Publications

• Air pollution remains a significant global health challenge and is increasingly recognized as a critical exposomic risk factor for adverse birth outcomes.
• What are the underlying biological mechanisms, and the critical exposure windows between prenatal air pollution exposure and low birth weight, preterm birth, and stillbirth?
• This new epidemiological review supports an association between maternal air pollution exposure and adverse birth outcomes
• A striking example: a 10 µg/m³ increase in fine particulate matter (PM_2.5) exposure during the second trimester has been associated with an 11.8 g reduction in birth weight and a 23.1% increase in the risk of preterm birth.
• Air pollution exposure linked to changes in placental morphology, perfusion, and metabolic function. Oxidative stress, inflammation, endocrine disruption, vascular dysfunction, and epigenetic modifications are considered key biological pathways through which air pollution may impair placental function.

This research has been made possible through a collaboration with the Department of General Paediatrics & Neonatology: The Children’s Hospital at Saarland University Hospital.

Read the full text here.

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.

Ischemic stroke is a leading cause of global morbidity and mortality, with seasonal variations potentially influencing both outcomes. While previous studies have suggested a pronounced association of the cold months with increased stroke morbidity and mortality, the evidence remains limited and inconsistent. This study aimed to assess seasonal variations in ischemic stroke hospital admissions and in-hospital case-fatality and complications in Germany over an 18-year period. This nationwide retrospective analysis included a total of 4,236,789 ischemic stroke hospitalizations in Germany between 2005 and 2022. Patients were categorized by season of hospital admission (winter, spring, summer, autumn). While ischemic stroke hospital admissions remained stable across seasons, in-hospital case-fatality was significantly increased during winter compared to summer. These findings highlight the need for targeted seasonal prevention and management strategies.

Noise pollution, particularly by aircraft, is a significant risk factor for cardiovascular disease. Aircraft noise activates stress response pathways in the brain, via the amygdala, the sympathetic nervous system and the hypothalamic–pituitary–adrenal axis. Male C57BL/6J mice were treated with citalopram (a selective serotonin (5-HT)-reuptake inhibitor) or diazepam (a benzodiazepine) 1 day before aircraft noise exposure for 4 days. In support of the stress response concept, we report here that noise exposure of mice implicates an increase in activity primarily in the left amygdala. Both neuro-active drugs, diazepam and citalopram, ameliorated the adverse cardiovascular and neurobiological effects of noise exposure, partially preventing blood pressure increases and endothelial dysfunction in both large (aorta) and small vessels (cerebral arterioles). Diazepam showed slightly greater efficacy. Noise exposure also increased markers of oxidative stress and inflammation in the heart and brain (cortex and hippocampus), and both drugs mostly prevented these pathophysiological changes. The study provides indirect evidence that modulating the stress response pathway may represent a pharmacological approach to mitigate the negative effects of noise exposure. 

Glioblastomas are the most prevalent and aggressive malignant brain tumors, characterized by hypertranscription and dependence on neurodevelopmental transcription factors. The transcriptional cycle is regulated by phosphorylation of the C-terminal domain (CTD) of RNA polymerase II (RNAPII) by transcriptional cyclin-dependent kinases (tCDKs), including CDK7, CDK9, CDK12, and CDK13. Here we find that glioblastoma stem cells (GSCs) are selectively sensitive to CDK12/CDK13 inhibition, whereas CDK7 and CDK9 inhibition cause non-specific cytotoxicity. This selective targeting halts GSC and organoid proliferation, curtails GSC invasion and suppresses tumor growth in a xenograft mouse model. In GSCs, CDK12/CDK13 inhibition leads to a rapid and genome-wide loss of serine-2 phosphorylation (pSer2) of the RNAPII CTD, abolishing transcriptional elongation and a transcriptional program sustained by key neurodevelopmental transcription factors. CDK12/CDK13 inhibition unexpectedly arrests DNA replication and replication fork progression in a manner distinct from the effect of inhibiting other tCDKs. This dramatic arrest precedes DNA damage response activation and cell cycle arrest, directly linking RNAPII elongation to replication fork dynamics and revealing a previously unrecognized dependence of DNA replication on CDK12/CDK13-RNAPII regulation.

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.

• In their recent report, the European Environment Agency’s (EEA) Environmental Noise in Europe 2025 report delivers an urgent message: transport noise is a major cardiovascular risk factor with significant public health, environmental, and economic consequences.
• Noise activates the sympathetic nervous system and the hypothalamic–pituitary–adrenal axis, releasing stress hormones that elevate blood pressure and heart rate. This neurohormonal storm induces oxidative stress and over time, these pathways accelerate hypertension, atherosclerosis, and heart failure - a progression comparable in magnitude to air pollution and smoking.
• For cardiologists, this report is not merely environmental; it is a cardiovascular call to action. The mechanistic evidence linking noise to endothelial dysfunction, oxidative stress, and inflammation is now robust and causal. Therefore, noise deserves equal attention to smoking cessation or hypertension management in clinical prevention strategies.

This invited editorial refers to ‘Cardiovascular disease averted by China’s clean air act and the potential benefit of further air pollution intervention: evidence based on the parametric G-computation’, by J. Xie et al., https://doi.org/10.1093/ eurjpc/zwag039.

International guidelines for the management of arterial hypertension fail to consider environmental pollutants as risk factors for the development of the disease and its cardiovascular complications. The reasoning behind this may stem from the failure to acknowledge compelling evidence from research on the cardiovascular effects of environmental pollution. In this narrative review, we summarize the effects of environmental air pollution and noise on individuals with arterial hypertension. We explore how these pollutants interact with other environmental and individual risk factors and discuss why such individuals should be considered a vulnerable group. We also discuss local studies to help national authorities adjust international recommendations to better fit the local context. In summary, national recommendations for managing hypertension should encompass more than just blood pressure goals and prescribed antihypertensive medications. Clinicians should recommend evidence-based behavioral changes related to environmental issues to individuals with arterial hypertension. These changes can help people with arterial hypertension control their blood pressure; delay adverse cardiovascular outcomes; and enhance the effectiveness of antihypertensive medications during episodes of poor air quality, environmental noise exposure, exposure to extremely cold or warm weather, or any combination of these risk factors. Guidelines must be adapted to account for environmental pollution, social factors, cultural norms, patient preferences, equity concerns, patient lifestyle, the healthcare system, and the economic situation in the region.

• This new randomised, double-blind crossover study of 74 healthy participants shows that a single night of road traffic noise can have measurable impacts on health.
• Participants exposed to nighttime traffic noise, typical of those living in a city, experienced impaired blood vessel function, raised heart rate, and blood protein changes linked to inflammation and stress responses.
• The findings, published in the journal Cardiovascular Research, could help explain why people exposed to long-term traffic noise have higher rates of high blood pressure and heart disease. The findings support calls for stricter noise regulation to improve cardiovascular health.

• The concentration of ultrafine particles (UFP) vary a lot depending on where and when they are measured. Due to their small size, UFPs can reach deep into the lungs and enter the bloodstream, potentially causing long term harm.
• Switzerland has contributed substantially to UFP research through measurement campaigns, mobile monitoring, and modelling studies.
• New research suggests that breathing in ultrafine particles over many years may affect heart health. However, there is still little strong evidence that short term exposure clearly increases the risk of illness or death.
• Ongoing Swiss and European projects, such as the MARKOPOLO project, aim to refine high-resolution spatiotemporal models, assess health impacts, and inform future air quality standards and regulatory frameworks for UFPs.

A review study by MARKOPOLO partners from the University Medical Center Mainz shows how environmental and living conditions shape the development and course of heart failure.

• The study looked at whether very small air pollution particles and everyday noise exposure can increase the risk of heart disease and metabolic problems. A few recent studies have associated ultrafine particulate matter (UFP) with metabolic disorders, contributing to cardiovascular disease, however, evidence is inconsistent.
• Researchers first examined 1,000 adults in one city to understand how pollution and noise in their living environment relate to their health, using location data and health measurements.
• A smaller group then took part in a short lifestyle program. This included simple changes like spending more time being active in green spaces and following a Mediterranean-style diet, to see if these habits can quickly improve health.
• This clinical trial with an interdisciplinary approach can provide new insights by evaluating the combined impact of UFP and noise on the indicators of metabolic syndrome and the effects of short-term lifestyle interventions, such as promoting physical activity in green spaces and healthy diets. It can strengthen the evidence base for pollution-disease associations and provide practical recommendations for reducing the burden of metabolic disorders and cardiovascular diseases.

Published in the European Heart Journal by European Society for Cardiology.

Published in the Global Heart Journal by World Heart Federation.

Published in the Journal of the American College of Cardiology (JACC). 

Published in Circulation, a journal by the American Heart Association.

• Particulate matter (PM) is a significant contributor to air pollution-associated negative health effects, and cardiovascular disease patients are more susceptible to air pollutionmediated damage of the heart and vessels. 
• This study investigated the protective effects against PM-induced cardiovascular damage by classic cardiovascular drugs. In mice, the cholesterol‑lowering drug atorvastatin and the ACE‑inhibitor captopril both reduced PM‑induced blood‑pressure spikes and partly restored endothelial health.
• Both drugs lowered harmful reactive‑oxygen‑species (ROS) production and decreased vascular NOX‑2 (a key enzyme that drives oxidative damage) caused by PM exposure. However, only a limited anti‑inflammatory impact was seen. Only captopril showed modest anti‑inflammatory effects in heart and lung tissue, while neither drug significantly lowered systemic inflammation in the plasma.
• These findings offer new insights into potential mitigation strategies for PM2.5-induced cardiovascular complications, particularly for patients at higher cardiovascular risk, like those with coronary artery or ischemic heart disease or hypertension.

• Transportation noise from road, rail, and aircraft traffic is now recognized as a major cardiovascular risk factor. In Europe, more than 113 million people are chronically exposed to levels above 55 dB(A), resulting in an estimated 1.3 million healthy life-years lost annually from traffic-related noise.
• Environmental noise triggers a cascade of biological stress responses that link chronic exposure to cardiovascular disease. Noise-induced activation of the brain’s stress path-ways leads to the release of catecholamines and glucocorticoids, oxidative stress, inflammation, and endothelial dysfunction. These mechanisms are further amplified by sleep disruption, circadian rhythm disturbance, and epigenetic modifications.
• The resulting vascular injury promotes hypertension, cardiac remodeling, and metabolic dysfunction, ultimately contributing to ischemic heart disease, stroke, heart failure, and increased cardiovascular mortality.
• Combined exposure to noise and air pollution further exerts additive or synergistic effects, underscoring the value of the exposome concept in identifying vulnerable populations. Transportation noise should therefore be considered an established cardiovascular risk factor, requiring equal priority in prevention guidelines and public health policy.

• Atmospheric pollution causes millions of excess deaths annually, with particulate matter (PM) being a major concern. While research has traditionally focused on PM, ultrafine particles (UFPs, diameter < 100 nm) have emerged as a critical human health risk due to their ability to penetrate deeply into the respiratory system, transmigrate into the bloodstream and induce systemic health impacts.
• This study delivers the first high-resolution global maps (1 km) of these particles by combining ground measurements with advanced machine-learning models (XGBoost model). The model reliably predicts particle number concentrations worldwide, showing strong contrasts: from just a few thousand particles per cubic centimeter in clean regions to over 40,000 in major cities.
• With ultrafine particles making up around 91% of all airborne particle counts, these new datasets offer a crucial foundation for better exposure studies and more accurate assessments of pollution-related health risks.

Keywords: Obesity, Aircraft Noise, Diabetes, Empagliflozin, Cardiovascular Complications, Metabolism, Oxidative Stress

• Noise as a cardiovascular risk factor: Environmental noise from road, rail, and air traffic is now firmly established as a major, widespread contributor to cardiovascular disease (CVD). Roughly one in three Europeans is chronically exposed to noise levels exceeding WHO guideline thresholds, significantly driving cardiovascular morbidity and mortality.
• Health outcomes: Strong meta-analytic evidence links transportation noise to ischemic heart disease, heart failure, stroke, hypertension, and type 2 diabetes. Experimental and clinical data implicate sympathetic nervous system activation, oxidative stress, inflammation, endothelial dysfunction, and circadian rhythm disruption as core biological pathways.
• The review calls for integrating noise into cardiovascular prevention strategies, emphasizing urban planning, public health policy, and clinical practice.
• Noise should be recognized and managed as a full-fledged cardiovascular risk factor, on par with established risks like smoking or hypertension.

• A commentary related to MARKOPOLO.

• Chronic traffic noise activates stress hormone pathways, disrupts sleep, and induces hypertension and vascular inflammation.
• Air pollution, fine particulate matter, particularly ultrafine particles (PM₂.₅, UFP), can penetrate deep into the lungs, enter the bloodstream, and promote oxidative stress, endothelial injury, and atherosclerosis.
• Increasingly frequent heatwaves place particular strain on elderly individuals and those with pre-existing cardiovascular disease. In cities, impervious surfaces and lack of greenery exacerbate “heat island” effects, increasing the risk of myocardial infarction and stroke.
• Persistent chemical pollutants such as pesticides, heavy metals, and PFAS (per- and polyfluoroalkyl substances), which degrade slowly or not at all, can enter the body through food and drinking water. Early studies suggest they can enhance inflammation, impair vascular function, and elevate long-term cardiovascular risk.

• A commentary related to MARKOPOLO.

• Circadian rhythms influence cardiovascular function and disease progression, shaping daily patterns in events like myocardial infarction, heart failure, and arrhythmias.
• Autonomic balance shifts over 24 hours, with parasympathetic dominance during sleep and sympathetic activation during the day, affecting cardiac recovery and stress response.
• Despite dampened rhythms in heart failure, circadian cycles remain present - offering potential for time-adapted diagnostics and therapies.
• Chronotherapy emerges as a promising approach to enhance cardiovascular treatment efficacy by aligning interventions with biological timing.

• A commentary on physical activity and air pollution.

• Environmental exposures like noise and air pollution are significant, modifiable risk factors for cardiovascular disease (CVD), acting alongside classic and behavioral risk factors such as hypertension, smoking, and diet.
• Both noise and air pollution induce oxidative stress and inflammation, with noise primarily affecting the brain and stress axis, while air pollution damages the lungs and circulatory system.
• The brain–heart axis is a key pathway in the development of CVD, with noise triggering neuroinflammation and stress hormone release, and air pollution contributing through direct brain uptake of particles and similar stress responses.
• Vascular dysfunction and atherosclerosis are common endpoints of both exposures, driven by shared biological mechanisms involving inflammation and impaired vascular signaling.
• Understanding these synergistic mechanisms is critical for prevention, especially in individuals with preexisting cardiovascular conditions, and highlights the need for targeted environmental health interventions.

• A combined mouse and human study by MARKOPOLO researchers from Mainz (University Medical Center, Max Planck Institute for Chemistry and Cyprus Institute) shows that shortterm exposure to synthetic nanoparticles (<250 nm) causes damage in remote organs, endothelial dysfunction and increased blood pressure, whereas microparticles (2-4 µm) accumulate in the lung leading to local pulmonary damage without blood pressure effects.
• The mouse study was based on advanced imaging techniques, functional measurements and biochemical parameters conducted in a joint effort of UMC-Mainz, MPIC, CyI and colleagues from the Leibniz Institute for Resilience Research and the Center for Thrombosis and Hemostasis.
• In a translational approach, estimations based on global human exposure data and hazard ratios from an epidemiological cohort study suggest a substantial cardiovascular disease burden attributable to ultrafine particles (UFPs, <100 nm). The team led by CyI and MPIC reports a yearly global cardiovascular disease incidence of 5.6 (95 % CI: 1.1–9.3) million, attributable to the exposure to UFPs, corresponding to 11-12 % of the total annual cardiovascular disease incidence at the global population level.
• These findings are worrisome and warrant further investigation since exposure to UFPs is so far not legally regulated (there are no legal limits) but obviously their contribution to the global burden of disease (and potentially premature deaths) is more pronounced than assumed.

• It is estimated that 2/3 of all chronic diseases are caused by environmental and lifestyle risk factors.
• Leading environmental risk factors for global death/disease are air pollution, hot/cold temperature, lead and unsafe water.
• The exposome concept describes the health impact by all environmental and lifestyle risk factors over entire life course.
• It also considers the biochemical changes (e.g. by OMICs signatures) by these risk factors in the human body.
• Besides chemical and physical pollution, the social environment such as economic status plays a major role for exposome.

• Healthy soil and clean water are essential to ecosystem sustainability and human well-being.
• Chemical pollution accounts for millions of premature deaths and non-communicable diseases, particularly CVD.
• Toxic chemicals cause cellular damage through oxidative stress, inflammation, and hormonal imbalances.
• Micro/nanoplastics, pervasive environmental contaminants, cause vascular injury, and transgenerational reproductive effects.
• Enhanced pollution controls and sustainable urban design may mitigate the global health impacts of environmental pollution.

• Transportation noise causes neurohormonal activation, sleep impairment and stress responses.
• Noise-induced stress hormone signaling via RAAS leads to inflammation, oxidative stress and cardiovascular dysfunction.
• Noise increases the risk of diabetes and other cardiometabolic diseases.
• Co-exposure to noise, air pollution or lack of green space causes cumulative increase of risk for diabetes.

• Hypertension is multifactorial. It results from a complex interplay of biological, genetic, and environmental factors.
• Environmental stressors play a major role - air, noise, and chemical pollution, built environments, and food systems significantly influence blood pressure levels.
• The "mosaic model", a conceptual framework, explains hypertension and views it as a network of interconnected causes rather than a single pathway. Identifying key nodes in this "mosaic" helps in targeting effective interventions at both the individual and societal levels.
• Public health strategies are crucial for controlling hypertension globally. Key approaches include improving urban planning, implementing policy changes, and integrating environmental risk assessments into clinical practice.