Influence of organic and inorganic soil pollutants on modifiable cerebrovascular disease risk factors

Abstract

Growing evidence indicates that chronic exposure to organic and inorganic soil pollutants may contribute to the development of cerebrovascular disease (CeVD) by modulating key, potentially reversible cardiometabolic risk factors. While the vascular consequences of air and water pollution are increasingly recognized, contaminated soils remain an underappreciated environmental reservoir of toxicants with potential health effects. Inorganic pollutants such as lead and cadmium, together with organic compounds including polycyclic aromatic hydrocarbons and polychlorinated biphenyls, can enter the human body through ingestion, inhalation of resuspended particulates, or, for some compounds, dermal absorption. Once absorbed, these pollutants disrupt metabolic and vascular homeostasis through converging mechanisms involving oxidative stress, endothelial dysfunction, and chronic low-grade inflammation. These processes promote the development of hypertension, insulin resistance, hyperglycemia, and dyslipidemia—well-established, modifiable risk factors for CeVD. Organic pollutants may further exacerbate metabolic toxicity through endocrine-disrupting effects and activation of the aryl hydrocarbon receptor, amplifying their cerebrovascular relevance. This review synthesizes experimental, epidemiological, and mechanistic evidence linking exposure to organic and inorganic soil pollutants with adverse alterations in blood pressure regulation, glucose metabolism, and lipid homeostasis. Despite growing concern, a critical knowledge gap remains in defining pollutant-specific associations with discrete cerebrovascular outcomes, largely due to limited integrative studies combining environmental exposure assessment with clinical biomarkers and longitudinal health data. Moreover, populations in industrially burdened or low-resource settings experience disproportionate exposure risks, reinforcing health inequities. Strengthening soil pollution surveillance, advancing remediation strategies, and incorporating environmental exposure histories into cardiovascular risk assessment may represent an upstream approach to reducing the global burden of CeVD.