化合物详情

Rapid hydrolysis in water to arsenic acids and hydrides.

Arsine was present in sewage sludge from a municipal wastewater treatment plant in Ruhrgebiet, Germany at a concentration of 0.76 ng/L. The compound was produced by pure cultures of anaerobic sewage sludge micorflora Methanobacterium formicicum, Methanosarcina, and Methanobacterium thermoautotrophicum; amounts of volatile arsine were 0.06-9.6, 0.2-1.0, and 0.073-12.6 ng, respectively(1).

It is strongly advised not to let the chemical enter into the environment.

Due to a number of acute arsine poisonings in ... zinc metallurgic plants, the environmental concentration of arsenic compounds were determined. In ... zinc metallurgy, the highest arsine concentration can occur: a) during zinc refining in the furnace ... b) during the refining furnace repair because of melting loss wetting. ... The high lead concentration at some work posts, both due to the multiple exceeding of the hygienic standard, and the simultaneous occurrence of lead and arsenic, ... create a potential possibility of forming more toxic compound, eg lead arsenide. In view of the carcinogenic exposure, it is important to take into account the possibility of interaction between arsenic and polycyclic aromatic hydrocarbons which occur during coke dry degassing.

The first signs of arsine exposure are difficultly breathing, headaches, vertigo, nausea, vomiting, abdominal pain, skin discoloration, and haemoglobinuria. (L11)

There is no antidote for arsine. Treatment is symptomatic and consists of measures to support respiratory, vascular, and renal function. Whole blood transfusions may be effective if significant haemolysis has occurred. (L11)

[lung & lymphatic cancer]

In this study the effect of sulfur, sulfur compounds, thiol-containing compounds, and thiol inhibitors on AsH(3)-induced disruption of membrane transport and hemolysis in human erythrocytes was investigated in vitro. Elemental sulfur, sodium thiosulfate, 5, 5'-dithio-bis(2-nitrobenzoic acid), and meso-2,3-dimercaptosuccinic acid were successful in delaying hemolysis, but the most successful agent was the sulfhydryl inhibitor, N-ethylmaleimide (NEM). This indicated that sulfhydryl groups, possibly membrane sulfhydryls, are major factors in the hemolytic mechanism of AsH(3). Measuring intracellular ion concentrations tested the effect of NEM on AsH(3)-induced disruption of membrane transport. AsH(3) alone caused all ions tested to flow with their concentration gradients: Intracellular K+...

Blood, kidneys, liver

LD50: 2.5 mg/kg (Intraperitoneal, Mouse) (T35) LC50: 20 ppm over 1 hour (Inhalation, Rat) (L1853)

Arsine exposure causes haemolytic anaemia, polyneuropathy, hypotension, and damage to the lungs, kidneys, liver, nervous system, heart, and blood-forming organs. (L11)

Hemolytic anemia - Decreased hemoglobin or number of red blood cells.

Inhalation

Arsine enters the bloodstream and crosses the alveolo-capillary membrane into red blood cells. Here it preferentially binds to hemoglobin and is oxidized to an arsenic dihydride intermediate and elemental arsenic, both of which are hemolytic agents. Arsine also depletes the reduced glutathione content of the red blood cells, resulting in the oxidation of sulfhydryl groups in hemoglobin and red cell membranes. These effects produce membrane instability, resulting in hemolysis. Arsine may also inhibit catalase, which leads to the accumulation of hydrogen peroxide. This destroys red cell membranes and may contribute to arsine-induced conversion of Fe+2 to Fe+3, which also impairs oxygen transport. (L11)

Chronic Inhalation: 0.016 mg/m3 (L134)

Oral Chronic Reference Dose Reference: CALEPA

A concentration of 500 ppm is lethal after exposure of a few minutes.

WHO= 0.002 mg/kg /Inorganic arsenic cmpd, as As; from table/

1, carcinogenic to humans. (L135)

LD50 Mouse ip 2.5 mg/kg

Fraction of Contaminant Absorbed in Gastrointestinal Tract: 1

CLASSIFICATION: A; human carcinogen. BASIS FOR CLASSIFICATION: Based on sufficient evidence from human data. An increased lung cancer mortality was observed in multiple human populations exposed primarily through inhalation. Also, increased mortality from multiple internal organ cancers (liver, kidney, lung, and bladder) and an increased incidence of skin cancer were observed in populations consuming drinking water high in inorganic arsenic. HUMAN CARCINOGENICITY DATA: Sufficient. ANIMAL CARCINOGENICITY DATA: Inadequate. /Inorganic Arsenic/ /based on former classification system/

Fraction of Contaminant Absorbed in Gastrointestinal Tract: 1