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Shocking Aspects of Nonconductive Plastics.

Toxic plasticizers in children’s toys and baby products hit public headlines 20 years ago, but exposure to these compounds is up to 25× higher in patients undergoing complex medical procedures. What are plasticizers, are they toxic and what are the arrhythmic consequences of the unknowing administration of them to our patients? The article in this issue of Circulation: Arrhythmia and Electrophysiology by Jaimes et al1 draws our attention toward these questions and the possible impact of plasticizers on arrhythmogenesis. Phthalate plasticizers (di-(2-ethylhexyl) phthalate [DEHP]) are hydrophobic chemicals abundantly used to make polyvinyl chloride products soft and flexible. These were patented over 70 years ago, and one of the first applications in 1952 was for the long-term storage of blood products.2 DEHP is noncovalently bonded to polyvinyl chloride and because of their hydrophobic nature can readily leach into solutions, especially lipophilic (TPN, pharmacologics) solutions or blood products. In the body, DEHP is converted to the active metabolite, MEHP, by lipase enzymes and is eliminated via the glucuronidation pathway.3 DEHP delivery is high in some of our sickest patients and is employed in procedures including extracorporeal membrane oxygenation, hemodialysis, cardiopulmonary bypass, blood transfusion, and catheter-based procedures. For example, plasticizers were recognized 3 decades ago4 to be present in serum of patients exposed to long cardiopulmonary bypass pump times. High levels of phthalates have been documented in children in neonatal intensive care units5–7 with levels >25-fold higher compared with the average environmental exposure for children8 at least, in part, due to an underdeveloped glucuronidation excretion pathway.9 One of the drivers for limiting storage time for blood products and mixing antibiotics immediately before use is the contribution of plasticizers to multiple metabolic abnormalities and endothelial dysfunction.10 Concluding that significant risk for iatrogenic toxicity may exist in vulnerable patients, the Food and Drug Administration issued a safety assessment of DEHP in 200111 and estimated a tolerable intake values based on animal studies. This was largely based on the effect of DEHP on the male reproductive system (thought to be the most sensitive organ system to DEHP) and while evidence of lung and liver toxicity were noted, no other elements were used for the tolerable intake calculation including cardiac toxicity. DEHP has been studied in multiple organ systems, including animal cardiac studies. In 1978, it was recognized by Aronson et al12 that an isolated rat heart preparation perfused with DEHP resulted in prolongation of the PR and QT intervals. Cardiac contractility and chronicity can be negatively affected by DHEP and MEHP.13,14 Furthermore, Gillum et al15 showed in an in vitro study of rat neonatal cardiomyocytes that DEHP slowed conduction velocity and reduced cellular EDITORIAL