Traffic-related environmental noise represents a widespread and relevant environmental factor in Europe that is associated with a substantial burden of disease. Current estimates indicate that a significant proportion of the population is exposed to noise levels linked to adverse health effects. Cardiovascular diseases are among the most extensively studied outcomes in this context. Epidemiological studies consistently demonstrate associations between long-term exposure to traffic noise and an increased risk of arterial hypertension, ischemic heart disease, myocardial infarction, heart failure and arrhythmias. These associations are often dose-dependent and also remain even after adjustment for air pollution. Experimental human studies provide complementary mechanistic evidence, showing that even short-term noise exposure can impair endothelial function, activate autonomic stress responses and disrupt sleep. Underlying mechanisms include activation of the sympathetic nervous system, dysregulation of the hypothalamic-pituitary-adrenal axis, oxidative stress and inflammatory processes. Overall, the available evidence supports a stronger consideration of traffic noise as a modifiable risk factor for cardiovascular disease. In addition to individual-level measures to reduce exposure, population-based strategies for noise reduction are essential.

Abstract:Nicotine is an independent and frequently underestimated cardiovascular risk factor. While prevention strategies have long focused on tobacco smoke and combustion products, current evidence clearly shows that nicotine itself is vasculotoxic, regardless of the delivery mode. Through sympathetic activation, blood pressure elevation, oxidative stress, endothelial dysfunction, and prothrombotic effects, nicotine drives the initiation and progression of cardiovascular disease. Most nicotine-associated mortality is cardiovascular and often occurs earlier than cancer outcomes. New nicotine products such as e-cigarettes, heat-not-burn devices, and oral nicotine pouches do not reduce this risk but increasingly shift exposure toward younger populations. A consistent, product-spanning early warning signal is the endothelial dysfunction, a validated predictor of future cardiovascular events, which is reversible only with complete nicotine abstinence. Unified, risk-based regulation of all nicotine-containing products is therefore a central pillar of effective cardiovascular prevention.

Loneliness has emerged as a significant and independent risk factor for cardiovascular disease (CVD), with epidemiological studies reporting an estimated 15%–30% increased risk across diverse populations and settings. This review synthesizes current evidence linking loneliness to major cardiovascular outcomes including coronary artery disease, heart failure, stroke, and all-cause mortality. This review is organized using a bio-psycho-social framework, examining biological mechanisms, psychological vulnerability, and social determinants contributing to cardiovascular risk. Within this framework, we examine biological mechanisms underlying this association, including chronic activation of stress response systems (hypothalamic–pituitary–adrenal axis and sympatho-adrenomedullary system), endothelial dysfunction, systemic inflammation, oxidative stress, and sleep disturbances. Among patients with established CVD, loneliness is highly prevalent (36%–45%) and associated with poor prognosis, reduced treatment adherence, and lower cardiac rehabilitation participation. We outline practical approaches for screening loneliness in clinical settings and discuss intervention strategies addressing social, emotional, and cognitive pathways. Recognition of loneliness as a modifiable cardiovascular risk factor represents an important opportunity for comprehensive patient care and secondary prevention strategies.

Healthy soils and clean water are essential for human survival, yet, both are increasingly compromised by chemical and plastic pollution. This preventable crisis causes an estimated 9 million premature deaths each year, including about 0.9 million linked to soil pollution and 1.3 million to water pollution. In 2019 alone, pollution contributed to 5.5 million cardiovascular deaths, underscoring its role in the global burden of non-communicable disease. A key underrecognized driver is the rapid rise in plastic production and plastic-associated chemicals. Global plastic output has increased more than 250-fold since 1950 and is projected to nearly triple by 2060, while less than 10% is effectively recycled. As highlighted by the Lancet Countdown on health and plastics, plastics threaten human health across their lifecycle, from fossil fuel extraction to waste, fragmentation, and environmental persistence. Soils and water systems are increasingly contaminated by heavy metals, pesticides, persistent synthetic chemicals, and micro- and nanoplastics. These pollutants degrade soil, reduce agricultural productivity, contaminate food chains, and spread through aquatic ecosystems, thereby amplifying disease risk. Micro- and nanoplastics have been detected in human blood, placenta, brain, and cardiovascular tissues, raising concern about biological effects. These exposures are drivers of cardiovascular disease. Despite their chemical diversity, they converge on shared mechanisms, including oxidative stress, inflammation, endocrine disruption, and circadian dysregulation. Their persistence reflects policy failure. Reducing soil, water, and plastic pollution must become a central pillar of cardiovascular prevention through enforceable, lifecycle-based policies that protect human health. #These authors contributed equally and should be considered as joint first and joint last authors.

Die Umgebungsluftverschmutzung ist einer der führenden modifizierbaren umweltbedingten Determinanten der kardiovaskulären Morbidität und Mortalität weltweit. Langfristige wie kurzfristige Exposition gegenüber Feinstaub und verkehrsbedingten Schadstoffen ist konsistent mit einem erhöhten Risiko für ischämische Herzkrankheit, Schlaganfall, Herzinsuffizienz, Arrhythmien und kardiovaskulären Tod assoziiert. Mechanistische Studien zeigen, dass inhalierte Schadstoffe pulmonalen und systemischen oxidativen Stress, Inflammation, endotheliale Dysfunktion, autonome Dysregulation und prothrombotische Veränderungen induzieren und damit eine biologische Plausibilität für diese Assoziationen liefern. Luftverschmutzung wirkt selten isoliert, sondern tritt typischerweise gemeinsam mit anderen Umweltstressoren wie Verkehrslärm, Hitze und eingeschränktem Zugang zu Grünflächen auf und betrifft überproportional sozioökonomisch benachteiligte und medizinisch vulnerable Gruppen. Diese Übersichtsarbeit fasst die aktuelle Evidenz zu den kardiovaskulären Effekten der Luftverschmutzung zusammen, hebt Hochrisikogruppen hervor und diskutiert klinische, bevölkerungsbezogene und gesundheitspolitische Strategien zur Reduktion von Exposition und Vulnerabilität. Wir argumentieren, dass die zeitgemäße kardiovaskuläre Prävention sich an aktuellen Befunden der Umweltgesundheitsforschung orientieren und sich an Verkehrs‑, Energie- und Städteplanung sowie die entsprechende Gesetzgebung anlehnen muss, um vulnerable Patientinnen, Patienten und Gemeinschaften effektiv zu schützen.

The microbiota shapes postnatal gut development and physiology. In the small intestine, epithelial-to-endothelial crosstalk governs the microbiota-induced remodeling of villus capillary networks essential for nutrient transport. The intestinal epithelial enzyme dual oxidase-2 (DUOX2), an established regulator of the microbiome-host interaction, exerts microbicidal functions through the generation of reactive oxygen species. However, its role in intestinal vascular development remains poorly understood. Here, we demonstrate a Toll-like receptor-2 (TLR2)-dependent regulatory pathway controlling DUOX2 expression that influences villus vascularization in the small intestine. Mice globally lacking DUOX2 activity exhibited a notable reduction in vascularization in the small intestine, accompanied by alterations in gut microbial community structure. Conversely, mice with an intestinal epithelial-specific deficiency of TLR2 displayed an increase in villus vascularization along with elevated expression levels of DUOX2. Notably, DUOX2 expression was strongly upregulated in intestinal epithelial biopsies from patients with Crohn’s disease. Similarly, inflammatory conditions induced by dextran sulfate sodium (DSS) treatment in mice resulted in increased epithelial Duox2 expression accompanied by enhanced villus vascularization. Together, our findings suggest a microbiota–TLR2–DUOX2 signaling axis in intestinal epithelial cells that promotes villus vascularization. This mechanism links microbial sensing in the intestinal epithelium to structural remodeling of the villus microvasculature during homeostasis and inflammation.

AIMS: Ultrafine particles (UFPs) smaller than 100 nm are ubiquitous in polluted air. Although they carry little mass, UFPs have a large exposure surface area, can bypass respiratory defences, translocate into the brain and bloodstream, and impact the heart and other organs. Here, we assess the role of UFPs in air quality and the health burden they impose. METHODS AND RESULTS: We integrated Earth observations with machine learning to estimate long-term UFP exposure at 1 km resolution, demonstrating that they pose a major air quality concern in urban environments, with annual mean concentrations typically ranging between 10,000 and 30,000 particles/cm-3. Model calculations suggest that black and organic carbon are primary components of pollution UFPs. Based on a meta-analysis of epidemiological cohort studies in Europe and North America, we derived a pooled hazard ratio for mortality and combined it with our UFP data. We estimate a mortality density of 35.7 (15.8-65.5) per 100,000 people annually in Europe, and 27.4 (12.9-47.4) per 100,000 in North America, the latter being close to the global mean. We find that UFP exposure and mortality densities are particularly high in South and Eastern Europe. Since observational data for other regions are limited, global calculations primarily depend on modelling. We indicatively estimate that 1.99 (0.81-3.89) million excess deaths per year are attributable to UFP exposure. This could account for approximately 5% of total mortality from non-communicable diseases, to a large degree (about half) due to cardiovascular conditions. Globally, about 91% of UFP-related excess mortality occurs in urban and suburban environments, and much of that (78%) in densely populated urban areas. CONCLUSION: Health-improving interventions should target combustion sources in cities, particularly those related to energy consumption, industry, and traffic. An annual air quality limit of 5,000 cm-3 could reduce global excess mortality by about 45%.

Environmental pollution-including air, noise, and light-and progressive climate change are major contributors to global health burdens, responsible for over 9 million premature deaths annuallysa. Among environmental exposures, air and noise pollution show the strongest epidemiological links to hypertension and cardiovascular disease, while emerging evidence also implicates light pollution, toxic metal exposure, and climate-related factors. Hypertension, the leading global cause of mortality, is increasingly recognized as a sentinel marker of environmental damage. Fine particulate matter (PM2.5) and road traffic noise exposure are associated with significant increase in hypertension prevalence and incidence. While historical guidelines overlooked environmental contributors, recent updates by the European Society of Hypertension (ESH) and European Society of Cardiology (ESC) have integrated environmental risk factors into hypertension management frameworks. This position paper from the ESH Working Group on Environment and Hypertension synthesizes current evidence on the epidemiology and pathophysiology of environmental pollution in the development of hypertension. It highlights the mechanistic pathways involving oxidative stress, vascular dysfunction, and neurohormonal dysregulation triggered by pollution exposure. Importantly, the paper outlines mitigation strategies at both population and individual levels, including legislative initiatives, urban planning, and personal exposure reduction techniques. Considering hypertension as an early manifestation of environmental harm offers a critical opportunity for preventive intervention. It is vital to emphasize strict blood pressure control, enhanced screening in high-risk populations and the integration of environmental exposure monitoring into clinical practice. This comprehensive document seeks to raise awareness among healthcare professionals and inform evidence-based strategies for reducing pollution-related hypertension and cardiovascular morbidity.

Tobacco use and emerging nicotine-delivery systems remain major, preventable drivers of cardiovascular disease worldwide. Although tobacco cigarette smoking has declined in some high-income regions, progress is uneven, with persistently high rates across parts of Europe, alongside rapidly expanding global markets for e-cigarettes, heated-tobacco products and oral nicotine formulations. Youth addiction to nicotine-containing products has emerged as an urgent public health challenge, as engineered e-cigarette devices delivering large nicotine doses facilitate early dependence and might establish lifelong exposure trajectories. Regulatory frameworks have not kept pace with this innovation, allowing new platforms to enter markets faster than safety evidence can mature. Leading cardiovascular societies and regulatory authorities agree that no nicotine-containing product can be safe for the cardiovascular system. Nicotine promotes sympathetic activation, haemodynamic stress, oxidative imbalance and inflammation, and endothelial nitric oxide synthase uncoupling and dysfunction, contributing to atherosclerotic plaque instability in animal models and humans. Studies in humans demonstrate adverse vascular responses across all nicotine-containing products, although interpreting studies requires caution and long-term outcome data are lacking. In this Review, we integrate mechanistic, biomarker, preclinical and clinical data to define a cardiovascular continuum of harm from nicotine-containing products, in which eliminating combustion reduces but does not eliminate vascular toxicity.

Umweltbedingte Risikofaktoren sind heute als wesentliche Determinanten der kardiovaskulären Krankheitslast anerkannt, aber bislang wenig in den klinischen Leitlinien repräsentiert. Externe Umweltexpositionen, wie Luftverschmutzung, Verkehrslärm, Hitze, Lichtverschmutzung, chemische Kontamination von Boden und Wasser, sowie die Stadtplanung, unser soziales Umfeld und Lebensstil tragen maßgeblich zur globalen Krankheitslast und vorzeitigen Todesfällen bei. Vor allem die Herz-Kreislauf-Morbidität und -Mortalität wird maßgeblich von diesen Umweltstressoren beeinflusst. Das Exposom-Konzept bietet dafür einen übergeordneten Rahmen, indem es lebenslange externe Expositionen mit Veränderungen in biologischen Prozessen, wie oxidativem Stress, Entzündungsreaktionen, Gefäßschäden, metabolischen Entgleisungen und Störung der zirkadianen Steuerung, unserer inneren Uhr, und daraus resultierenden chronischen Erkrankungen und Todesfällen assoziiert. Umweltexpositionen erhöhen nicht nur das Risiko für chronische Erkrankungen in gesunden Menschen, sondern verstärken klassische Risikofaktoren, verschlechtern die Prognose vulnerabler Gruppen und eröffnen so konkrete Präventions- und Interventionsmöglichkeiten in der ambulanten und stationären Versorgung. Praktisch tätige Kardiologinnen und Kardiologen können Umweltbelastungen systematisch in die Anamnese integrieren, besonders gefährdete Personen identifizieren, verhaltensbezogene Schutzmaßnahmen empfehlen, interdisziplinär mit Hausärzten und Arbeitsmedizinern zusammenarbeiten und sich zugleich gesundheitspolitisch für herzgesündere Lebenswelten einsetzen. Diese Übersichtsarbeit fasst die aktuelle Evidenz zu den Auswirkungen des Exposoms auf die Herz-Kreislauf-Gesundheit zusammen und leitet daraus Empfehlungen für Kardiologen ab. Ziel ist es, das Exposom aus der Perspektive der täglichen Versorgung zu betrachten: von der Risikostratifikation über patientennahe Interventionen bis hin zu strukturellen Maßnahmen auf Ebene von Praxis, Klinik und Gesellschaft.

Environmental risk factors-air pollution, noise, heat, chemical contamination, and light pollution-are increasingly recognized as key contributors to cardiovascular disease but remain underrepresented in clinical guidelines and public health strategies. This comprehensive review, developed under the auspices of the European Society of Cardiology (ESC), synthesizes current evidence on the cardiovascular consequences of environmental exposures. Building on prior ESC recommendations on air pollution, the consensus statement extends the focus to include climate change, urban heat islands, chemical pollutants, noise, and light pollution, highlighting their shared pathophysiological mechanisms: oxidative stress, inflammation, endothelial dysfunction, and circadian disruption. Epidemiological and experimental studies confirm that these exposures exacerbate the incidence of coronary artery disease, stroke, heart failure, arrhythmias, and hypertension-even at levels below existing regulatory thresholds. It is proposed the exposome framework as a conceptual tool to understand the cumulative lifetime impact of environmental hazards on cardiovascular health. Special attention is given to vulnerable populations, including children, the elderly, socioeconomically disadvantaged groups, and patients with pre-existing cardiovascular disease. The document outlines urgent research needs, such as the need for high-resolution exposure data, exploration of gene-environment interactions and molecular pathways, and the development of real-world and mechanistic studies assessing interventions. Mitigation strategies are discussed across individual, clinical, and policy levels, with a call for heart-healthy urban design, stricter emissions legislation, and equitable access to clean environments. Cardiologists are uniquely positioned to advocate for environmental cardiovascular health, bridging the gap between science, clinical care, and policy. This statement aims to accelerate that translation by raising awareness and promoting action across disciplines.

Air pollution remains a significant global health challenge and is increasingly recognized as a critical exposomic risk factor for adverse birth outcomes. Although numerous epidemiological studies have linked prenatal air pollution exposure to low birth weight, preterm birth, and stillbirth, important uncertainties remain regarding the underlying biological mechanisms, critical exposure windows, and the interplay between different pollutants and susceptibility factors. This narrative review synthesizes epidemiological findings and mechanistic evidence identified through literature searches in PubMed, Scopus, and Web of Science to provide a comprehensive overview of how maternal exposure to air pollutants affects fetal development and pregnancy outcomes. The reviewed epidemiological evidence largely supports an association between maternal air pollution exposure and adverse birth outcomes. For example, a 10 µg/m3 increase in fine particulate matter (PM2.5) exposure during the second trimester has been associated with an 11.8 g reduction in birth weight and a 23.1

Environmental risk factors are recognized as essential determinants of the cardiovascular disease burden but are still poorly represented in clinical guidelines. External environmental exposures such as air pollution, traffic noise, heat, light pollution, chemical contamination of soil and water as well as urban planning, our social environment and lifestyle contribute significantly to the global disease burden and premature deaths. In particular, cardiovascular morbidity and mortality are significantly influenced by these environmental stressors. The exposome concept provides an overarching framework for this by associating lifelong external exposures with changes in biological processes such as oxidative stress, inflammatory responses, vascular damage, metabolic dysregulation, disturbances of circadian regulation, our circadian clock, and the resulting chronic diseases and deaths. Environmental exposures not only increase the risk of chronic diseases in healthy individuals but also amplify classic risk factors, worsen the prognosis for vulnerable groups, and thus open concrete prevention and intervention opportunities in outpatient and inpatient care. Practicing cardiologists can systematically integrate environmental exposures into medical history taking, identify particularly at-risk individuals, recommend behavior-related protective measures, work interdisciplinarily with general practitioners and occupational physicians, and at the same time advocate for heart-healthier living environments in health policy. This review summarizes the current evidence on the impact of the exposome on cardiovascular health and derives recommendations for cardiologists from it. The goal is to view the exposome from the perspective of daily care: from risk stratification to patient-centered interventions to structural measures at the level of practice, clinic, and society.

The exposome refers to the total environmental exposures a person encounters throughout life, and its relationship with human health is increasingly studied. This non-systematic review focuses on recent research investigating the effects of environmental factors—such as air pollution, noise, greenspace, neighborhood walkability, and metallic pollutants—on atherosclerosis, a major cause of cardiovascular disease. Studies show that long-term exposure to airborne particulate matter can impair endothelial function and elevate adhesion molecule levels, leading to vascular damage. Nighttime traffic noise also negatively impacts endothelial health. On the other hand, living in areas with more greenspace and better neighborhood walkability is linked to reduced arterial stiffness, suggesting protective cardiovascular effects. Mechanisms involved include oxidative stress, inflammation, and sympathetic activation from air pollution and noise. Metallic pollutants, including lead, cadmium, and arsenic, are linked to early signs of atherosclerosis through mechanisms involving oxidative stress. However, the effects of specific pollutants and their interactions remain incompletely understood. There is a growing need to mitigate harmful environmental exposures, such as air pollution and noise, while promoting beneficial ones like greenspace, to improve cardiovascular health. Emerging technologies like remote sensing and artificial intelligence can help further our understanding of how the exposome influences cardiovascular outcomes. More research is necessary to clarify the impact of specific pollutants as well as their interactions and how they contribute to atherosclerosis.

Environmental stressors in the modern world can fundamentally affect human physiology and health. Exposure to stressors like air pollution, heat, and traffic noise has been linked to a pronounced increase in non-communicable diseases. Specifically, aircraft noise has been identified as a risk factor for cardiovascular and metabolic diseases, such as arteriosclerosis, heart failure, stroke, and diabetes. Noise stress leads to neuronal activation with subsequent stress hormone release that ultimately activates the renin-angiotensin-aldosterone system, increases inflammation and oxidative stress thus substantially affecting the cardiovascular system. However, despite the epidemiological evidence of a link between noise stress and metabolic dysfunction, the consequences of exposure at the molecular, metabolic level of the cardiovascular system are largely unknown. Here, we use a murine model system of short-term aircraft noise exposure to show that noise stress profoundly alters heart metabolism. Within 4 days of noise exposure, the heart proteome and metabolome bear the hallmarks of reduced potential for generating ATP from fatty-acid beta-oxidation, the tricarboxylic acid cycle, and the electron transport chain. This is accompanied by the increased expression of glycolytic metabolites, including the end-product, lactate, suggesting a compensatory shift of energy production towards anaerobic glycolysis. Intriguingly, the metabolic shift is reminiscent of what is observed in failing and ischaemic hearts. Mechanistically, we further show that the metabolic rewiring is likely driven by reactive oxygen species (ROS), as we can rescue the phenotype by knocking out NOX-2/gp91phox, a ROS inducer, in mice. Our results suggest that within a short exposure time, the cardiovascular system undergoes a fundamental metabolic shift that bears the hallmarks of cardiovascular disease. These findings underscore the urgent need to comprehend the molecular consequences of environmental stressors, paving the way for targeted interventions to mitigate health risks associated with chronic noise exposure in modern, environments heavily disturbed by noise pollution.

Chronic non-communicable diseases (NCDs) account for 2/3 of global deaths annually, primarily due to an aging population and external risk factors such as air/water/soil pollution, traffic noise, mental stress, and climate change emanating from the environment. These factors contribute to premature deaths and loss of healthy life years, as reflected by disability-adjusted life years. The exposome concept was proposed 16 years ago as a new research field to investigate environment-health associations, also by considering the underlying pathophysiological pathways. The exposome describes lifelong environmental exposures, besides pollutants also socioeconomic and lifestyle factors, aiming to explain the associated diseases and deaths. The exposome can be divided into the specific and general external environment and further subcategories such as organ-specific exposomes as well as spatially and temporally restricted pollutomes. The exposome also shows considerable interaction with genetic predisposition and pre-established chronic diseases, characteristics of the vulnerable groups. The present overview provides background information on the impact of the environment on health and disease by considering recent data of the Global Burden of Disease Study. We also explain the exposome concept with the help of selected studies, briefly describe how the exposome is measured, and discuss biomarkers identified by exposomic research and their impact on the development and progression of atherosclerosis. Major pathophysiological pathways comprise exacerbated stress hormone signaling, oxidative stress, inflammation and circadian rhythm dysregulation promoting impairment of cardiometabolic function. The present overview highlights the relevance of the exposome for future health research and preventive medicine, especially concerning cardiovascular diseases and therapy.