Arsine is an inorganic compound with the formula AsH3. This flammable, pyrophoric, and highly toxic gas is one of the simplest compounds of arsenic. [1] Arsine has a garlic-like or fishy odour that can be detected at concentrations of 0.5 ppm and above. Because arsine is non-irritating and produces no immediate symptoms, persons exposed to hazardous levels may be unaware of its presence. Arsine is water soluble. [2] Arsine is formed when arsenic comes in contact with an acid. [3]

Uses [2,3]

Arsine is used as a doping agent in the semiconductor industry and in the manufacture of crystals for fiberoptics and computer chips. It is used infrequently in galvanizing, soldering, etching, burnishing, and lead plating. It was also investigated as a warfare agent during World War II, but it was never used on the battlefield.

Sources & Routes of Exposure

Sources of Exposure [2]

Arsine gas is formed when arsenic-containing materials react with freshly formed hydrogen in water or acids. Exposure may result when arsenic containing metals (i.e., metal vats) undergo acid washes. Unintentional exposures have also occurred during refining of ores (e.g., lead, copper, zinc, iron, and antimony ores) that contain arsenic.

Routes of Exposure [2]

  • Inhalation is the major route of exposure. The odour threshold of arsine is 10-fold greater than the Occupational Safety and Health Administration (OSHA) permissible exposure limit. Odour is not an adequate indicator of arsine’s presence and does not provide reliable warning of hazardous concentrations. Arsine is heavier than air and hazardous concentrations may develop quickly in enclosed, poorly ventilated, or low-lying areas.
  • Skin/Eye Contact: There is little information about direct toxic effects of arsine on the skin or eyes, or about absorption through the skin. Exposure to liquefied arsine (the compressed gas) can result in frostbite.
  • Ingestion of arsine itself is unlikely because it is a gas at room temperature. However, metal arsenides are solids that can react with acidic gastric contents, releasing arsine gas in the stomach.

Health Effects [2]

Acute Exposure

After absorption by the lungs, arsine enters red blood cells (RBC) where different processes may contribute to haemolysis and impairment of oxygen transport. Inhibition of catalase may lead to accumulation of hydrogen peroxide which, as an oxidiser, destroys red cell membranes and may contribute to arsine-induced conversion of Fe+2 to Fe+3, which also impairs oxygen transport. Arsine preferentially binds to haemoglobin, and is oxidised to an arsenic dihydride intermediate and elemental arsenic, both of which are haemolytic agents. Arsine toxicity involves depletion of reduced glutathione. Therefore, people deficient in the enzyme glucose-6-phosphate-dehydrogenase (G6PD) are more susceptible to haemolysis following arsine exposure. Pre-existing cardiopulmonary or renal conditions, iron deficiency, and/or pre-existing anaemia may result in more severe outcomes if haemolysis occurs. Contact with the skin or eyes is not expected to result in systemic toxicity. Ingestion of arsine is unlikely, but ingestion of metallic arsenides can lead to arsine gas production and toxicity.


Acute intravascular haemolysis develops within hours and may be severe during the first 2 or 3 days following exposure. Free haemoglobin levels in plasma rise (levels greater than 2 g/dL have been reported). Anaemia ensues subsequent to haemolysis. Anaemia may develop quickly and be severe. Leukocytosis and signs of intravascular coagulation can be observed during the haemolytic phase. Methemoglobinaemia can be of concern in infants and toddlers. Children may be more vulnerable to loss of effectiveness of haemoglobin because of their relative anaemia compared to adults.


A garlic odour may be present on the breath. Delayed accumulation of fluid in the lungs may occur after massive exposure. Dyspnoea may be due to lack of oxygen secondary to haemolysis. Children may be more vulnerable to gas exposure because of relatively higher minute ventilation per kg and failure to recognise the need to promptly evacuate an area when exposed.


Kidney failure due to acute tubular necrosis is a significant sequela of arsine exposure. Haemoglobin in the urine is thought to be the major cause of damage to the kidneys; however, a direct toxic effect of arsine or deposition of the arsine-haemoglobin-haptoglobin complex may also play a role. Urinalysis shows large amounts of protein and free haemoglobin usually without intact RBCs. Urine may be unusually coloured (e.g., brown, red, orange, or greenish). Decreased urinary output may develop within 24-48 hours.


Nausea, vomiting, and crampy abdominal pain are among the first signs of arsine poisoning. Onset varies from a few minutes to 24 hours after exposure.


The characteristic bronze tint of the skin caused by arsine toxicity is induced by haemolysis and may be caused by haemoglobin deposits. The bronze coloration is not jaundice, although jaundice may develop later as a result of significant haemolysis. Contact with liquefied arsine (compressed gas) can cause frostbite.


Headache is often an early sign of exposure. CNS disorders can develop several days after severe exposure; signs include restlessness, memory loss, disorientation, and agitation. Some exposed persons experience signs of peripheral nerve damage 1-2 weeks after exposure. There are case reports of polyneuropathy developing 1-6 months after arsine exposure.


Right upper quadrant pain, hepatomegaly, elevated serum globulin, elevated liver enzymes and prolonged prothrombin time have been observed.


Skeletal muscle injury or necrosis have been reported. Muscle pain and twitches, myoglobinuria, elevated levels of serum creatine phosphokinase (CPK), and aldolase have been observed.


Cardiovascular effects may include moderate and transient sinus tachycardia secondary to haemolysis or anaemia, hypovolemia or acute pulmonary oedema, hypotension and cardiovascular shock due to direct effects on the myocardium and hyperkalaemia, elevation of the T-wave (ECG) and various degrees of heart block, and general vasoconstriction due to peripheral hypoxia.


Watery eyes, photophobia, blurred vision, and red staining of the conjunctiva may appear early after exposure.

Chronic Exposure

Chronic arsine exposure can result in gastrointestinal upset, anaemia, and damage to lungs, kidneys, liver, nervous system, heart, and blood-forming organs. There is little information regarding health effects of chronic low-level exposures to arsine.


There are no data on the carcinogenicity of arsine in humans or in experimental animals. However, arsine is oxidised to the same trivalent and pentavalent forms of arsenic as those seen after drinking-water or inhalation exposure to arsenic compounds known to present a cancer hazard. The Department of Health and Human Services (DHHS), the International Agency for Research on Cancer (IARC), and the Environmental Protection Agency (EPA) have classified inorganic arsenic as a human carcinogen based on sufficient evidence from human data.

Reproductive and Developmental Effects

Arsine should be treated as a potential teratogenic agent. Although the reproductive effects of acute or chronic exposure to arsine are unknown, some related inorganic arsenicals produce a broad spectrum of adverse developmental effects in animals. Animal studies indicated that in arsine-exposed mothers, arsenic crosses the placenta and reaches the foetus; however, no adverse developmental effects were observed.

Safety [5]

First Aid Measures

  • Inhalation: Immediately remove to fresh air. If not breathing, give artificial respiration. If breathing is difficult, qualified personnel may give oxygen. Call a physician. Symptoms may be delayed. Consider any exposure as a potentially toxic dose.
  • Skin contact: Adverse effects not expected from this product. The liquid may cause frostbite. For exposure to liquid, immediately warm frostbite area with warm water not to exceed 105°F (41°C). Water temperature should be tolerable to normal skin. Maintain skin warming for at least 15 minutes or until normal colouring and sensation have returned to the affected area. In case of massive exposure, remove clothing while showering with warm water. Seek medical evaluation and treatment as soon as possible.
  • Eye contact: Immediately flush eyes thoroughly with water for at least 15 minutes. Hold the eyelids open and away from the eyeballs to ensure that all surfaces are flushed thoroughly. Contact an ophthalmologist immediately.
  • Ingestion: Ingestion is not considered a potential route of exposure.

Fire Information

  • Arsine is a toxic, flammable liquefied gas.
  • Vapour forms explosive mixtures with air and oxidising agents.
  • If leaking gas catches fire, do not extinguish flames.
  • Flammable and toxic vapours may spread from leak and could explode if reignited by sparks or flames.
  • Vapours are heavier than air and may collect in low spots. Explosive atmospheres may linger.
  • Evacuate all personnel from the danger area. Use self-contained breathing apparatus (SCBA) and protective clothing.
  • Immediately cool containers with water from maximum distance.
  • Stop flow of gas if safe to do so, while continuing cooling water spray.
  • Remove ignition sources if safe to do so.
  • Remove containers from area of fire if safe to do so.

Exposure Controls and Personal Protection

Engineering Controls

  • Use an explosion-proof local exhaust system.
  • Local exhaust and general ventilation must be adequate to meet exposure standards.
  • Use explosion proof equipment and lighting.

Personal Protective Equipment

The following personal protective equipment is recommended when handling arsine:

  • Hand protection: Neoprene rubber.
  • Eye protection: Wear safety glasses when handling cylinders; vapour-proof goggles and a face shield during cylinder change out or whenever contact with product is possible. Select eye protection in accordance with OSHA 29 CFR 1910.133.
  • Skin and body protection: Wear metatarsal shoes and work gloves for cylinder handling, and protective clothing where needed. Wear appropriate chemical gloves during cylinder change out or wherever contact with product is possible. Select per OSHA 29 CFR 1910.132, 1910.136, and 1910.138.
  • Respiratory protection: When workplace conditions warrant respirator use, follow a respiratory protection program that meets OSHA 29 CFR 1910.134, ANSI Z88.2, or MSHA 30 CFR 72.710 (where applicable). Use an air-supplied or air-purifying cartridge if the action level is exceeded. Ensure that the respirator has the appropriate protection factor for the exposure level. If cartridge type respirators are used, the cartridge must be appropriate for the chemical exposure (e.g., an organic vapour cartridge). For emergencies or instances with unknown exposure levels, use a self-contained breathing apparatus (SCBA).
  • Thermal hazard protection: Wear cold insulating gloves when transfilling or breaking transfer connections.

Regulation [6]

United States

OSHA: The United States Occupational Safety & Health Administration has set the following Permissible Exposure Limits (PEL) for arsine of:

  • General Industry: 29 CFR 1910.1000 Z-1 Table — 0.05 ppm, 0.2 mg/m3 TWA
  • Maritime: 29 CFR 1915.1000 Table Z-Shipyards — 0.05 ppm, 0.2 mg/m3 TWA

ACGIH: The American Conference of Governmental Industrial Hygienists has set a Threshold Limit Value (TLV) for arsine of 0.005 ppm, 0.016 mg/m3 TWA

NIOSH: The National Institute for Occupational Safety and Health has set a Recommended Exposure Limit (REL) for arsine of 0.002 mg/m3 Ceiling (15 min); Potential Carcinogen


Safe Work Australia: Safe Work Australia has established a Time Weighted Average Concentration for arsine of 0.05 ppm, 0.16 mg/m3 for a 40-hour work week.