Hemoglobin poisoning

Carbon monoxide poisoning results when carbon monoxide replaces oxygen bound to hemoglobin. The oxygenated form of hemoglobin, Hb 02 carries 02 to the lungs. 

Not only 02 molecules but also other groups can be bound to the iron atom of hemoglobin. Specifically, carbon monoxide molecules can be so attached and, in fact, CO is more firmly bound to hemoglobin than is O2. This is one detail of the carbon monoxide poisoning mechanism. If we breathe a mixture of CO and 02 molecules, the CO molecules are preferentially picked up by the red blood cells. Since the sites... 

In humans, severe cases of acrylonitrile poisoning have resulted in low grade anemia (Wilson 1944 Wilson et al. 1948), but complete recovery was reported. Chronic occupational exposure to low levels of acrylonitrile has not resulted in detectable effects on the hematological system (Sakurai et al. 1978). In intermediate and chronic studies in animals, decreased red cell count, hemoglobin concentration and hematocyte were observed (Bio/dynamics 1980a, 1980b, 1980c Quast et al. 

A case report of acute arsine poisoning in which a 27-y-old man was exposed to arsine during chemical manufacturing was reported by Pinto (1976). The subject was exposed to arsine as a result of arsine production via a reaction between a galvanized bucket and an arsenic-containing sulfuric acid solution. The exposure (duration not specified) produced toxic effects characterized by abdominal cramping, thoracic discomfort, and hematuria. Over the next week, the patient s hematocrit declined from 42.5 to 27.1 and hemoglobin dropped from 14.1 to 9.5 g/dL even with medical intervention (blood transfusions and mannitol diuresis). Nine hours after exposure, blood arsenic was 159 g/dL and urinary arsenic was 1862 ug/L. 

Kleinfeld (1980) reported a case of arsine poisoning in a 31-y-old man. The exposure to arsine occurred from a leaking canister thought to be empty. The exposure duration was estimated to be 1-2 min, but no actual or estimated arsine concentrations were available. The victim presented with hematuria. On hospital admission, no intact erythrocytes were present in the urine, hematocrit was 43%, and hemoglobin was 9.8 g/ dL. The hematocrit dropped to as low as 18%, the correction of which required one unit of packed cells. Based upon the exposure history and the subject s note of a "garlicky" odor, the diagnosis was arsine-induced hemolytic anemia. Urinary arsenic was 7.2 mg/L on admission and 0.1 mg/L 4 d later. The patient was subsequently discharged. 

Data from case reports indicated that there is usually a 1- to 24-h delay between exposure and onset of signs and symptoms of poisoning. Additionally, hematologic parameters (e.g., hemoglobin, hematocrit levels) appear to be progressively affected for several days after the exposure. Hence although the exposure is acute, the most serious adverse effect may be delayed by several hours or days. 

Phosgene poisoning may cause respiratory and cardiovascular failure which results in low plasma volume, increased hemoglobin concentration, low blood pressure, and an accumulation of fluid in the lungs. There is no antidote for phosgene, and treatment consists of support of respiratory and cardiovascular functions. 

Cumulative poison Highly irritating to eyes and throat Permanent corneal damage Skin rash followed by blistering Interferes with blood hemoglobin functioning... 

Nitrites may be used as an antidote for cyanide poisoning if given rapidly. They convert hemoglobin to methemoglobin, which binds cyanide in the blood before reaching the tissues. Oxygen is also given if possible. 

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