How good are the numbers for cigarette tar at predicting deliveries of carbon monoxide, hydrogen cyanide, and acrolein?

1981 ◽  
Vol 7 (5) ◽  
pp. 801-808 ◽  
Author(s):  
J. C. Young ◽  
J. C. Robinson ◽  
W. S. Rickert
2019 ◽  
Author(s):  
Stephanie T Weiss ◽  
Kathryn W Weibrecht

This review looks at the potential causes, diagnoses, and possible treatments for three asphyxiant gases: carbon monoxide, hydrogen cyanide, and hydrogen sulfide, Exposure to these gases can lead to central nervous system depression, unconsciousness, and death due to tissue hypoxia. These gases are among the most common causes of fatalities related to toxic gas poisoning, with carbon monoxide responsible for 36% and hydrogen sulfide 7.7%. It is necessary to remove victims affected by poisoning immediately from the source of the toxic gas, administer oxygen, and assess their stability. As symptoms of these gases can differ widely, ranging from broad and unspecific to highly morbid, and may require different levels of care, the correct diagnosis should also rely on inferences from the patient history and the context of the admission, including evidence of fire and chemical reactions. Normobaric oxygen and hyperbaric oxygen are the two main treatments for carbon monoxide, although studies have been inconclusive in regards to the effectiveness of hyperbaric oxygen. The Cyanokit (containing hydroxocobalamin) is considered to be more effective for hydrogen cyanide when compared with the Cyanide Antidote Kit due to the former’s low toxicity and high effectiveness. Hydrogen sulfide is often used as a suicide agent, the mortality of which is close to 100%. Figures show the mechanisms by which the asphyxiant gases carry out their negative effects on the human body. Tables show the half-life of carboxyhemoglobin with oxygen therapy and a comparison between the Cyanide Antidote Kit and the Cyanokit. This review contains 3 figures, 13 tables, and 44 references.  Keywords: Inhalation, poisoning, carbon monoxide, cyanide, methemoglobin, carboxyhemoglobin, hydrogen sulfide, smoke


1993 ◽  
Vol 19 (3) ◽  
pp. 540-543
Author(s):  
Makoto Akiyoshi ◽  
Satoru Hisaki ◽  
Takashi Fukuda ◽  
Eiji Obata ◽  
Koji Ando

2017 ◽  
Vol 846 (1) ◽  
pp. 60 ◽  
Author(s):  
Dongwoo T. Chung ◽  
Tony Y. Li ◽  
Marco P. Viero ◽  
Sarah E. Church ◽  
Risa H. Wechsler

2010 ◽  
Vol 35 (8) ◽  
pp. 577-591 ◽  
Author(s):  
Zhaozhi Wang ◽  
Fuchen Jia ◽  
E. R. Galea

1898 ◽  
Vol 73 (0) ◽  
pp. 255-258 ◽  
Author(s):  
John Wade ◽  
Laurence C. Panting

1984 ◽  
Vol 2 (1) ◽  
pp. 20-36 ◽  
Author(s):  
David A. Purser

A bioassay model has been developed to test the time course and degree of in capacitation produced by exposures to thermal decomposition products from polymeric materials. A battery of physiological tests was used during separate exposures to atmospheres of carbon monoxide, hydrogen cyanide, hypoxia, hypercapnia and heated air. Each atmosphere was designed to simulate one aspect of the conditions commonly encountered in fires. Measurements were made of the animals' respiration, cardiac function and respiratory blood gases. Neurological function was monitored by measurements of the elec troencephalogram, auditory cortical evoked potentials and peripheral nerve con duction velocity. Hypoxia (10% oxygen) caused muscle weakness, a decrease in nerve conduction velocity, abnormal cardiac function accompanied by a fall in blood pressure and central nervous system depression. At 1000 ppm carbon monoxide, venous carboxyhaemoglobin levels reached 30%. There was a reduc tion of nerve conduction velocity and in some cases severe central nervous system depression. At 60 ppm hydrogen cyanide had a slight depressive effect on the central nervous system, while at 80-150 ppm severe central nervous system depression and incapacitation occurred. The main result of 5% carbon dioxide exposure was a three-fold increase in respiratory minute volume. It is concluded that the model is capable of detecting early physiological signs of in capacitation induced by fire conditions. It is suggested that exposures to a com bination of hydrogen cyanide and carbon monoxide with accompanying changes in cerebral blood flow during attempts to escape from fires may be a cause of col lapse and subsequent death.


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