Micro‐ and Nanoplastics and Cardiovascular Disease: Evidence, Mechanisms, and Unresolved Questions

Micro‐ and nanoplastics (MNPs), conventionally defined as plastic debris of 1 μm–5 mm (microplastics) and below 1 μm (nanoplastics), have been recovered from human blood, myocardium, atherosclerotic plaque and thrombi, and a single prospective cohort has linked their presence in carotid plaque to a more than four‐fold excess of myocardial infarction, stroke or death. This review assembles the quantitative human and experimental evidence and tests it against the standard required of a causal exposure. Across small, heterogeneous studies using different matrices and analytical platforms, MNPs are detected in 58%–84% of cardiovascular‐relevant samples, although the control arm of the only case–control comparison was positive in 31.8%. A second, independent coronary case–control study has reproduced the detection signal and shown it to be graded by clinical presentation, but the outcome estimate, a hazard ratio of 4.53 (95% confidence interval 2.00–10.27), still rests on one unreplicated cohort of 257 patients, derives from a cross‐sectional plaque measurement, and has drawn published methodological correspondence. Experimental studies define a cascade that converges on the effector pathways established for fine particulate air pollution: reactive‐oxygen‐driven endothelial dysfunction with endothelial nitric oxide synthase uncoupling and glycocalyx injury; scavenger‐receptor‐mediated macrophage uptake that activates the NLRP3 inflammasome and interleukin‐1β, the axis whose therapeutic neutralization lowers cardiovascular events; and surface‐charge‐dependent platelet activation feeding immunothrombosis. Biological effect is governed by particle size, surface charge and the biomolecular corona rather than by polymer identity, and in rodents the smallest particles translocate to brain and placenta. That mechanistic literature is built almost entirely on pristine polystyrene delivered at bolus dose, and none of it is benchmarked against a human internal dose, which has never been quantified. The evidence satisfies several Bradford Hill considerations but leaves temporality, consistency and human dose–response unresolved, and it can exclude neither reverse causation nor confounding by shared exposures. The only independent predictor of MNP detection in coronary blood identified so far is smoking history. MNPs are therefore a biologically plausible candidate cardiovascular exposure that has not been shown to cause disease. Standardized measurement, independent prospective cohorts and exposure‐reduction trials are the immediate requirements of the field.