Research timeline and gaps: Microplastics and Cardiovascular Disease

Selected publication milestones, not an exhaustive history or discovery priority claim.

2016 — Repeated PIVUS sampling maps compound-specific serum trends; kinetics is distinct from clinical risk. Original PMID27542758.

2017 — Contaminated-water distribution predicts PFHxS trends within the shared PIVUS cohort. Original PMID28780137.

2019 — Prospective PFAS-diabetes results include mostly nonsignificant inverse associations, a boundary against uniform metabolic-harm inference. Original PMID30622063.

2021 — Particle-exposed endothelial/immune models demonstrate activation while leaving human clinical dependency unresolved. Original PMID34788346.

2022 — A contamination-aware pyrolysis workflow detects polymer mass in human blood. Original PMID35367073.

2022 — Randomized donation lowers selected serum PFAS without established clinical health improvement. Original PMID35394514.

2022 — Anionic particles produce biophysical endothelial leakiness, broadening mechanisms beyond inflammatory markers. Original PMID35963861.

2023 — A sensitized high-fat ApoE mouse platform shows administered particle-associated atherosclerosis; dose translation remains open. Original PMID37144527.

2023 — Cardiac-surgery tissue and paired blood analyses highlight clinical procedural sources and diseased-tissue selection. Original PMID37440474.

2024 — A prospective carotid-surgery cohort links plaque polymers to later infarction, stroke or all-cause death, without proving causality. Original PMID38446676.

2024 — Randomized-sequence resin treatment lowers serum PFAS; concentration is its primary outcome. Original PMID38367552.

2024 — Barrier impairment associates with CNS particle burden without a particle-cytokine association. Original PMID39366047.

2025 — A post-MI clinical cohort adds coronary PVC/event association, with ambiguous indexed numerical wording retained as a limitation. Original PMID40007360.

2025 — Mouse imaging demonstrates particle-phagocyte obstruction and reduced microvascular flow under administered exposure. Original PMID39841831.

2025 — Prospective PFAS/lipidomics case-control work links chemicals with post-PCI events, while causal mediation remains unisolated. Original PMID40571603.

2025 — Lean LDLR-deficient mice show a male-versus-female atherosclerosis boundary under daily gavage. Original PMID41275764.

2025 — Small crossover interventions distinguish enhanced chemical excretion from serum concentration and clinical benefit. Original PMID40974835.

Research gaps

Standardized particle-resolved internal dosimetry and procedural contamination controls across human cohorts.

Independent prospective clinical-event cohorts outside pre-existing disease/surgical selection, with cardiovascular death separated from all-cause death.

Validated natural exposure-mitigation contrasts and causal instruments; no unethical deliberate human exposure trial is required.

Realistic dose, polymer/size/surface, sex/genotype and additive controls for mediator-specific vascular experiments.

Controlled human plastic-particle burden removal with clinical benefit-harm endpoints, distinct from chemical serum kinetics.

Compound-specific PFAS clinical-event attribution and controlled removal-health outcomes, rather than extrapolation from lipids or blood concentration.

Boundary experiment

A prospective natural exposure-mitigation study compares baseline-defined communities affected by a specific verified source with matched independent control communities. Register polymer/particle sizes, chemical coexposures, repeated internal-dose assays, clean procedural blanks, baseline vascular risk and adjudicated myocardial infarction/stroke/cardiovascular-death endpoints. Separately randomize a lawful safe chemical-burden-lowering strategy in appropriately eligible PFAS-exposed adults to prespecified clinical function/health and harm outcomes; do not equate serum decline with success.