Carbon monoxide acute

The Du Pont HaskeU Laboratory for Toxicology and Industrial Medicine has conducted a study to determine the acute inhalation toxicity of fumes evolved from Tefzel fluoropolymers when heated at elevated temperatures. Rats were exposed to decomposition products of Tefzel for 4 h at various temperatures. The approximate lethal temperature (ALT) for Tefzel resins was deterrnined to be 335—350°C. AH rats survived exposure to pyrolysis products from Tefzel heated to 300°C for this time period. At the ALT level, death was from pulmonary edema carbon monoxide poisoning was probably a contributing factor. Hydrolyzable fluoride was present in the pyrolysis products, with concentration dependent on temperature. 

The toxic symptoms from inhalation of nickel carbonyl are beUeved to be caused by both nickel metal and carbon monoxide. In many acute cases the symptoms ate headache, di22iQess, nausea, vomiting, fever, and difficulty in breathing. If exposure is continued, unconsciousness follows with subsequent damage to vital organs and death. Iron pentacarbonyl produces symptoms similar to nickel carbonyl but is considered less toxic than nickel carbonyl. 

The Reppe process for manufacture of acrylic esters uses acetylene and carbon monoxide, with a nickel carbonyl catalyst having high acute and longterm toxicity, to react with an alcohol to make the corresponding acrylic ester ... 

The nervous system is vulnerable to attack from several directions. Neurons do not divide, and, therefore, death of a neuron always causes a permanent loss of a cell. The brain has a high demand for oxy gen. Lack of oxygen (hypoxia) rapidly causes brain damage. This manifests itself both on neurons and oligodendroglial cells. Anoxic brain damage may result from acute carbon monoxide, cyanide, and hydrogen sulfide poisonings. Carbon monoxide may also be formed in situ in the metabolism of dichloromethylene. 

The following factors have been suggested as alternatives to consider when presented with a potential case of exposure to carbon monoxide diabetic ketoacidosis, hypothyroidism and myxedema coma, labyrinthitis, and lactic acidosis toxic exposures resulting in methemoglobinemia ingestion of alcohols or narcotics and diseases that cause gastroenteritis, encephalitis, meningitis, and acute respiratory distress syndrome. 

Smith J, Brandon S Morbidity from acute carbon monoxide poisoning at a three-year follow-up. Br Mciy 1 318-321, 1973... 

Penney DG. Acute carbon monoxide poisoning animal model A review. Toxicology 1990 62 123. Penny DG. A review Hemodynamic response to carbon monoxide. Environ Health Perspect 1988 77 121. Rocco TP, Fang JC. Pharmacological treatment of heart failure. In Brunton L, Lazo J, Parker K, eds. 

Oxo plants employ mixtures of highly toxic, flammable gases under pressure at high temperatures and require strict adherence to established operating safety codes and emergency reporting procedures to local, state, and federal authorities. I11 the United States, carbon monoxide is classified as both an acute, fire, and sudden release hazard. 

In the evaluation of toxic characteristics of an inhalable environmental chemical (e.g., carbon monoxide, volatile chemical, or aerosol/particulate), determination of acute inhalation toxicity is an initial study step. It provides information on health hazards likely to arise from short-term exposure by inhalation. Data from an acute test help to establish a dose regimen in subchronic (and other) studies, and may provide additional information on a chemical s mode of toxic action. 

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