Inequalities in income and education are associated with survival differences after out-of-hospital cardiac arrest : nationwide observational study

Published online: 12 November 2021Background: Despite the acknowledged importance of socioeconomic factors as regards cardiovascular disease onset and survival, the relationship between individual-level socioeconomic factors and survival after out-of-hospital cardiac arrest is not established. Our aim was to investigate whether socioeconomic variables are associated with 30-day survival after out-of-hospital cardiac arrest. Methods: We linked data from the Swedish Registry for Cardiopulmonary Resuscitation with individual-level data on socioeconomic factors (ie, educational level and disposable income) from Statistics Sweden. Confounding and mediating variables included demographic factors, comorbidity, and Utstein resuscitation variables. Outcome was 30-day survival. Multiple modified Poisson regression was used for the main analyses. Results: A total of 31 373 out-of-hospital cardiac arrests occurring in 2010 to 2017 were included. Crude 30-day survival rates by income quintiles were as follows: Q1 (low), 414/6277 (6.6%); Q2, 339/6276 (5.4%); Q3, 423/6275 (6.7%); Q4, 652/6273 (10.4%); and Q5 (high), 928/6272 (14.8%). In adjusted analysis, the chance of survival by income level followed a gradient-like increase, with a risk ratio of 1.86 (95% CI, 1.65–2.09) in the highest-income quintile versus the lowest. This association remained after adjusting for comorbidity, resuscitation factors, and initial rhythm. A higher educational level was associated with improved 30-day survival, with the risk ratio associated with postsecondary education ≥4 years being 1.51 (95% CI, 1.30–1.74). Survival disparities by income and educational level were observed in both men and women. Conclusions: In this nationwide observational study using individual-level socioeconomic data, higher income and higher educational level were associated with better 30-day survival after out-of-hospital cardiac arrest in both sexes

Air Pollution Exposure—A Trigger for Myocardial Infarction?

The association between ambient air pollution exposure and hospitalization for cardiovascular events has been reported in several studies with conflicting results. A case-crossover design was used to investigate the effects of air pollution in 660 first-time myocardial infarction cases in Stockholm in 1993–1994, interviewed shortly after diagnosis using a standard protocol. Air pollution data came from central urban background monitors. No associations were observed between the risk for onset of myocardial infarction and two-hour or 24-hour air pollution exposure. No evidence of susceptible subgroups was found. This study provides no support that moderately elevated air pollution levels trigger first-time myocardial infarction

Air Pollution and Inflammation (Interleukin-6, C-Reactive Protein, Fibrinogen) in Myocardial Infarction Survivors

BACKGROUND: Numerous studies have found that ambient air pollution has been associated with cardiovascular disease exacerbation. OBJECTIVES: Given previous findings, we hypothesized that particulate air pollution might induce systemic inflammation in myocardial infarction (MI) survivors, contributing to an increased vulnerability to elevated concentrations of ambient particles. METHODS: A prospective longitudinal study of 1,003 MI survivors was performed in six European cities between May 2003 and July 2004. We compared repeated measurements of interleukin 6 (IL-6), fibrinogen, and C-reactive protein (CRP) with concurrent levels of air pollution. We collected hourly data on particle number concentrations (PNC), mass concentrations of particulate matter (PM) < 10 microm (PM(10)) and < 2.5 microm (PM(2.5)), gaseous pollutants, and meteorologic data at central monitoring sites in each city. City-specific confounder models were built for each blood marker separately, adjusting for meteorology and time-varying and time-invariant covariates. Data were analyzed with mixed-effects models. RESULTS: Pooled results show an increase in IL-6 when concentrations of PNC were elevated 12-17 hr before blood withdrawal [percent change of geometric mean, 2.7; 95% confidence interval (CI), 1.0-4.6]. Five day cumulative exposure to PM(10) was associated with increased fibrinogen concentrations (percent change of arithmetic mean, 0.6; 95% CI, 0.1-1.1). Results remained stable for smokers, diabetics, and patients with heart failure. No consistent associations were found for CRP. CONCLUSIONS: Results indicate an immediate response to PNC on the IL-6 level, possibly leading to the production of acute-phase proteins, as seen in increased fibrinogen levels. This might provide a link between air pollution and adverse cardiac events

Mixtures of long-term exposure to ambient air pollution, built environment and temperature and stroke incidence across Europe

Introduction: The complex interplay of multiple environmental factors and cardiovascular has scarcely been studied. Within the EXPANSE project, we evaluated the association between long-term exposure to multiple environmental indices and stroke incidence across Europe. Methods: Participants from three traditional adult cohorts (Germany, Netherlands and Sweden) and four administrative cohorts (Catalonia [region Spain], Rome [city-wide], Greece and Sweden [nationwide]) were followed until incident stroke, death, migration, loss of follow-up or study end. We estimated exposures at residential addresses from different exposure domains: air pollution (nitrogen dioxide (NO2), particulate matter < 2.5 μm (PM2.5), black carbon (BC), ozone), built environment (green/blue spaces, impervious surfaces) and meteorology (seasonal mean and standard deviation of temperatures). Associations between environmental exposures and stroke were estimated in single and multiple-exposure Cox proportional hazard models, and Principal Component (PC) Analyses derived prototypes for specific exposures domains. We carried out random effects meta-analyses by cohort type. Results: In over 15 million participants, increased levels of NO2 and BC were associated with increased higher stroke incidence in both cohort types. Increased Normalized Difference Vegetation Index (NDVI) was associated with a lower stroke incidence in both cohort types, whereas an increase in impervious surface was associated with an increase in stroke incidence. The first PC of the air pollution domain (PM2.5, NO2 and BC) was associated with an increase in stroke incidence. For the built environment, higher levels of NDVI and lower levels of impervious surfaces were associated with a protective effect [%change in HR per 1 unit = −2.0 (95 %CI, −5.9;2.0) and −1.1(95 %CI, −2.0; −0.3) for traditional adult and administrative cohorts, respectively]. No clear patterns were observed for distance to blue spaces or temperature parameters. Conclusions: We observed increased HRs for stroke with exposure to PM2.5, NO2 and BC, lower levels of greenness and higher impervious surface in single and combined exposure models

Long-term exposure to transportation noise and risk of incident stroke:A pooled study of nine scandinavian cohorts

BACKGROUND: Transportation noise is increasingly acknowledged as a cardiovascular risk factor, but the evidence base for an association with stroke is sparse. OBJECTIVE: We aimed to investigate the association between transportation noise and stroke incidence in a large Scandinavian population. METHODS: We harmonized and pooled data from nine Scandinavian cohorts (seven Swedish, two Danish), totaling 135,951 participants. We identified residential address history and estimated road, railway, and aircraft noise for all addresses. Information on stroke incidence was acquired through link-age to national patient and mortality registries. We analyzed data using Cox proportional hazards models, including socioeconomic and lifestyle con-founders, and air pollution. RESULTS: During follow-up (median = 19:5 y), 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 indi-vidual-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 ≤2:5 lm (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

Long-term exposure to low-level air pollution and incidence of chronic obstructive pulmonary disease: The ELAPSE project.

BACKGROUND: Air pollution has been suggested as a risk factor for chronic obstructive pulmonary disease (COPD), but evidence is sparse and inconsistent. OBJECTIVES: We examined the association between long-term exposure to low-level air pollution and COPD incidence. METHODS: Within the 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE) study, we pooled data from three cohorts, from Denmark and Sweden, with information on COPD hospital discharge diagnoses. Hybrid land use regression models were used to estimate annual mean concentrations of particulate matter with a diameter < 2.5 µm (PM2.5), nitrogen dioxide (NO2), and black carbon (BC) in 2010 at participants' baseline residential addresses, which were analysed in relation to COPD incidence using Cox proportional hazards models. RESULTS: Of 98,058 participants, 4,928 developed COPD during 16.6 years mean follow-up. The adjusted hazard ratios (HRs) and 95% confidence intervals for associations with COPD incidence were 1.17 (1.06, 1.29) per 5 µg/m3 for PM2.5, 1.11 (1.06, 1.16) per 10 µg/m3 for NO2, and 1.11 (1.06, 1.15) per 0.5 10-5m-1 for BC. Associations persisted in subset participants with PM2.5 or NO2 levels below current EU and US limit values and WHO guidelines, with no evidence for a threshold. HRs for NO2 and BC remained unchanged in two-pollutant models with PM2.5, whereas the HR for PM2.5 was attenuated to unity with NO2 or BC. CONCLUSIONS: Long-term exposure to low-level air pollution is associated with the development of COPD, even below current EU and US limit values and possibly WHO guidelines. Traffic-related pollutants NO2 and BC may be the most relevant

Long-term air pollution exposure and Parkinson's disease mortality in a large pooled European cohort: An ELAPSE study

BACKGROUND: The link between exposure to ambient air pollution and mortality from cardiorespiratory diseases is well established, while evidence on neurodegenerative disorders including Parkinson's Disease (PD) remains limited. OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and PD mortality in seven European cohorts. METHODS: Within the project 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE), we pooled data from seven cohorts among six European countries. Annual mean residential concentrations of fine particulate matter (PM 2.5), nitrogen dioxide (NO 2), black carbon (BC), and ozone (O 3), as well as 8 PM 2.5 components (copper, iron, potassium, nickel, sulphur, silicon, vanadium, zinc), for 2010 were estimated using Europe-wide hybrid land use regression models. PD mortality was defined as underlying cause of death being either PD, secondary Parkinsonism, or dementia in PD. We applied Cox proportional hazard models to investigate the associations between air pollution and PD mortality, adjusting for potential confounders. RESULTS: Of 271,720 cohort participants, 381 died from PD during 19.7 years of follow-up. In single-pollutant analyses, we observed positive associations between PD mortality and PM 2.5 (hazard ratio per 5 µg/m 3: 1.25; 95% confidence interval: 1.01-1.55), NO 2 (1.13; 0.95-1.34 per 10 µg/m 3), and BC (1.12; 0.94-1.34 per 0.5 × 10 -5m -1), and a negative association with O 3 (0.74; 0.58-0.94 per 10 µg/m 3). Associations of PM 2.5, NO 2, and BC with PD mortality were linear without apparent lower thresholds. In two-pollutant models, associations with PM 2.5 remained robust when adjusted for NO 2 (1.24; 0.95-1.62) or BC (1.28; 0.96-1.71), whereas associations with NO 2 or BC attenuated to null. O 3 associations remained negative, but no longer statistically significant in models with PM 2.5. We detected suggestive positive associations with the potassium component of PM 2.5. CONCLUSION: Long-term exposure to PM 2.5, at levels well below current EU air pollution limit values, may contribute to PD mortality

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

Cardiovascular effects of short-term exposure to air pollution : Exploring potential pathways and susceptible subgroups

Cardiovascular disease is the most common cause of mortality globally, with a number of contributing risk factors. Ambient air pollution represents a universally present risk factor with a substantial preventive potential. Although the relationship between exposure to air pollution and all-cause mortality, or even cardiovascular mortality, has been relatively well established, the details of how, when, who and even how much remain unclear. This thesis focuses on understanding associations between short-term exposure to air pollution and cardiovascular disease, with special attention to ischemic heart disease and ventricular arrhythmias. In the first paper we conducted a case-crossover study with 660 first-time myocardial infarctions in Stockholm, interviewed shortly after diagnosis to determine time of disease onset. Air pollution levels 2 and 24 hours preceding the time of onset were compared in the same individual with 3-4 equally long control periods without myocardial infarction matched by time of day and day of week within the same calendar month. No associations were found between air pollution levels and myocardial infarction in the main analyses or in subgroup analyses. Atherosclerosis is an inflammatory disease leading to a number of cardiac disorders including myocardial infarction. Low-grade inflammation, measured by slight increases in blood markers such as interleukin-6 (IL-6), has been associated with poorer prognosis for heart disease and mortality. In a multi-center study involving 6 European cities and 1003 myocardial infarction survivors we conducted repeated (5.8 in average) blood sampling for inflammatory markers including IL-6, and genotyped for single nucleotide polymorphisms (SNPs) in inflammatory genes. In the second paper results are presented for associations between interleukin-6 (IL6) genotypes and mean IL-6 plasma levels using mixed model analyses with random intercepts. Four SNPs showed associations with IL-6 levels with eg 6.3% (95% confidence interval 1.7-11.2%) increased IL-6 per minor alleleof an IL6 SNP labeled rs1800795. In the third paper we analyzed the effect modification of selected SNPs in theIL6 gene and the fibrinogen alpha- (FGA) and beta-chain (FGB) genes on the IL-6 response to preceding air pollution levels. We found associations demonstrating gene-environment interaction effects for an IL6 SNP and a FGB SNP. Strongest effects were found when patients with the minor alleles of FGB rs1800790 were exposed to carbon monoxide in the 6-11 hour exposure-window prior to sampling. In homozygotes for this allele a 10% (4.6-16%) increased mean IL-6 was observed per 0.64 mg/m3 increase of pollutant. In the fourth paper we studied the relationship between air pollution levels 2 and 24 hours preceding ventricular arrhythmias in 211 patients with implantable cardioverter defibrillators in Stockholm and Gothenburg using a similar methodology as in Paper I. We found associations for ventricular arrhythmias and 2 hour exposure to particulate pollution indicating an odds ratio of 1.31 (1.00-1.72) per 13.2 μg/m3 PM10. Interaction analyses showed strongest effects for events occurring closer to the monitoring station, outdoors and in Gothenburg. Conclusions: Air pollution exposure was not associated with the onset of myocardial infarction in our sample. Four strongly correlated polymorphisms in the IL6 gene were associated with plasma IL-6 levels implicating that variants in the IL6 gene affect the inflammatory status of myocardial infarction survivors and potentially their future prognosis. The air pollution effect on IL-6 levels was modified by variations in the IL6 and FGB genes. This suggests that if inflammation is a pathway for the air pollution effect on heart disease, these genetic variations may lead to some people being more susceptible to air pollution than others. Particulate air pollution was associated with ventricular arrhythmias already after 2 hours of exposure giving further support to the hypotheses that air pollution may contribute to dysfunctional autonomic regulation of the electrical conduction of the heart and be an important alternative explanation for the cardiovascular mortality seen in association with air pollution

Arbete efter hjärtinfarkt – en kunskapssammanställning

De senaste ca 20-30 åren har det skett en fortlöpande förändring av flera faktorer som påverkar risken för hjärtinfarkt i Sverige. Mycket tyder på att flera riskfaktorer för hjärtinfarkt har minskat samtidigt som de diagnostiska kriterierna har skärpts, vilket gör att vi idag kan identifiera tillståndet i ett tidigare skede och innan stor skada har skett. Till detta har behandlingsarsenalen och strukturen kring uppföljning och rehabilitering efter hjärtinfarkt stärkts. En genomgången hjärtinfarkt innebär en period av sjukskrivning men för en mycket stor andel av fallen är en full återgång till arbete möjlig. Risken för reinfarkt och hjärtsvikt efter hjärtinfarkt är idag låg. Inom vissa yrken kan olika former av hjärtsjukdom vara en riskfaktor för att arbetet utförs sämre eller innebär en risk för tredje person. Särskilda bestämmelser, som kan innebära begränsningar i möjligheterna att återgå i dessa arbeten, gäller därför för yrkesförare, lokförare, piloter, rök- och kemdykare, samt vid arbete med hög höjdskillnad. Det är sannolikt att risken för reinfarkt påverkas av samma riskfaktorer som för primär infarkt. Sammanställningen av olika arbetsmiljöfaktorers betydelse för insjuknande i hjärtkärlsjukdom har visat starka eller måttligt starka belägg för flera exponeringar som är vanliga i dagens arbetsliv. Bland de kemiska arbetsmiljöfaktorerna finns en tydliga tydlig koppling till exponering för bland annat motoravgaser och kvarts (stendamm). Misstankarna är också relativt starka att exponering för svetsrök är förknippat med en ökad risk för hjärtsjukdom. För psykosociala och organisatoriska arbetsmiljöfaktorer finns en ökad risk i samband med exponering för job strain (spänt arbete), och här finns även direkta belägg för att job strain utgör en riskfaktor för reinfarkt. Nattarbete är sannolikt förknippat med en ökad risk för infarkt, men kunskaperna om betydelsen av olika skiftscheman är ofullständig. En ökad risk för hjärtsjukdom har även rapporterats i samband med osäkra anställningar och långa arbetsveckor. Betydelsen av fysiskt tungt arbete för primära infarktrisken är oklar och behöver klarläggas genom ytterligare studier. Exponering för buller i arbetet är förknippat med blodtrycksförhöjning, men beläggen för ett samband med kardiovaskulära sjukdomar är mer svaga. Dagens forskning kring hjärtinfarktpatienter fokuserar mycket på effekten av behandling och rehabilitering för framtida risk medan kunskapsfältet för hur arbetsmiljöfaktorer ökar hälsorisken hos patienter med genomgången infarkt är mycket begränsad. För att fortsätta utveckla hälsosamma arbetsmiljöer efterlyser vi framtida forskning om betydelsen av olika arbetsmiljöfaktorer för risken att återinsjukna i infarkt