 105%. A proportional hazards model was used to estimate adjusted hazard ratios with 95% confidence intervals (CIs). The model was stratified by hospital and adjusted for age, sex, comorbidities, hospital stays in the year preceding the index visit, marital status, length of education, and weekday/weekend timing of visit. RESULTS: A total of 816,832 patients with 2,084,554 visits were included. Mean hospital bed occupancy was 93.3% (SD 3.3%). In total, 28,112 patients died within 30 days, and 17,966 patients died inhospital. Hospital bed occupancy was not associated with 30-day mortality (hazard ratio for highest category of occupancy ≥105% was 1.10; 95% CI 0.96 to 1.27) or inhospital mortality. Patients discharged from the ED at occupancy levels greater than 89% had a 2% to 4% higher risk of revisits to the ED within 7 days. A 10% increase in hospital bed occupancy was associated with a 16-minute increase (95% CI 16 to 17 minutes) in ED length of stay and 1.9-percentage-point decrease (95% CI 1.7 to 2.0 percentage points) in admission rate. CONCLUSION: We did not find an association between increasing hospital bed occupancy and mortality in our sample of 6 EDs in Stockholm Region, Sweden, despite increased length of stay in the ED and a decline in admissions for inpatient care.

Emergency department crowding associated with increased 30-day mortality: a cohort study in Stockholm Region, Sweden, 2012 to 2016.

OBJECTIVES: Emergency department (ED) crowding is a major problem across the world. Studies investigating the association between crowding and mortality are many, but the quality is inconsistent and there are very few large, high-quality multicenter studies that are properly designed to deal with confounding due to case mix. The aim of this study is to investigate the association between ED crowding and 30-day mortality. METHODS: We conducted an observational cohort study at all 7 EDs in Stockholm Region, Sweden 2012-2016. The crowding exposure was defined as the mean hourly ED census during the shift that the exposed patient arrived, divided with the expected ED census for this shift. The expected ED census was estimated using a separate linear model for each hospital with year and shift as predictors. The exposure was categorized in 3 groups: reference (lowest 75% of observations), moderate (75%-95% of observations), and high (highest 5% of observations). Hazard ratios (HR) for all-cause mortality within 30 days were estimated with a Cox proportional hazards model. The model was adjusted for age, sex, triage priority, arrival hour, weekend, arrival mode, chief complaint, number of prior hospital admissions, and comorbidities. RESULTS: 884,228 patients who visited the ED 2,252,656 times were included in the analysis. The estimated HR (95% confidence interval) for death within 30-days was 1.00 (0.97-1.03) in crowding category 75%-95% and 1.08 (1.03-1.14) in the 95%-100% category. CONCLUSIONS: In a large cohort study including 7 EDs in Stockholm Region, Sweden we identified a significant association between high levels of ED crowding and increased 30-day mortality.

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.

Ozone and cardiac arrest: The role of previous hospitalizations.

BACKGROUND: Several studies have reported associations between exposure to particulate matter and incidence of out-of-hospital cardiac arrest (OHCA) and some have observed associations with ozone (O3). There are no studies investigating susceptibility based on previous disease history to short-term O3 exposure and the risk of OHCA. AIM: To investigate the role of previous cardiovascular-related hospitalizations in modifying the associations between the risk of OHCA and short-term increase in O3 concentrations. METHODS: A time-stratified case-crossover analysis of 11,923 OHCA registered in the Swedish Register for Cardiopulmonary Resuscitation from 2006 to 2014 was performed. Using personal identification numbers, OHCA were linked to all previous hospitalizations in Sweden since 1987 to create susceptible groups based on the principal diagnosis code at discharge. Susceptibility was based on hospitalization for i) acute myocardial infarction; ii) heart failure; iii) arrhythmias; iv) diabetes; v) hypertension; and vi) stroke. Moving 2 and 24-h averages for O3, PM2.5, PM10, and NO2 were constructed from hourly averages. RESULTS: A 10 µg/m3 higher 2-h average O3 concentration was associated with a 2% higher risk of OHCA (95% CI, 0% 3%). Associations were similar for 24-h average O3 and in individuals with or without hospitalizations for AMI, heart failure, diabetes, hypertension or stroke. Individuals with previous hospitalizations for arrhythmias had a lower risk of OHCA with higher O3. No associations were observed for other pollutants. CONCLUSIONS: Short-term exposure to O3 was associated with an elevated risk of OHCA, however, previous hospitalizations for cardiovascular diseases were not associated with additionally augmented risks.

Long- and short-term air pollution exposure and measures of arterial stiffness in the Framingham Heart Study.

BACKGROUND: Studies of air pollution exposure and arterial stiffness have reported inconsistent results and large studies employing the reference standard of arterial stiffness, carotid-femoral pulse-wave velocity (CFPWV), have not been conducted. AIM: To study long-term exposure to ambient fine particles (PM2.5), proximity to roadway, and short-term air pollution exposures in relation to multiple measures of arterial stiffness in the Framingham Heart Study. METHODS: We assessed central arterial stiffness using CFPWV, forward pressure wave amplitude, mean arterial pressure and augmentation index. We investigated long-and short-term air pollution exposure associations with arterial stiffness with linear regressions using long-term residential PM2.5 (2003 average from a spatiotemporal model using satellite data) and proximity to roadway in addition to short-term averages of PM2.5, black carbon, particle number, sulfate, nitrogen oxides, and ozone from stationary monitors. RESULTS: We examined 5842 participants (mean age 51 ±â€¯16, 54% women). Living closer to a major roadway was associated with higher arterial stiffness (0.11 m/s higher CFPWV [95% CI: 0.01, 0.22] living <50 m vs 400 ≤ 1000 m). We did not observe association between arterial stiffness measures and long-term PM2.5 or short-term levels of PM2.5, particle number, sulfate or ozone. Higher levels of black carbon and nitrogen oxides in the previous days were unexpectedly associated with lower arterial stiffness. CONCLUSIONS: Long-term exposure to PM2.5 was not associated with arterial stiffness but positive associations with living close to a major road may suggest that pollutant mixtures very nearby major roads, rather than PM2.5, may affect arterial stiffness. Furthermore, short-term air pollution exposures were not associated with higher arterial stiffness.

Susceptibility to short-term ozone exposure and cardiovascular and respiratory mortality by previous hospitalizations.

BACKGROUND: Ozone (O3) has been associated with cardiorespiratory mortality although few studies have explored susceptible populations based on prior disease. We aimed to investigate the role of previous hospitalization on the association between short-term exposure to O3 and cardiovascular (CV) and respiratory mortality. METHODS: We performed time series analyses using generalized additive models and case-crossover on 136,624 CV and 23,281 respiratory deaths in Stockholm County (1990-2010). Deaths were linked to hospital admissions data. We constructed 2-day and 7-day averages using daily 8-h maximum for O3 and hourly values for PM2.5, PM10, NO2, and NOx from a fixed monitor. RESULTS: We observed a 0.7% (95% CI: 0.1%, 1.3%) and 2.7% (95% CI: 0.8%, 4.6%) higher risk of CV and respiratory death per 10 µg/m3 higher 2-day and 7-day average O3 respectively. Individuals previously hospitalized for myocardial infarction demonstrated 1.8% (95% CI: 0.4%, 3.4%) higher risk of CV death per 10 µg/m3 higher 2-day average O3 and similar associations were observed in individuals with no previous hospitalization for any cause. Individuals with previous hospitalizations did not show susceptibility towards O3-related risk of respiratory mortality. We observed no associations for other pollutants. CONCLUSION: Short-term ozone exposure is associated with CV and respiratory mortality and our results may suggest higher susceptibility to CV mortality following O3 exposure in individuals previously hospitalized for myocardial infarction. Higher risks were also observed in individuals with cardiovascular death as their first presentation of disease.