Di(2-ethylhexyl) phthalate (DEHP) exposure during cardiopulmonary bypass: A narrative review of human clinical evidence and future directions.
The coronary story today is physiology, not grafts.
Continuous thermodilution in 51 patients with anomalous aortic origin of a coronary artery showed that the high-risk anatomic triad (intramural segment, acute take-off, slit-like ostium) produces measurably reduced hyperemic flow (179 vs 290 mL/min) and elevated microvascular resistance at rest and under stress.
BackgroundDi(2-ethylhexyl) phthalate (DEHP) is widely used as a plasticizer in polyvinyl chloride medical devices employed during cardiopulmonary bypass (CPB). Although migration from these devices and blood-storage systems has long been recognized, the human clinical evidence remains limited and methodologically heterogeneous.MethodsThis narrative review used a structured search of PubMed/MEDLINE, Scopus, and Google Scholar from database inception through 23 August 2026. Original peer-reviewed human clinical studies measuring parent DEHP or its metabolites in blood, plasma, or urine among patients undergoing CPB were eligible for the primary synthesis. Relevant mechanistic, biomaterial, transfusion-medicine, guideline, and regulatory sources were used for context.ResultsThe searches identified 237 database records; 33 duplicates were removed, and 204 unique records were screened. Thirteen full-text reports were assessed, and seven human clinical studies published between 1983 and 2025 were included. Across adult and pediatric settings, perioperative increases in parent DEHP and/or urinary or circulating metabolites were documented. The studies implicated multiple sources, including CPB components, blood-storage systems, and ancillary blood-contacting devices, but none provided complete patient-level source apportionment. DEHP-free tubing reduced, but did not eliminate, exposure. RBC washing reduced DEHP and MEHP in vitro, but a reduction in patient-level internal exposure has not been established.ConclusionHuman clinical evidence consistently demonstrates internal exposure to DEHP or its metabolites during cardiac surgery involving CPB. However, small heterogeneous cohorts, variable analytes and sampling schedules, and limited outcome follow-up preclude causal inference regarding clinical harm. Prospective multicenter studies using standardized biomonitoring and source-apportionment methods are required.
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