Long-term exposure to air pollution is associated with survival following acute coronary syndrome.
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ABSTRACT: Aims
The aim of this study was to determine (i) whether long-term exposure to air pollution was associated with all-cause mortality using the Myocardial Ischaemia National Audit Project (MINAP) data for England and Wales, and (ii) the extent to which exposure to air pollution contributed to socioeconomic inequalities in prognosis.Methods and results
Records of patients admitted to hospital with acute coronary syndrome (ACS) in MINAP collected under the National Institute for Cardiovascular Outcomes Research were linked to modelled annual average air pollution concentrations for 2004-10. Hazard ratios for mortality starting 28 days after admission were estimated using Cox proportional hazards models. Among the 154 204 patients included in the cohort, the average follow-up was 3.7 years and there were 39 863 deaths. Mortality rates were higher for individuals exposed to higher levels of particles with a diameter of ≤2.5 µm (PM2.5; PM, particulate matter): the fully adjusted hazard ratio for a 10 µg/m(3) increase in PM2.5 was 1.20 (95% CI 1.04-1.38). No associations were observed for larger particles or oxides of nitrogen. Air pollution explained socioeconomic inequalities in survival to only a small extent.Conclusion
Mortality from all causes was higher among individuals with greater exposure to PM2.5 in survivors of hospital admission for ACS in England and Wales. Despite higher exposure to PM2.5 among those from more deprived areas, such exposure was a minor contribution to the socioeconomic inequalities in prognosis following ACS. Our findings add to the evidence of mortality associated with long-term exposure to fine particles.
SUBMITTER: Tonne C
PROVIDER: S-EPMC3640199 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundBarriers to healthcare are common in the USA and may result in worse outcomes among hospital survivors of an acute coronary syndrome (ACS).ObjectiveTo examine the relationship between barriers to healthcare and 2-year mortality after hospital discharge for an ACS.DesignLongitudinal study.SettingSurvivors of an ACS hospitalization were recruited from 6 medical centers in central Massachusetts and Georgia in 2011-2013.PatientsStudy participants with a confirmed ACS reported whether they had a financial-related healthcare barrier, no usual source of care, or a transportation-related healthcare barrier around the time of hospital admission.InterventionsNone.MeasurementsCox regression analyses calculated adjusted hazard ratios (aHRs) for 2-year all-cause mortality for the three healthcare barriers while controlling for several demographic, clinical, and psychosocial characteristics.ResultsThe mean age of study participants (n = 2008) was 62 years, 33% were women, and 77% were non-Hispanic white. One third of patients reported a financial barrier, 17% lacked a usual source of care, and 12% had a transportation barrier. Five percent (n = 100) died within 2 years after hospital discharge. Compared to patients without these barriers, those lacking a usual source of care and with barriers to transportation experienced significantly higher mortality (aHRs 1.40, 95% CI 1.30 to 1.51 and 1.46, 95% CI 1.13 to 1.89, respectively). Financial barriers were not associated with all-cause mortality (aHR 0.79, 95% CI 0.60 to 1.06).LimitationsObservational study with other unmeasured potentially confounding prognostic factors.ConclusionsAbsence of an established usual source of care and inconsistent transportation availability were associated with a higher risk for dying after an ACS. Patients with these barriers to follow-up care may benefit from more intensive follow-up and support.
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Project description:BackgroundLong-term exposures to air pollution has been reported to be associated with inflammation and oxidative stress. However, the underlying metabolic mechanisms remain poorly understood.ObjectivesWe aimed to determine the changes in the blood metabolome and thus the metabolic pathways associated with long-term exposure to outdoor air pollution and ambient temperature.MethodsWe quantified metabolites using mass-spectrometry based global untargeted metabolomic profiling of plasma samples among men from the Normative Aging Study (NAS). We estimated the association between long-term exposure to PM2.5, NO2, O3, and temperature (annual average of central site monitors) with metabolites and their associated metabolic pathways. We used multivariable linear mixed-effect regression models (LMEM) while simultaneously adjusting for the four exposures and potential confounding and correcting for multiple testing. As a reduction method for the intercorrelated metabolites (outcome), we further used an independent component analysis (ICA) and conducted LMEM with the same exposures.ResultsMen (N?=?456) provided 648 blood samples between 2000 and 2016 in which 1158 metabolites were quantified. On average, men were 75.0?years and had an average body mass index of 27.7?kg/m2. Almost all men (97%) were not current smokers. The adjusted analysis showed statistically significant associations with several metabolites (58 metabolites with PM2.5, 15 metabolites with NO2, and 6 metabolites with temperature) while no metabolites were associated with O3. One out of five ICA factors (factor 2) was significantly associated with PM2.5. We identified eight perturbed metabolic pathways with long-term exposure to PM2.5 and temperature: glycerophospholipid, sphingolipid, glutathione, beta-alanine, propanoate, and purine metabolism, biosynthesis of unsaturated fatty acids, and taurine and hypotaurine metabolism. These pathways are related to inflammation, oxidative stress, immunity, and nucleic acid damage and repair.ConclusionsUsing a global untargeted metabolomic approach, we identified several significant metabolites and metabolic pathways associated with long-term exposure to PM2.5, NO2 and temperature. This study is the largest metabolomics study of long-term air pollution, to date, the first study to report a metabolomic signature of long-term temperature exposure, and the first to use ICA in the analysis of both.
| S-EPMC7788989 | biostudies-literature
Project description:BackgroundExposure to air pollution has been consistently associated with cardiovascular morbidity and mortality, but mechanisms remain uncertain. Associations with blood pressure (BP) may help to explain the cardiovascular effects of air pollution.ObjectiveWe examined the cross-sectional relationship between long-term (annual average) residential air pollution exposure and BP in the National Institute of Environmental Health Sciences' Sister Study, a large U.S. cohort study investigating risk factors for breast cancer and other outcomes.MethodsThis analysis included 43,629 women 35-76 years of age, enrolled 2003-2009, who had a sister with breast cancer. Geographic information systems contributed to satellite-based nitrogen dioxide (NO2) and fine particulate matter (? 2.5 ?m; PM2.5) predictions at participant residences at study entry. Generalized additive models were used to examine the relationship between pollutants and measured BP at study entry, adjusting for cardiovascular disease risk factors and including thin plate splines for potential spatial confounding.ResultsA 10-?g/m(3) increase in PM2.5 was associated with 1.4-mmHg higher systolic BP (95% CI: 0.6, 2.3; p < 0.001), 1.0-mmHg higher pulse pressure (95% CI: 0.4, 1.7; p = 0.001), 0.8-mmHg higher mean arterial pressure (95% CI: 0.2, 1.4; p = 0.01), and no significant association with diastolic BP. A 10-ppb increase in NO2 was associated with a 0.4-mmHg (95% CI: 0.2, 0.6; p < 0.001) higher pulse pressure.ConclusionsLong-term PM2.5 and NO2 exposures were associated with higher blood pressure. On a population scale, such air pollution-related increases in blood pressure could, in part, account for the increases in cardiovascular disease morbidity and mortality seen in prior studies.
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