Arsine exposure

Human TClo values of 3 ppm (no duration specified) and 325 micrograms per cubic meter (lig/m3) (0.1 ppm) (no duration specified) have been reported (RTECS 1987). Henderson and Haggard (1943) (as cited in AIHA1993) noted that exposure of humans to arsine at 3-10 ppm for a few hours may result in signs and symptoms of poisoning. Similar to the data set for acute lethality, most information on nonlethal effects of arsine exposure in humans are case reports representing exposure estimates. 

Landrigan et al. (1982) conducted an epidemiologic survey to evaluate occupational exposure to arsine in a lead-acid battery manufacturing plant. Arsine concentrations ranged from nondetectable to 49 /breathing zone samples. A high correlation was found between urinary arsenic concentration and arsine exposure (r=0.84 p=0.0001 for an n of 47). Additionally, arsine levels above 15.6 /ig/m3 (=0.005 ppm) were associated with urinary arsenic concentrations in excess of 50 //g/L. The investigators concluded that exposure to a 200 /ig/m3 arsine exposure standard would not prevent chronic increased absorption of trivalent arsenic. 

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. 

Several reports identified nonlethal effects in humans acutely exposed to arsine. These reports, however, lacked definitive exposure data but verified hematologic disorders leading to renal failure as critical effects of arsine exposure. Bulmer et al. (1940) (as cited in Elkins 1959) reconstructed an exposure incident at a gold extraction facility and estimated that subchronic (up to 8 mon) exposure to 0.12 ppm arsine resulted in jaundice and anemia (see Section 2.2.1). The lack of definitive exposure data for humans necessitates the use of animal data for quantitative estimation of AEGL values. Derivation of AEGL-2 values based upon limited human data (Flury and Zernik 1931) was considered but rejected because the data were poorly documented and inconsistent with other data showing lethality at lower cumulative exposures. 

Consistent with the human responses to arsine exposure, observations in several animal species (rats, mice, and hamsters) indicated hematologic involvement. Cumulative exposures of 540-1,800 ppm-min produced decreases in hematocrit levels, RBC counts, packed cell volumes, and increases in absolute and relative spleen weights (consistent with erythrocyte damage). For acute exposures, the exposure-response curve is steep generally less than a 10-fold difference between no-effect and lethality exposures. 

Risk, M., and L.Fuortes. 1991. Chronic arsenicalism suspected from arsine exposure A case report and literature review. Vet. Hum. Toxicol. 33 590-595. 

Reference Peterson, D.P., and M.H.Bhattacharyya. 1985. Hematological responses to arsine exposure quantitation of exposure response in mice. Fundam. Appl. Toxicol. 5 499-505... 

Arsine affects the ability of the blood system to carry oxygen by destroying red blood cells. The lack of oxygen rapidly affects all body tissues, especially the central nervous system. Arsine may also affect the kidneys, liver, and heart. Most deaths related to arsine exposure are believed to be secondary to acute renal failure. Arsine is carcinogenic. 

What Immediate Health Effects May Result from Arsine Exposure ... 

There are no specific tests for arsine exposure. However, blood, urine and other tests may show if there has been any serious injury to the lungs, blood cells, kidneys, or nerves. 

Caution Arsine is a flammable and highly toxic gas that does not provide adequate warning of hazardous levels. Inhalation is the major route of arsine exposure, although there is little information about absorption through the skin or toxic effects on the skin or eyes. Contact with liquid arsine may result in frostbite. 

Field First Aid Evacuate the Hot Zone at once when there is any release of arsine consider any victims who may have inhaled arsine to have suffered a potentially toxic dose. Although small amounts of arsine can be trapped in the victim s clothing or hair, these quantities are not likely to cause a danger for first response personnel outside the Hot Zone. Toxic effects could be delayed for up to two to twenty-four hours after exposure arsine exposure victims should all be evaluated at a medical facility. There is no specific antidote for arsine treatment is symptomatic and consists of actions to support respiratory, vascular, and renal functions. 

With arsine exposure, there may be potential severe hemolysis (the breakdown of red blood cells and the release of hemoglobin). Ensure adequate oxygenation by arterial blood measurement or pulse oxygenation monitoring. Use diuretics to maintain urinary flow. 

Extremities - possible paresthesias and Mees lines with chronic arsenic toxicity from arsine exposure. 

Blood and urine arsenic levels are elevated aeutely 0 A 24-h urine arsenie may help in monitoring ehronic, low-level arsine exposures... 

Chronic arsenic toxicity - patients surviving acute arsine exposure may develop chronic arsenic toxicity, including anemia and peripheral neuropathy. 

The main chronic effect of arsine exposure (low dose) in humans is anemia. Repeated exposure to arsine may also damage the kidneys, liver, heart, and nervous system. There is a concern about the formation of carcinogenic arsenic from long-term exposure to arsine. 

In acute exposure prompt medical attention is critical. The victim should be immediately removed to fresh air and away from the source of exposure. Oxygen should be provided if there is a respiratory distress. Initial therapy should be directed at stopping the ongoing hemolysis by performing exchange transfusion. Currently there is no other treatment to decrease arsine hemolysis however, studies in vitro have shown that some dithiol chelators (meso-2,3-dimercaptosuccinic acid, DMSA 2,3-dimercapto-l-propanesulfonic acid, DMPS and 2,3-butanedithiol) are effective (see Further Reading). This should be followed by aims to restore renal function or compensate for lost renal function (hemodialysis). This process does not remove any formed arsenic from the exposed body. Administration of dimercaprol (British Anti-Lewisite, BAL) has no effect on arsine hemolysis, but it lowers blood arsenic levels resulting from arsine exposure. The use of chelators must be... 

Ayala-Fierro F, Baldwin AL, Wilson LM, Valeski JE, and Carter DE (2000) Structural alterations in the rat kidney after acute arsine exposure. Laboratory Investigation 80(1) 87-97. 

Figure 4-41. Representation of the atomic layer epitaxial (ALE) process, (i) TMGa exposure, leaving a Ga layer (ii), (iii) arsine exposure, leaving an As layer (iv), (v) the cycle begins to repeat.

Bone marrow depression, anemia, leukopenia, and basophilic stippling are associated with chronic arsenic exposure. Arsine (AsHj) poisoning can produce widespread hemolysis. Cirrhosis, ascites, and destruction of renal tissues have been reported. Arsine exposure may also cause renal failure (Forth et al. 1996). 

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