Characterization of emissions of dioxins and furans from ethylene dichloride, vinyl chloride monomer and polyvinyl chloride facilities in the United States. Consolidated report.

This is the consolidated report of emissions of PCDD/F from facilities in the organic chemical manufacturing chain leading to polyvinyl chloride. Data have been gathered from facilities in the US and Canada from a number of manufacturers and at various steps in the manufacturing process. Estimates of US emissions or transfers of PCDD/F were generated on an "Upper Bound" and "Most Likely" basis. The Most Likely estimate of US emissions of PCDD/F to the open environment, that is, air, water and land surface by facilities in this chain, based on evaluation of non-detects at one-half the detection limit is about 12 g I-TEQ per year. On this same basis, an estimated 19 g is disposed of in secure landfills.

Characterization of emissions of dioxins and furans from ethylene dichloride (EDC), vinyl chloride (VCM) and polyvinylchloride (PVC) manufacturing facilities in the United States. I. Resin, treated wastewater, and ethylene dichloride.

Under the auspices of its Dioxin Characterization Program, members of The Vinyl Institute (VI), have analyzed for potential polychlorinated dibenzodioxin/furan (PCDD/F) concentrations in polyvinylchloride (PVC) resins, treated wastewater effluent and ethylene dichloride (EDC) product at EDC, vinyl chloride monomer (VCM) and PVC manufacturing facilities in the U.S. and Canada. No 2,3,7,8-tetrachlorodibenzodioxin (TCDD) was detected in any sample analyzed under the program to date. Trace concentrations (low pg/g) of PCDD/F were detected in only a few samples of PVC resins and EDC product. Treated wastewater contained low ppq concentrations of PCDD/F. All concentrations are expressed as Toxic Equivalents (TEQ). Extrapolation of these data shows that the contribution of EDC/VCM/PVC manufacturing via these media constitutes substantially less than 1 percent of the estimated annual U.S. dioxin releases to the environment.

Pericarditis associated with acral erythema of chemotherapy: a syndrome of cutaneous and serosal toxicities?

A nineteen-year-old woman whose Hodgkin's disease had relapsed experienced acral erythema in association with a asymptomatic pericardial friction rub following autologous bone marrow transplantation. An echocardiogram revealed a large pericardial and right pleural effusion. Since blood cultures gave negative results, renal function was normal, and the patient had neither neutropenia nor elevated temperature, an infectious cause was deemed unlikely and invasive procedures were not performed. These effusions resolved spontaneously. We propose that this patient's acral erythema and associated pericardial and pleural inflammation represent cutaneous and serosal toxic reactions to high-dosage chemotherapy that occur with the onset of leukocyte recovery. If so, acral erythema may signal the beginning of a toxic drug reaction. The appearance of erythema associated with lymphocyte recovery is due to immune hypersensitivity secondary to immaturity of the reconstituting immune system. Thus, we recommend that patients with acral erythema be examined for pleuropericarditis, especially if they experience chest pain.