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Updated: Apr 21, 2026

Aggravation of Myocardial Ischemia upon Particulate Matter Exposure in Atherosclerosis Animal Model
Published on: December 10, 2021
Metal exposure in heart disease
1Department of Medicine, University Medical Centre Mannheim, University of Heidelberg, Heidelberg, Germany; Clinical Research Center for Reproduction and Genetics in Hunan Province, Reproductive and Genetic Hospital of CITIC-Xiangya, Changsha, Hunan, China; IMD Institut Für Medizinische Diagnostik Berlin-Potsdam GbR, Berlin, Germany; Institute of Reproductive and Stem Cell Engineering, NHC Key Laboratory of Human Stem Cell and Reproductive Engineering, School of Basic Medical Science, Central South University, Changsha, China.
Abstract:
Coronary heart disease (CHD) remains a leading cause of morbidity and mortality worldwide. In addition to classical risk factors, environmental exposures to toxic metals have been increasingly associated with cardiovascular risk in epidemiological studies. This narrative review summarizes current PubMed-indexed literature on the association of lead, cadmium, arsenic, mercury, and chromium with CHD, with emphasis on epidemiological evidence, mechanistic studies, and clinical implications. Literature was selected to cover major human observational studies, relevant experimental data, and translational reports addressing exposure pathways, biomarkers, vascular mechanisms, and prevention. Available epidemiological evidence suggests that chronic exposure to lead, cadmium, and arsenic is associated with higher risks of hypertension, atherosclerotic cardiovascular disease, and cardiovascular mortality, whereas the evidence for mercury and chromium is more heterogeneous and context-dependent. Mechanistic evidence, derived mainly from experimental and translational studies, indicates that these metals can promote oxidative stress, inflammation, endothelial dysfunction, disturbed lipid handling, mitochondrial injury, and, in some cases, epigenetic remodeling, thereby contributing to atherogenesis and plaque progression. However, the strength of evidence differs across metals and mechanisms, and causal interpretation remains strongest where experimental plausibility and human data converge. Clinically, heavy metal exposure should be considered in selected patients with CHD, particularly those with atypical risk profiles, relevant environmental or occupational exposure histories, or unexplained disease progression despite optimal standard management. Whole blood and urine measurements remain the preferred biomarkers in most settings, whereas hair analysis requires cautious interpretation. Prevention focuses on exposure reduction through water and food safety, emission control, smoking cessation, and targeted public health measures. Overall, toxic metals represent a plausible and likely underrecognized contributor to cardiovascular disease that deserves greater integration into cardiovascular prevention and environmental health research.
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