Publications

• 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.