The above information was obtained from the National Institute for Occupational
Safety and Health's computerized Registry of Toxic Effects of Chemical
Substances (RTECS), and from the National Library of Medicine's computerized
chemical dictionary file CHEMLINE. Registered trademark information is not
included in these files. Therefore, some of the above synonyms and identifiers may
be trademarked but are not so indicated above.
ARSINE (Arsenic Hydride) POISONING IN THE WORKPLACE
August 3, 1979
The National Institute for Occupational Safety and Health (NIOSH) recommends
that appropriate work practices be implemented to reduce the risk of worker
exposure to arsine (AsH3) gas, There is a high potential for the generation of
arsine gas when inorganic arsenic is exposed to nascent (freshly formed) hydrogen.
This recommendation is based on several reports of worker exposure to arsine
resulting in severe toxic effects or death. Most of the reported cases occurred
when arsine was accidently generated during an industrial process. NIOSH would
like to inform the occupational health community of some of the circumstances in
which workers have been poisoned by arsine, with particular emphasis on the
underlying mechanisms of generating the gas. We request that producers and
distributors of arsenic and materials containing arsenic transmit information to
their customers and employees, and that professional associations and unions
inform their members.
Stibine (SbH3), another toxic gas, is formed when antimony is exposed to nascent
hydrogen. In most situations where arsine can be formed stibine can also be
formed if antimony is present. Therefore, similar work practices should be
implemented to reduce the risk of worker exposure to stibine.
Background
Identified in 1775, arsine is a highly poisonous, colorless, nonirritating gas with a
mild garlic odor. It is soluble in water, and slightly soluble in alcohol and alkalies.
When nascent hydrogen is generated in the presence of arsenic, or when water
reacts with a metallic arsenide, arsine evolves. Most cases of arsine poisoning
have been associated with the use of acids and crude metals, one or both of which
contained arsenic as an impurity. Ores contaminated with arsenic can liberate
arsine when treated with acid.1 Arsine is commercially
produced for use in organic synthesis, and the processing of solid state electronic components.
In industrial settings arsine poisoning generally results from the accidental
formation of arsine gas. Most reported cases of exposure to arsine have occurred
during the smelting and refining of metals. However, there are many other
situations where exposures to lethal concentrations of the gas have been reported
including galvanizing, soldering, etching and lead plating operations. Arsine can be
produced by fungi (especially in sewage) in the presence of arsenic. The renewed
interest in coal as a source of energy causes concern for a possible increase in the
number of exposures to arsine, because coal contains considerable quantities of
arsenic. The processes for converting coal to gas and other by-products should
include preventative measures aimed at reducing the chance of transformation of
the arsenic impurities into arsine.1
Occupational Standards and
Exposures
The current Department of Labor, Occupational Safety and Health Administration
(OSHA) standard for occupational exposure to arsine is 0.05 ppm (0.2 mg/cu m of
air) as a time-weighted average in any 8-hour work shift of a 40-hour work week.
The present OSHA standard for occupational exposure to stibine to 0.1 ppm (0.5
mg/cu m of air) in any 8-hour work shift of a 40-hour work week.2
The 1975 NIOSH Criteria Document on inorganic arsenic recommended that worker exposure
to inorganic arsenic and to arsine be limited to 0.002 mg (2.0 ยต) of arsenic/cu m of
air as determined by a 15-minute sampling period. The document states that the
short-term limit is intended to achieve the greatest practicable reduction in
worker exposure while avoiding spurious sampling results which can be produced by
natural background concentrations of inorganic arsenic.3 The 1978 NIOSH
criteria document on antimony recommended the retention of the specific Federal
limit for occupational exposure to antimony, without recommending a limit for
stibine.4
The NIOSH National Occupational Hazard Survey (NOHS) estimates that approximately
900,000 workers are occupationally exposed to identified sources of arsenic
for varying periods of time during the workday. This estimate is not, however,
based on actual workplace environmental exposure measurements. However,
arsenic is a widespread element, and therefore unidentified exposures can occur in
unsuspected work situations. The NOHS estimate for occupational exposure to
antimony is approximately l,7OO,OOO workers.5
Toxicity
The first case of arsine poisoning was reported in 1815 after a German chemist
died from an exposure to arsine in his laboratory. From 1815 to 1928, 247 cases of
arsine poisoning were reported. From 1928 to 1974 an additional 207 cases were
reported, of which 51 (25%) were fatal.1
Acute Arsine Toxicity - Arsine is the most acutely toxic form of arsenic and one of
the major industrial causes of sudden extensive hemolysis (destruction of red blood
cells). It has the ability to combine with hemoglobin within the red blood cell,
causing destruction or severe swelling of the cell, rendering it nonfunctional.1
Inhalation of 250 ppm (800 mg/cu m) of arsine gas is instantly lethal. Exposures of
25-50 ppm (80-160 mg/cu m) for one-half hour are lethal, and 10 ppm (32 mg/cu m)
is lethal after longer exposures. The Mean Lethal Dose (MLD) is unknown for man,
but in small mammals it is about 0.5 mg/kg body weight.6
The characteristic features of acute arsine poisoning are abdominal paint bloody
urine, and jaundice (yellow discoloration of the skin). Initial symptoms of arsine
poisoning are headache, malaise, weakness, dizziness difficult breathing,
abdominal pain, nausea, and vomiting, which are usually first noticed 2 to 24 hours
after exposure. Bloody urine, light to dark red, is frequently noticed 4-6 hours
after exposure to arsine and is often followed by jaundice 12-48 hours later. An
unusual bronze discoloration of the skin can often be observed accompanying the
jaundice. If the arsine exposure is severe, the products resulting from the
breakdown of red blood cells and hemoglobin will clog the kidneys, causing a
reduction in the amount of urine formed, sometimes to the point of complete
blockage of urine formation. Other toxic effects of arsine include damage to the
liver and heart, either by direct actions of arsine in the cells or due to the
formation of arsenic.1,7
Chronic Arsine Toxicity - Most reported cases of arsine poisoning have been acute
or sub-acute in nature, usually resulting from a single short exposure or from
breathing the gas for a few hours. In one report of chronic arsine poisoning, it was
noted that arsine in very small concentrations appeared to exert a cumulative,
damaging effect. This was manifested by a progressive drop in the number of red
blood cells and in the hemoglobin level. The exposed victims experienced shortness
of breath on exertion, and a general feeling of weakness. However, in relation to
the degree of blood destruction, the degree of known disability experienced by the
victims of chronic arsine poisoning was less than expected.8
Chronic Arsenic Toxicity - Since inorganic arsenic is needed to generate arsine,
prolonged exposures to low levels of arsine are likely to occur under conditions
where workers are also exposed to inorganic arsenic. Once arsine is inhaled, it
breaks down, releasing inorganic arsenic into the blood stream. The worker's risk
of arsenic poisoning is therefore increased by the combination of inorganic arsenic
exposure and the breakdown of arsine. A number of signs and symptoms are
associated with arsenic poisoning. When ingested arsenic compounds can cause
nausea, vomiting and diarrhea within a few hours. Dermatitis may be observed
after chronic ingestion but the typical signs include increased pigmentation, and
thickening of the skin on the palms and soles of the feet. Changes in the heart's
performance as measured by the electrocardiogram (ECG) have been reported
after chronic arsenic intoxication. Observed ECG changes regressed after arsenic
exposure ceased. Decreased numbers of red and white blood were reported in
cases of chronic intoxication but these changes also regressed after arsenic
ingestion ended. Skin cancer has long been considered a consequence of arsenic
exposure, however multiple cancers of the internal organs have also been reported.3
Case Reports - Most cases of arsine poisoning occur after the accidental
generation of the gas in the workplace. During recent years of may incidents have
involved a reaction between arsenic and aluminum, with the subsequent release of
hydrogen in the presence of water to permit the formation of arsine gas.9 Tables
1, 2, and 3 list examples of accidental arsine poisoning reported in the literature.
TABLE 1. Examples of workers poisoned by arsine in smelting and refining
operations.
Three workers were poisoned while using a jackhammer to remove slag
from ladles. To reduce dust, water was sprayed on the slag. The water
reacted with the arsenide of the alkali metal, generating arsine.9
A worker was poisoned while cleaning an obstructed industrial drain
which contained acid liquors with arsenic impurities. A galvanized
shovel and bucket were used to carry the sludge from the drain. The
acidic arsenic liquor reacted with the zinc coating of the bucket and
produced arsine.10
Thirteen workers were poisoned (3 died) during the purification of lead
alloys. Arsine fumes were generated by moisture reacting with
aluminum arsenide in metal dross.11
A worker was poisoned during reclamation of metal from flue dust
obtained from blast furnaces. Zinc, water, and sulphuric acid had been
added to the dust. Upon heating with steam, arsine was formed because
arsenic impurities and nascent hydrogen were both present.12
TABLE 2. Examples of workers poisoned by arsine in enclosed spaces.
Two workers were poisoned while cleaning an aluminum trailer tank
with a phosphoric acid solution. The tank had been used 6 months
previously for the transport of a 42% solution of sodium arsenite (weed
killer). Since that time it had been cleaned with steam and detergent,
and used for storage and transportation of alcohol and other industrial
solvents. Before assigning the trailer to another client, a thorough
cleaning job was ordered, which required the hand application of the
acid cleaner. Subsequently, arsine was generated by a reaction between
the acid cleaner and the aluminum which had arsenic impurities.13
Three workers were poisoned while using an aluminum ladder to descend
into a chemical evaporation tank containing a few inches of sodium
arsenite. The aluminum ladder reacted with the sodium arsenite,
liberating arsine.14
Eight sailors were poisoned when a cylinder containing arsine developed
a leak, emitting the gas into the airspace of a cargo hold on board a
freighter.15
TABLE 3. Examples of workers poisoned by arsine in miscellaneous occupational
settings.
A worker was poisoned while pouring freshly diluted commercial
hydrochloric acid through the pipes of a water jacket. The manufacturer
had added sodium arsenite and aniline hydrochloride to the acid to
act as inhibitors to the corrosive action of the acid. Subsequently the
mixture of water and sodium arsenite under these conditions led to the
generation of arsine.16
Five workers were poisoned while washing aluminum slag to dissolve out
soluble constituents. Apparently, the copper in this mixture was
contaminated with arsenic.17
Eight children and one adult were poisoned on a farm while cleaning a
dipping vat. Two years before, arsenic had been used in the vat as an
insecticide. Later, with another insecticide, superphosphate was added
to create an acid medium, thereby leading to arsine production.18
Two workers were poisoned after a commercial drain cleaner was added
to a drain which contained water and arsenic residues. The drain
cleaner contained sodium hydroxide, sodium nitrate, and aluminum
chips. These chemicals reacted to produce onascent hydrogen, which
bonded with the arsenic, leading to generation of arsine.19
Although the accidents illustrated in the above tables differ with respect to the
surrounding circumstances, the basic reactions leading to arsine formation are
similar. Arsine usually evolved when nascent hydrogen was generated in the
presence of arsenical compounds or by the hydrolysis of a metallic arsenide in
contact with water. Invariably, there was an acid medium where metal was
present (e.g., dross residues galvanized implements, aluminum tanks or
implements) thereby creating the key ingredients necessary for arsine formation.
A more recent area of concern involves the recycling of batteries. Lead alloys in
car batteries contain antimony as a hardener, with arsenic and silver added to
inhibit corrosion. In the production of "maintenance-free" bateries, calcium is
added to the lead alloys as a hardening agent. During recycling, arsine can be
released if scrap containing arsenic is melted down with the "maintenance-free"
batteries containing calcium. When the scrap mixture is in the molten state,
calcium arsenide is formed. As cooling occurs, the calcium arsenide floats to the
surface as part of the dross, and in the presence of water, arsine evolves.20
Other Considerations
Stibine (SbH3; hydrogen antimonide; antimony hydride; antimony trihydride)-
Antimony (Sb) can be converted to stibine by a similar series of reactions required
to convert arsenic to arsine. Stibine equals or surpasses arsine in toxicity, and
causes a specific toxic action which closely resembles that of arsine.21 Although
stibine is chemically similar to arsine, it is less stable. Probably because of this
instability fewer cases of stibine poisoning have been reported.22 Stibine can
evolve when certain alloys containing antimony (Sb) are treated with acid and
subjected to electrolytic action, when certain antimony compounds are treated
with steam, or whenever nascent hydrogen comes in contact with metallic
antimony or with a soluble antimony compound.
When stibine enters the bloodstream, it reacts with the hemoglobin of red blood
cells, leading to destruction of the cells.21 Stibine exerts a direct effect on the
brain tissue cells, leading to various degrees of degeneration.23 Victims of
stibine poisoning have experienced marked weakness headache, nausea, severe
abdominal and lower back pain, and blood in the urine. These symptoms are similar
to those caused by arsine toxicity.24
NIOSH Recommendation
In light of the serious and accidental nature of exposure to arsine and/or stibine,
NIOSH recommends that steps be taken to prevent exposure to these gases.
Whenever the possibility exists for either gas being generated, such as when
working with metals (crude, drosses, or implements made of metal) care should be
taken to assure that arsenic and antimony do not react with any sources of fresh
hydrogen. Similarily, when working with arsenical compounds care should always
be taken to prevent the inadvertant generation of hydrogen gas in the presence of
arsenicals. In all occupational settings where there is arsenic, workers should be
informed of the possibility of arsine formation when there is nascent (freshly
formed) hydrogen present. Likewise, workers exposed to antimony compounds
should be informed of the possibility of exposure to stibine when freshly formed
hydrogen is present.
Further research on the chronic and acute effects of exposure to arsine and stibine
is needed. Although the acute toxicity of arsine in humans is fairly well defined,
very little information is available on long term effects of exposure to arsine with
simultaneous exposure to other arsenic compounds. In addition more research into
methods of sampling for the presence of arsine and stibine in air is needed, for both
monitoring and documentation purposes.
In the event arsine and/or stibine is generated, immediate steps should be taken to
remove workers from the contaminated environment. In cases of exposure or
when any symptoms are first observed prompt medical attention is imperative.
Treatment of arsine poisoning should include: (a) immediate blood exchange
transfusion to replace the destroyed red blood cells, and also to remove arsenic
and the hemoglobin-arsine complex; (b) the adminstration of therapeutic amounts
of dimercaprol (BAL); and (c) dialysis should be started if the patient has suffered
kidney damage. Exchange transfusions lower blood arsenic levels, but dialysis,
though it may be life-saving, does not remove arsenic from the patient. Therefore,
efforts should be made to remove arsenic from the victim's body.25 Other
medical support measures should be utilized as indicated.
[signature]
Anthony Robbins, M.D.
Director
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Copies of this and other NIOSH documents are available from: