E X T O X N E T
Extension Toxicology Network
A Pesticide Information Project of Cooperative Extension Offices of
Cornell University, Michigan State University, Oregon State University, and
University of California at Davis. Major support and funding was provided
by the USDA/Extension Service/National Agricultural Pesticide Impact
TRADE OR OTHER NAMES
Current trade or other names include Fastphos, Fumitoxin, Gastoxin, Max-
Kill, Phosfume, Phostoxin and Weevilcide (1, 4). Al-phos, Celphide, Celphine,
Celphos, Detia-Gas-Ex, and Quick Tox may have been used in previous
formulations (1, 3).
Aluminum Phosphide is a Restricted Use Pesticide so may be purchased and
used only by certified applicators (2). It is in EPA Toxicity Class I and
products containing it must bear the signal word DANGER (1, 2). Aluminum
Phosphide was first registered for use in the United States in the late 1950s
Aluminum phosphide is an inorganic phosphide used to control insects and
rodents in a variety of settings. It is mainly used as an indoor fumigant at
crop transport, storage or processing facilities (or in shipholds, railcars,
etc.) for both food and non-food crops (1, 3). It may also be used as an
outdoor fumigant for burrowing rodent and mole control, or in baits for rodent
control in crops (3).
Aluminum Phosphide is available in pellet and tablet form, and is also
available in porous blister packs, sachets or as dusts (3, 4). As in the case
of Phostoxin, it may be formulated as 55% active ingredient along with
ammonium carbamate and inert ingredients (3, 5).
Phostoxin and aluminum phosphide are not absorbed dermally; main routes
of exposure are through ingestion and inhalation (5). They are highly toxic
via both these routes. The reported rodent oral LD50 is 11.5 mg/kg for
Phostoxin, with that for the technical compound presumably lower (4, 5).
Aluminum phosphide ingested orally reacts with water and stomach acids to
produce phosphine gas, which may account in a large part for observed toxicity
(6, 7). Phosphine generated in the gastrointestinal tract is readily absorbed
into the bloodstream, and it is readily absorbed through the lung epithelium
(6). Phosphine may cause denaturing of oxyhemeglobin (the carrier for
systemic distribution of oxygen) as well as enzymes important for respiration
and metabolism, and may also have effects on cellular membranes (9). Inhaled
aluminum phosphide dust undergoes the same reaction in the moist air sacs of
the lung, although at a lower rate, resulting in similar local and systemic
effects (6, 7).
The rodent 4-hour inhalation LC50 for phosphine gas (the product of
phosphide reaction with water) is widely reported as 15 mg/meters cubed (15
ug/L, or approximately 10.7 ppm) (6,7). Recent study indicates that the
rodent 4-hour inhalation LC50 may exceed 15 mg/meters cubed (8). In this
study, male and female rats experienced no mortality at one-time 6-hour
exposure levels of 15 mg/meters cubed (8). Red mucous discharge from the
nostrils ceased during a 14-day recovery period; postmortem examination
revealed no gross or microscopic treatment-related effects (8).
Symptoms of mild to moderate acute aluminum phosphide toxicity include
nausea, abdominal pain, tightness in chest, excitement, restlessness,
agitation and chills (5, 6). Symptoms of more severe toxicity include,
diarrhea, cyanosis, difficulty breathing, pulmonary edema, respiratory
failure, tachycardia (rapid pulse) and hypotension (low blood pressure),
dizziness and/or death (6, 7). Convulsions have been reported in lab animals
exposed to high concentrations of phosphine (6). Severe exposure may also
result in proteinuria or glucosuria (low molecular weight proteins or glucose
in the urine) indicating kidney damage (7).
Pathological examination of exposed laboratory animal tissue and results
of post-mortem examinations of phosphine poisoning victims generally indicate
hypoxia, with evidence of local trauma in the gastrointestinal tract or lungs,
liver, kidneys and central nervous system (6).
Data from a cohort of occupationally-exposed Indian agricultural
fumigation workers undergoing single exposures of approximately 1-3 mg/meters
cubed (0.71 - 2.22 ppm) revealed reversible (within 2 weeks) symptoms of mild
acute exposure (of the types noted above) (7).
Rats fed aluminum phosphide-fumigated chow averaging 0.51 ppm phosphine
residues (approximately 0.43 mg/kg/day) showed no differences from the control
animals with respect to blood or urine chemistry and no observable differences
in tissue structure (7). It was reported that workers had probably
encountered similar exposures on an intermittent basis (in some cases over as
long as a 20 year period) and had yet to show signs of toxicity (7), which
suggests that chronic effects may be minor or have a very long latency period.
Inhalation studies were conducted on the effects of phosphine gas on male
and female rats exposed at levels of 0.5, 1.5, and 4.5 mg/meters cubed for six
hours per day over a 13 week period (8). Higher exposure groups (7.5 and 15
mg/meters cubed) were added following preliminary acute test results (8).
Results indicated that 15 mg/meters cubed was lethal to 4 out of ten female
rats following three days of exposure (8). Significant treatment-related
effects on body weight and decreased food consumption were seen across all
treatment groups and sexes, but were reversible (8). Decreases in red-blood
cell counts, hemoglobin, hematocrit and increased platelet counts were seen in
male rats of the 4.5 mg/meters cubed group (8). Dose-related changes in blood
urea nitrogen and other clinical parameters were also seen across exposure
groups (8). Post-mortem examination of test animals revealed microscopic
lesions in the outer cortex of the kidneys of rats exposed to 15 mg/meters
cubed, but not at lower exposure levels (8). All of these effects were
apparently reversible following a four-week recovery period (8).
Post-mortem examination of test animals revealed apparently reversible
damage to seminal vesicles in male rats exposed to 1.5 mg/meters cubed
phosphine (8). Pregnancy rates for female rats exposed to 4.5 mg/meters cubed
on days 6-10 of gestation were comparable to those in the unexposed group (8).
No adverse effects on uterine implantation were seen in the 0.3, 3 and 4.5
mg/meters cubed exposure groups, although a statistically significant
elevation in resorptions was seen in the 0.015 mg/meters cubed exposure group
(8). Thus, this effect may not be dose-related as it there was not increased
effect with increased dose. The available evidence for reproductive effects
in animals suggest that reproductive effects are not likely in humans under
No effects on fetal birthweights or sex ratios were seen in offspring of
rats exposed to up to 4.5 mg/meters cubed for six hours a day on days 6-10 of
gestation (8). No statistically significant differences in development or
morphology were seen in the offspring of rats in the exposed groups versus
unexposed groups upon external, visceral or skeletal evaluation (8). The
available evidence for teratogenic effects in animals suggests that such
effects are not likely in humans under normal conditions.
No evidence was available regarding the ability of aluminum phosphide or
phosphine to cause mutations or increase the mutation rate. Studies of human
lymphocyte cultures exposed under laboratory conditions showed significant
increases in phosphine-induced total chromosomal aberrations (e.g. gaps,
deletions, breaks or exchanges) with increasing phosphine concentrations (9).
In the same study, analysis of lymphocyte cultures drawn from fumigators
(using phosphine exclusively) exposed to phosphine showed significant
increases in the same types of chromosomal aberrations.
No data are currently available; it is possible that some testing on the
oncogenicity may be initiated in the near future (4).
Acute toxicity resulting from aluminum phosphide exposure is apparent
most immediately in the heart and lungs; it may also affect the central
nervous system, liver and kidneys (6).
Fate in Humans & Animals
As stated above, aluminum phosphide rapidly reacts with water to form
highly toxic phosphine gas. It has been reported that aluminum phosphide may
be absorbed directly into the bloodstream, although this is probably a very
minor route of entry (10). That phosphine which is not expired through the
lungs may be metabolized to phosphates, hypophosphite and phosphite (1, 10).
Effects on Birds
The precise oral or inhalation median lethal doses for aluminum phosphide
or phosphine in birds are not known. It is reported that exposure of turkeys
and hens to 211 and 224 mg/meters cubed for 74 and 59 minutes respectively
resulted in labored breathing, swelling of organs, tonic-clonic convulsions
and death (11). Due to the mechanism of action it is likely that it could
similarly affect other bird species at similar levels of exposure.
Fortunately, such exposure is not very likely, as phosphine is rapidly
dissipated in open air.
Effects on Aquatic Species
The reported acute LC50 is 4.1 ug/L in rainbow trout, indicating very
high toxicity (12). No data were available regarding the specific toxicity of
aluminum phosphide or of phosphine to other fish or aquatic species (e.g. LC50
or EC50 values), but due to the mechanism of action it is likely that it will
be very highly toxic to them as well. Such exposure is unlikely; aluminum
phosphide will rapidly react to form phosphine gas, which is somewhat soluble
in water, but will mainly bubble up into the air (2).
Effects on Other Animals (Non target species)
No data were available.
Breakdown of Chemical in Soil and Groundwater
Aluminum phosphide will breakdown spontaneously in the presence of water
to form a gaseous product, and so it is non-persistent and non-mobile in the
soil environment, and poses no risk to groundwater.
Breakdown of Chemical in Surface Water
It is highly unlikely that aluminum phosphide or phosphine will be found
in surface waters.
Breakdown of Chemical in Vegetation
No data were available.
PHYSICAL PROPERTIES AND GUIDELINES
Aluminum phosphide is a greenish gray solid at room temperature. Hydrogen
phosphide (phosphine) gas, produced by reaction with aluminum phosphide in
contact with water (even at ambient humidity), has an odor similar to garlic
or decaying fish (2, 5).
|RfD: ||0.004 mg/kg/day (13)
|PEL/TLV: ||For phosphine 0.42 mg/meters cubed (0.3 ppm) (14)
|Chemical Name: ||aluminum phosphide
|Molecular Weight: ||57.95 (3)
|Water solubility: ||Insoluble; reactive with water to form hydrogen phosphide (phosphine), H3P (3)
|Solvent solubility: ||Not Available
|Melting Point: ||1,000 degrees C (5)
|Vapor Pressure: ||negligible @ 25 degrees C (5)
|Partition Coefficient (octanol/water): ||Not Available
|Adsorption Coefficient: ||Not Available
Degesch America, Inc.
275 Triangle Dr.
P. O. Box 116
Weyers Cave, VA 24486 USA
Review by Basic Manufacturer:
Comments solicited: June, 1995
Comments received: January, 1996
Royal Society of Chemistry. 1991 (as updated). The Agrochemicals
Handbook, Royal Society of Chemistry Information Services, Cambridge, UK.
Meister, R.T. (ed.). 1992. Farm Chemicals Handbook '92, Meister
Publishing Co., Willoughby, OH.
US Environmental Protection Agency. 1992. Office of Pesticides and
Toxic Substances, Fact Sheet Number 118: Aluminum Phosphide/Magnesium
Phosphide. Washington, DC.
Shaheen, D. 1996. Technical Vice President, Degesch America, Inc.,
Weyers cave, VA, Personal Communication.
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Phosphide, Phostoxin, Degesch America, Weyers Cave, VA.
Gehring, P.J., Nolan, R.J., Watanabe, P.G. and Schumann, A.M. 1991.
Chapter 14: Solvent, Fumigants and Related Compounds, In Hayes, W.J. and
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Garry, V.F., Griffith, J., Danzl, T. J., Nelson, R. J., Whorton, E.
B., Krueger, L. A. and Cervenka, J., Human Genotoxicity: Pesticide
Applicators and Phosphine. Science 246 (35) pp. 251-254.
World Health Organization (WHO). 1988. Environmental Health
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phosphine. Archiv fur Toxikologie, 24(23):164-187.
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U.S. Environmental Protection Agency. 1994. File: Aluminum
Phosphide Integrated Risk Information System (IRIS). US EPA, Washington, DC.
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