Cardiovascular disease burden from ambient air pollution in Europe reassessed using novel hazard ratio functions

European Heart Journal, Journal Year: 2019, Volume and Issue: 40(20), P. 1590 - 1596

Published: Feb. 22, 2019

Ambient air pollution is a major health risk, leading to respiratory and cardiovascular mortality. A recent Global Exposure Mortality Model, based on an unmatched number of cohort studies in many countries, provides new hazard ratio functions, calling for re-evaluation the disease burden. Accordingly, we estimated excess mortality attributed Europe.The functions have been combined with ambient exposure data estimate impacts Europe 28 countries European Union (EU-28). The annual rate from 790 000 [95% confidence interval (95% CI) 645 000-934 000], 659 CI 537 000-775 000) EU-28. Between 40% 80% are due events, which dominate outcomes. upper limit includes events other non-communicable diseases, currently not specified. These estimates exceed analyses, such as Burden Disease 2015, by more than factor two. We that reduces mean life expectancy about 2.2 years annual, attributable per capita 133/100 year.We provide novel suggesting substantially higher previously assumed, though subject considerable uncertainty. Our results imply replacing fossil fuels clean, renewable energy sources could reduce loss pollution.

Language: Английский

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Loss of life expectancy from air pollution compared to other risk factors: a worldwide perspective

Cardiovascular Research, Journal Year: 2020, Volume and Issue: 116(11), P. 1910 - 1917

Published: Jan. 24, 2020

Long-term exposure of humans to air pollution enhances the risk cardiovascular and respiratory diseases. A novel Global Exposure Mortality Model (GEMM) has been derived from many cohort studies, providing much-improved coverage fine particulate matter (PM2.5). We applied GEMM assess excess mortality attributable ambient on a global scale compare other factors.We used data-informed atmospheric model calculate worldwide PM2.5 ozone pollution, which was combined with estimate disease-specific loss life expectancy (LLE) in 2015. Using this model, we investigated effects different sources, distinguishing between natural (wildfires, aeolian dust) anthropogenic emissions, including fossil fuel use. all is estimated at 8.8 (7.11-10.41) million/year, an LLE 2.9 (2.3-3.5) years, being factor two higher than earlier estimates, exceeding that tobacco smoking. The mean rate about 120 per 100 000 people/year much exceeded East Asia (196 000/year) Europe (133 000/year). Without would increase by 1.1 (0.9-1.2) years 1.7 (1.4-2.0) removing potentially controllable emissions. Because dust wildfire emission control impracticable, significant unavoidable.Ambient one main health risks, causing LLE, especially through It causes rivals strongly exceeds violence (all forms together), i.e. order magnitude (LLE 0.3 respectively).

Language: Английский

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Environmental determinants of cardiovascular disease: lessons learned from air pollution

Nature Reviews Cardiology, Journal Year: 2020, Volume and Issue: 17(10), P. 656 - 672

Published: May 7, 2020

Language: Английский

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Updated Cardiovascular Prevention Guideline of the Brazilian Society of Cardiology - 2019

Arquivos Brasileiros de Cardiologia, Journal Year: 2019, Volume and Issue: unknown

Published: Jan. 1, 2019

Introducao A doenca cardiovascular (DCV) e a principal causa de morte no Brasil mundo, determinando aumento da morbidade incapacidade ajustadas pelos anos vida. Embora as taxas mortalidade disability-adjusted life year (DALY) padronizadas por idade estejam diminuindo Brasil, possivelmente como resultado politicas saude bem-sucedidas, o numero total destas esta aumentando principalmente devido ao envelhecimento adoecimento populacao. presenca dos fatores risco classicos (hipertensao, dislipidemia, obesidade, sedentarismo, tabagismo, diabetes [...]

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Fine particulate air pollution and human mortality: 25+ years of cohort studies

Environmental Research, Journal Year: 2019, Volume and Issue: 183, P. 108924 - 108924

Published: Nov. 14, 2019

Much of the key epidemiological evidence that long-term exposure to fine particulate matter air pollution (PM2.5) contributes increased risk mortality comes from survival studies cohorts individuals. Although first two these studies, published in mid-1990s, were highly controversial, much has changed last 25 + years. The objectives this paper are succinctly compile and summarize findings cohort using meta-analytic tools address several controversies. Independent reanalysis substantial extended analysis original have been conducted many additional a wide variety cohorts, including constructed public data leveraging natural experiments published. Meta-analytic estimates mean distribution effects currently available, provide adverse associations with all-cause, cardiopulmonary, lung cancer mortality.

Language: Английский

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Ambient air pollution and cardiovascular diseases: An umbrella review of systematic reviews and meta‐analyses

Journal of Internal Medicine, Journal Year: 2022, Volume and Issue: 291(6), P. 779 - 800

Published: Feb. 9, 2022

Abstract The available evidence on the effects of ambient air pollution cardiovascular diseases (CVDs) has increased substantially. In this umbrella review, we summarized current epidemiological from systematic reviews and meta‐analyses linking CVDs, with a focus geographical differences vulnerable subpopulations. We performed search strategy through multiple databases including articles between 2010 31 January 2021. quality assessment evaluated strength evidence. Of 56 included reviews, most studied outcomes were stroke (22 reviews), all‐cause CVD mortality, morbidity (19). strongest was found higher short‐ long‐term exposure mortality morbidity, stroke, blood pressure, ischemic heart (IHD). Short‐term exposures to particulate matter <2.5 μm (PM 2.5 ), <10 10 nitrogen oxides (NO x ) consistently associated risks hypertension triggering myocardial infarction (MI), (fatal nonfatal). Long‐term PM largely risk atherosclerosis, incident MI, hypertension, mortality. Few other arrhythmias, atrial fibrillation, or failure but they generally reported positive statistical associations. Stronger associations in Asian countries subpopulations, especially among elderly, cardiac patients, people weight status. Consistent experimental data, comprehensive review strong that levels increase IHD. These results emphasize importance reducing alarming across globe, Asia,

Language: Английский

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Oxidative stress pathways of air pollution mediated toxicity: Recent insights

Redox Biology, Journal Year: 2020, Volume and Issue: 34, P. 101545 - 101545

Published: May 23, 2020

Ambient air pollution is a leading environmental cause of morbidity and mortality globally with most the outcomes cardiovascular origin. While numerous mechanisms are proposed to explain link between pollutants events, evidence supports role for oxidative stress as critical intermediary pathway in transduction systemic responses system. Indeed, alterations vascular function step development cardiometabolic disorders such hypertension, diabetes, atherosclerosis. This review will provide an overview impact particulate gaseous on from human animal studies published last five years. We discuss current gaps knowledge date implicating emphasis inhalational exposures. conclude identification gaps, exhortation further elucidate mediated effects.

Language: Английский

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Air pollution and cardiovascular disease: car sick

Cardiovascular Research, Journal Year: 2019, Volume and Issue: unknown

Published: Aug. 20, 2019

Abstract The cardiovascular effects of inhaled particle matter (PM) are responsible for a substantial morbidity and mortality attributed to air pollution. Ultrafine particles, like those in diesel exhaust emissions, major source nanoparticles urban environments, it is these particles that have the capacity induce most significant health effects. Research has shown exposure can many detrimental on system both acutely chronically. This review provides an overview PM pollution, with emphasis ultrafine vehicle exhaust. We consider biological mechanisms underlying postulate dysfunction may be implicated other organ systems. employment multiple strategies tackle especially from vehicles, likely accompanied by improvements health.

Language: Английский

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Environmental Noise-Induced Effects on Stress Hormones, Oxidative Stress, and Vascular Dysfunction: Key Factors in the Relationship between Cerebrocardiovascular and Psychological Disorders

Oxidative Medicine and Cellular Longevity, Journal Year: 2019, Volume and Issue: 2019, P. 1 - 13

Published: Nov. 11, 2019

The role of noise as an environmental pollutant and its adverse effects on health are being increasingly recognized. Beyond direct the auditory system (e.g., hearing loss tinnitus induced by exposure to high levels noise), chronic low-level causes mental stress associated with known cardiovascular complications. According recent estimates World Health Organization, traffic is responsible for a more than 1.5 million healthy life years per year in Western Europe alone, major part related annoyance, cognitive impairment, sleep disturbance. Underlying mechanisms noise-induced centered increased hormone levels, blood pressure, heart rate, which turn favor development cerebrocardiovascular disease such stroke, arterial hypertension, ischemic disease, myocardial infarction. Furthermore, also symptoms psychological disorders depression anxiety, further increase maladaptive coping alcohol tobacco use). From molecular point view, experimental studies suggest that can thereby triggering inflammatory oxidative pathways activation nicotinamide adenine dinucleotide phosphate oxidase, uncoupling endothelial/neuronal nitric oxide synthase inducing endothelial neuronal dysfunction. This review elucidates underlying relationship between disorders, focusing signaling including autonomous nervous endocrine association inflammation, stress, vascular

Language: Английский

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Oxidative Stress: A Unifying Paradigm in Hypertension

Canadian Journal of Cardiology, Journal Year: 2020, Volume and Issue: 36(5), P. 659 - 670

Published: Feb. 25, 2020

The etiology of hypertension involves complex interactions among genetic, environmental, and pathophysiologic factors that influence many regulatory systems. Hypertension is characteristically associated with vascular dysfunction, cardiovascular remodelling, renal stimulation the sympathetic nervous system. Emerging evidence indicates immune system also important activated cells migrate accumulate in tissues promoting inflammation, fibrosis, target-organ damage. Common to these processes oxidative stress, defined as an imbalance between oxidants antioxidants favour leads a disruption oxidation-reduction (redox) signalling control molecular Physiologically, reactive oxygen species (ROS) act molecules cell function through highly regulated redox-sensitive signal transduction. In hypertension, stress promotes posttranslational modification (oxidation phosphorylation) proteins aberrant consequent tissue Many enzymatic systems generate ROS, but NADPH oxidases (Nox) are major sources heart, vessels, kidneys, Expression activity Nox increased responsible for disease. Here we provide unifying concept where common mediator underlying hypertension. We focus on some novel concepts whereby ROS function, aldosterone/mineralocorticoid actions, immunoinflammation, all contributing development

Language: Английский

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