Exposure to environmental toxicants and cardiovascular disease risk: a population-based study

Environmental toxicants represent an important yet often overlooked contributor to the development and progression of cardiovascular disease (CVD). This population-based study investigates the associations between exposure to various environmental chemicals and CVD risk using data from the National Health and Nutrition Examination Survey (NHANES). We analyzed 82 chemical exposures in a nationally representative cohort of 11,308 U.S. adults, 11% of whom had a diagnosis of CVD. The sample consisted of 48.5% males and 51.5% females, with 76.5% under the age of 65. Multiple imputation was employed to address missing data, and logistic regression models were applied to estimate associations between toxicant levels and CVD outcomes. A total of 37 environmental chemicals were significantly associated with increased CVD risk. Stratified analysis revealed demographic-specific patterns: women and younger adults showed higher susceptibility to exposures such as nicotine metabolites, polycyclic aromatic hydrocarbons (PAHs), and volatile organic compounds (VOCs), while older adults (aged ≥ 65) demonstrated stronger associations with phthalate and plasticizer metabolites. To further explore potential biological mechanisms, mediation analyses were conducted using peripheral blood biomarkers, including white blood cells, neutrophils, platelets, and monocytes. These immune and inflammatory markers mediated 2.3–15.4%, 2.7–26.5%, 4.9–23.4%, and 4.2–21.6% of the total toxicant-related CVD effects, respectively. Our findings suggest that diverse classes of environmental toxicants contribute meaningfully to cardiovascular risk and may do so, in part, through inflammatory or immune-mediated pathways. These results support the integration of environmental exposure assessments into cardiovascular risk evaluation and point to the need for early preventive strategies, especially in vulnerable subgroups. Further research is warranted to elucidate causal pathways and inform regulatory policies aimed at mitigating exposure to harmful environmental agents.