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Title: Phosgene

 [1];  [1]
  1. ORNL
Publication Date:
Research Org.:
Oak Ridge National Lab. (ORNL), Oak Ridge, TN (United States)
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DOE Contract Number:
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Country of Publication:
United States

Citation Formats

Bast, Cheryl B, and Glass-Mattie, Dana F. Phosgene. United States: N. p., 2015. Web. doi:10.1016/B978-0-12-800159-2.00025-7.
Bast, Cheryl B, & Glass-Mattie, Dana F. Phosgene. United States. doi:10.1016/B978-0-12-800159-2.00025-7.
Bast, Cheryl B, and Glass-Mattie, Dana F. 2015. "Phosgene". United States. doi:10.1016/B978-0-12-800159-2.00025-7.
title = {Phosgene},
author = {Bast, Cheryl B and Glass-Mattie, Dana F},
abstractNote = {},
doi = {10.1016/B978-0-12-800159-2.00025-7},
journal = {},
number = ,
volume = ,
place = {United States},
year = 2015,
month = 1

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  • Inhalation is the most important route of exposure for phosgene. A latency period occurs before phosgene affects the target organ, the lungs. The odor threshold is between 0.5 and 1.5 ppm, and the odor has been described as similar to newly-mown hay. Toxic effects have been reported at concentrations below the threshold. On initial exposure, phosgene can undergo hydrolysis and form hydrogen chloride which can be slightly irritating to the upper respiratory tract and eyes; the amount formed is limited by the low water solubility of phosgene. Once inhaled to the lower respiratory tract, phosgene undergoes an acylation reaction withmore » amino, hydroxyl and sulfhydryl groups causing destruction of protein, lipids, and disruption of cellular functions. In response to this destruction, after a latency period of 1-24 hours, a breakdown in the blood-air barrier occurs and protein rich fluid accumulates in the lungs. Most commonly, death occurs within 48 hours after exposure from a progressive pulmonary edema and anoxia. At very high concentrations, death can occur from acute heart failure prior to the start of the pulmonary edema. Data on humans are limited to occupational exposures or accounts from the use of phosgene in World War I. Animal studies with phosgene show a steep dose-response curve for pulmonary edema and mortality. Animal studies also indicate little species variability as all species exposed developed similar clinical signs (dyspnea, pulmonary edema, labored breathing) and histopathological lesions in the lungs. While there are no chronic animal data, subchronic studies indicate little accumulation of phosgene or increased severity of lesions with continuous exposure.« less
  • The exchange reaction /sup 12/COCl/sub 2/+/sup 13/COarrow-right-left/sup 13/COCl/sub 2/+ /sup 12/CO is theoretically expected to have a separation factor of 1.04 at 60degreeC, and of 1.07 at -35degreeC. Pure COCl/sub 2/ and a series of COCl/sub 2/--CO gaseous mixtures were irradiated either with the 253.7 nm mercury line or the light of a medium pressure mercury lamp (above 200 nm). The /sup 13/C distribution in the photostationary state has shown separation factors ranging from 1.092 at 60degreeC to 1.170 at -35degreeC for the 253.7 line and from 1.059 at 60degreeC to 1.067 at 25degreeC at irradiation with the medium pressuremore » lamp. The increase of the factors above the theoretically predicted values is attributed to differences in the fine structure of /sup 12/COCl/sub 2/ and /sup 13/COCl/sub 2/ predissociation spectra. The possibility of improving the selectivity of the separation process is analyzed. (AIP)« less
  • Experiments were made with a batch reactor to determine the effect of gas pressures, temperature, and gamma radiation intensity on the reaction of CO + Cl/sub 2/ ..-->.. COCl/sub 2/. Oxygen and a large ratio of reactor surface to volume retarded the reaction, but inert gases had no effect. A low-temperature reactor system is proposed to take advantage of the conditions which give a high reaction rate with gamma radiation and a simple scheme of product purification.
  • In this study, the authors demonstrated the acute pulmonary cellular changes associated with phosgene exposure, by both light (L.M.) and electron microscopy (E.M.). Adult, unanesthetized sheep were exposed for 10 minutes to either 767 ppm/min of phosgene or room air. Four hours post exposure, all animals were killed, wet lung weight was obtained, and lung tissue was collected for L.M. and E.M. In sheep exposed to phosgene, wet lung weight was significantly higher. Grossly, the lung was congested and edematous. Alveolar and interstitial edema, fibrin and neutrophil exudation in the air spaces, and increased alveolar macrophages, were prominent by L.M.more » E.M. of Type I pneumocytes showed intracellular swelling, necrosis, and denuding of basement membrane with preservation of the tight junctions. Type II pneumocytes showed loss of lamellar bodies, cytoplasmic swelling, and damage to the endoplasmic reticulum. Endothelial cells showed increased density and vesicular activity, cytoplasmic swelling, and displacement of basement membrane. This study supports the biochemical data the authors previously reported.« less