Poisoning arsine

Depletes RBC glutathione, causing cell membrane instability and hemolysis 

Population All, esp workers exposed to metal refining, lead 

Abdomen, flank - pain Abdomen - pain Arterial press - low Breath, odor - garlic Breathing - difficult (dyspnea) Breathing - rapid (tachypnea) 

conjunctivae - red stain Head - pain (headache) 

Liver - enlarged (hepatomegaly) Mentation - disorientation Mentation - memory loss Mentation - restless, agitated Mentation - weakness (malaise) Muscles - cramps Muscles - pain (myalgia) 

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Case reports are available regarding lethal effects of acute exposure to arsine (Pinto et al. 1950 Morse and Setterlind 1950 Hesdorffer et al. 1986). However, no definitive quantitative exposure data accompany these reports. Signs and symptoms varied depending on the exposure situation but usually included abdominal and muscle pain, nausea and diarrhea, hematuria, and oliguria. Delayed lethality, common in arsine poisoning, varied considerably. 

Pinto (1976) also reported similar characteristics regarding acute arsine poisoning. Although, an exposure concentration was unavailable, exposure to newly formed arsine for less than 1 h resulted in severe (likely fatal without medical intervention of exchange transfusion) signs and symptoms, including... 

Numerous cases of arsine poisoning have been reported (Elkins and Fahy 1967 DePalma 1969). However, these reports lack definitive exposure concentration data and usually lack exposure duration data as well. Some of the more recent and complete reports involving nonlethal consequences are described in the following section. These reports do not provide quantitative data suitable for AEGL derivations, but they do provide valuable insight into the nature and progression of arsine poisoning in humans. In most cases, the severity of the effects was usually sufficient to necessitate medical intervention to prevent lethality. Some of the more prominent reports and those with the best descriptive data have been summarized, but the overview is by no means exhaustive. 

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. 

Numerous case reports are available regarding the lethal and nonlethal toxicity of arsine in humans, but definitive exposure concentration or duration data are lacking. Although the case reports are of limited use for quantitative estimates of exposure limits, they do provide qualitative information about the nature of arsine poisoning in humans. Some estimated human toxicity values are available and are summarized in Table 2-3. 

TABLE 2-3 Acute Toxicity Values for Arsine Poisoning in Humans... 

Urinary arsenic is routinely evaluated in victims of arsine poisoning. Urine arsenic in unexposed people is <50 figfL (Landrigan et al. 1982). These authors reported that 15.6 fig of arsine/m3 is associated with urinary arsenic of 50 jug/L. Other studies of urinary arsenic levels have also been reported, but the post-exposure time of measurement varies considerably, and there are no corresponding exposure correlates. Urinary arsenic levels in humans poisoned by arsine include 3.08 mg/L (Spolyar and Harger 1950), 1.14 mg/L, and 2.25 mg As/L (Elkins and Fahy 1967) 20 mg/L, 220 mg/L (24 h post-exposure) (Uldall et al. 1970), 130 mg/L, 175 mg/L (Uldall et al. 1970), and 0.43 mg As/L (24 h post-exposure) (De Palma 1969)... 

Delayed neurologic and psychiatric disorders following acute arsine exposures have been reported (Frank 1976). Exposure concentrations were not provided, but duration of exposure ranged from 10 to 90 min. Within hours after the exposures, characteristic signs of arsine poisoning (e.g., hemolysis and hematuria) were observed. Polyneuropathies and neuropsychiatric syndromes were detected at 1-36 mon after the acute exposures to arsine. 

Bulmer, F.M.R., H.E.Rothwell, S.S.Polack, and D.W.Stewart, D.W. 1940. Chronic arsine poisoning among workers in the cyanide extraction of gold from metallic dross. Arch. Ind. Hyg. Occup. Med. 1 419. 

Elkins, H.B, and J.P.Fahy. 1967. Arsine poisoning from aluminum tank cleaning. Ind. Med. Surg. 36 747-749. 

Labes, R. 1926. The mechanism of arsine poisoning. Dtsch. Med. Wochenschr. 52 2152-2154. 

Pinto, S.S. 1976. Arsine poisoning Evaluation of the acute phase. J. Occup. Med. 22 633-635. 

There is no antidote for arsine poisoning, but its effects can be treated. The doctor may give the exposed patient fluids through a vein to protect the kidneys from damage. For severe poisoning, blood transfusions and cleansing of the blood (hemodialysis) maybe needed. 

Toxicology. Arsine is a severe hemolytic agent abdominal pain and hematuria are cardinal features of arsine poisoning and are frequently accompanied by jaundice. 

Fowler BA, Weissberg JB Arsine poisoning. N Engl J Med 19hm 1-1114, 1974... 

Teitelbaum DT, Kier LC Arsine poisoning. Arch Environ Health 19 133-143, 1969... 

Bulmer FMR et al Chronic arsine poisoning among workers employed in the cyanide extraction of gold A report of fourteen cases. J Ind Hyg Toxicol 22 111-124, 1940... 

Closely monitor serum electrolytes, calcium, BUN, creatinine, hemoglobin, and hematocrit. For victims of arsine poisoning, avoid high levels of fluid replacement to avoid the onset of congestive heart failure symptoms. 

Respiratory symptoms Administer supplemental oxygen by mask. Bronchospasms Treat with aerosolized bronchodilators or cardiac sensitizing agents. (Arsine poisoning is not known to pose additional risk during the use of bronchial or cardiac sensitizing agents). 

Arsine, the most toxic form of arsenic, exhibits some characteristics that may make it useful as a chemical warfare (CW) agent. Arsine is a colorless, odorless, nonirritating gas and is 2.5 times denser than air (Henriksson et al, 1996 Pullen-James and Woods, 2006 Thomas and Young, 2001). At concentrations above 0.5 ppm, a garlic-like odor may be noted, but arsine is toxic at much lower concentrations. Acute arsine poisoning due to inhalation of arsine gas (AsHs) is rare but has no known antidote. It is the most acutely toxic form of arsenic causing rapid and severe hemolysis immediately on exposure. The mechanisms of hemolysis are not completely understood. Arsine has a short half-life (27-96 h) and is converted to various arsenic derivatives. Although it... 

Arsine poisoning can lead to acute renal tubular necrosis and ultimately to oliguric/anuric renal failure (Rogge et al, 1983). Renal failure can be attributed to (1) direct effect of arsine on renal tissue, (2) heme-pigment nephropathy, or... 

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