Distribution of Di(2-Ethylhexyl) Phthalate and Products in Blood and Blood Components

Rock, G.; Labow, Rosalind S.; Tocchi, Monika

doi:10.2307/3430198

Cited by 20 publications

(19 citation statements)

References 15 publications

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“…Thus, this material is a likely candidate for a mediator of FX1I activation. Furthermore, many plastics re lease migrants remaining from the polymerization process, or leach plasticizers [27] which may interact with cell mem branes and plasma proteins [28]. The activation of factor XII by plasmin has been proposed by other investigators [6]; however, we failed to detect plasmin activity in these samples.…”

Section: Coagulation Activation In Platelet Concentratescontrasting

confidence: 53%

Coagulation Factor Activation in Stored Platelet Concentrates is Modulated by the Platelets

Gyöngyössy-Issa¹,

Black²,

Devine³

1996

Vox Sanguinis

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To assess alterations in coagulation proteins in stored platelet concentrates, we used a series of platelet parameters and measures of coagulation activation to compare samples collected before unit donation, during the processing of platelet concentrates (PC) from CPDA-1 blood, and in storage up to 5 days as well as stored platelet-poor plasma (PPP). Storage-dependent increases in activated partial thromboplastin time and prothrombin time were seen in both PC and PPP. However, FVII, FXI, FXII, kailikrein activity and prothrombin FI.2 levels remained unchanged in stored PC. Surprisingly, in stored PPP, significant alterations in FX11, FVII, kallikrein and prothrombin FI.2 levels were seen. Platelet morphology and surface marker studies demonstrated platelet activation during storage. These data suggest that the presence of platelets in the CLX storage container partially suppresses coagulation activation at significant cost to platelet viability.

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Section: Coagulation Activation In Platelet Concentratescontrasting

confidence: 53%

Coagulation Factor Activation in Stored Platelet Concentrates is Modulated by the Platelets

Gyöngyössy-Issa¹,

Black²,

Devine³

1996

Vox Sanguinis

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“…Extraction occurs either by leaching or after an extracting material (blood, IV¯uids) diffuses into the PVC matrix and dissolves the plasticizer, which is relatively lipophilic. [Nass, 1977;Rock et al, 1986;Lundberg and Nilsson, 1994]. Temperature, mechanical agitation, storage time, chemical nature of the medical device contents, and DEHP concentration in the device in¯uence the degree of leaching, which can vary from a fraction to 10±15% of the available DEHP [Nass, 1977;Kevy and Jacobson, 1982;Lundberg and Nilsson, 1994;Latini and Avery, 1999].…”

Section: Medical Exposuresmentioning

confidence: 99%

Health risks posed by use of Di-2-ethylhexyl phthalate (DEHP) in PVC medical devices: A critical review

et al. 2001

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Background Polyvinyl chloride plastics (PVC), made flexible through the addition of di‐2‐ethylhexyl phthalate (DEHP), are used in the production of a wide array of medical devices. From the late 1960s, leaching of DEHP from PVC medical devices and ultimate tissue deposition have been documented. Methods A critical review of DEHP exposure, metabolism, and toxicity data from human and animals studies was undertaken. A brief analysis of alternatives to DEHP‐plasticized PVC for use in medical device manufacture was completed. Results DEHP leaches in varying concentrations into solutions stored in PVC medical devices. Certain populations, including dialysis patients and hemophiliacs may have long‐term exposures to clinically important doses of DEHP, while others, such as neonates and the developing fetus, may have exposures at critical points in development. In vivo and in vitro research links DEHP or its metabolites to a range of adverse effects in the liver, reproductive tract, kidneys, lungs, and heart. Developing animals are particularly susceptible to effects on the reproductive system. Some adverse effects in animal studies occur at levels of exposure experienced by patients in certain clinical settings. DEHP appears to pose a relatively low risk of hepatic cancer in humans. However, given lingering uncertainties about the relevance of the mechanism of action of carcinogenic effects in rodents for humans and interindividual variability, the possibility of DEHP‐related carcinogenic responses in humans cannot be ruled out. Conclusions The observed toxicity of DEHP and availability of alternatives to many DEHP‐containing PVC medical devices presents a compelling argument for moving assertively, but carefully, to the substitution of other materials for PVC in medical devices. The substitution of other materials for PVC would have an added worker and community health benefit of reducing population exposures to DEHP, reducing the creation of dioxin from PVC production and disposal, and reducing risks from vinyl chloride monomer exposure. Am. J. Ind. Med. 39:100–111, 2001. © 2001 Wiley‐Liss, Inc.

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“…Higher concentrations could not be used, as the chemicals precipitated and produced etchings in the dishes. In blood products stored in poly(vinyl chloride) plastic bags (in which DEHP was used as a plasticizer), DEHP has been found in concentrations exceeding the highest level used in the present work (Rock et al, 1986). For clofibrate, the therapeutic plasma concentration is around 50 #M (Olivier et al, 1988).…”

Section: Resultsmentioning

confidence: 83%

Morphological transformation and catalase activity of syrian hamster embryo cells treated with hepatic peroxisome proliferators, TPA and nickel sulphate

1990

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The abilities of the hepatic peroxisome proliferators (HPPs) clofibrate, di(2-ethylhexyl)phthalate (DEHP), mono(2-ethylhexyl)-phthalate (MEHP), 2,4-dichlorophenoxy acetic acid (2,4-D), 2,4,5-trichlorophenoxy acetic acid (2,4,5-T) and tiadenol to induce morphological transformation and to increase the catalase activity of Syrian hamster embryo (SHE) cells were studied. DEHP, MEHP, clofibrate and tiadenol induced morphological transformation of SHE cells and increased the catalase activity. DEHP was more potent than clofibrate and tiadenol in both inducing catalase and morphological transformation, while MEHP seemed more potent than DEHP in inducing catalase, but not morphological transformation, 2,4,5-T and 2,4-D did not induce morphological transformation, but 2,4,5-T was more potent than clofibrate in increasing the catalase activity. These results show that several HPPs induce morphological transformation of SHE cells and an increase in the catalase activity. There is, however, no direct connection between these two parameters, as seen from the results of 2,4,5-T. The tumor promoter TPA, and the metal salt nickel sulphate, induced morphological transformation of SHE cells without any appreciable increase in the catalase activity. These results further corroborate the dissociation between induction of morphological transformation and the increase in catalase activity.

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Distribution of Di(2-Ethylhexyl) Phthalate and Products in Blood and Blood Components

Cited by 20 publications

References 15 publications

Coagulation Factor Activation in Stored Platelet Concentrates is Modulated by the Platelets

Coagulation Factor Activation in Stored Platelet Concentrates is Modulated by the Platelets

Health risks posed by use of Di-2-ethylhexyl phthalate (DEHP) in PVC medical devices: A critical review

Morphological transformation and catalase activity of syrian hamster embryo cells treated with hepatic peroxisome proliferators, TPA and nickel sulphate

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