Air Pollution and Vascular Biomaterial Remodeling
Kratka vsebina
Air pollution is increasingly recognised as an independent cardiovascular risk factor. Fine particulate matter and ultrafine particles can transport toxic elements and metalloids, promoting systemic inflammation, oxidative stress, endothelial dysfunction, and vascular injury. Toxic elements such as cadmium, lead, mercury, arsenic, nickel, and chromium may contribute to vascular damage, while essential trace elements, including selenium, zinc, copper, manganese, and molybdenum, support redox balance and cellular homeostasis. However, the role of toxic–essential element imbalance in cardiovascular disease remains insufficiently understood. Recent translational studies combine environmental exposure assessment, human biomonitoring, and vascular phenotyping. Exposure is typically evaluated using environmental data together with biomarkers measured in blood and urine. Cardiovascular status can be assessed through non-invasive vascular measurements and, where clinically indicated, analysis of vascular tissue obtained during surgery. Advanced analytical methods enable quantification of toxic and essential elements and evaluation of their associations with vascular alterations. Chronic exposure to air pollution–related toxic elements is expected to be associated with endothelial dysfunction, inflammation, and early vascular remodeling. Imbalances between toxic and essential elements may correlate with the severity of vascular injury. Combining biomonitoring with tissue-level analysis may therefore provide new mechanistic insights and support the identification of early biomarkers of environmentally driven vascular damage. Overall, integrating environmental exposure assessment, biomonitoring, and vascular tissue analysis offers a promising framework for understanding environmentally related cardiovascular disease. Considering both toxic and essential elements may improve cardiovascular risk assessment, early detection, and the development of targeted preventive strategies.
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