Human & Experimental Toxicology (2005) 24: 27 /33
www.hetjournal.com
Occupational exposure to aluminium
phosphide and phosphine gas? A suspected
case report and review of the literature
DL Sudakin*
Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR, USA
The manufacture and application of aluminium phosphide fumigants pose risks of inhalation exposure to
phosphine gas. This article presents a case report
of suspected inhalation exposure to phosphine gas in
a manufacturing facility for aluminium phosphide
fumigants, which was associated with acute dyspnoea,
hypotension, bradycardia and other signs of intoxication.
These symptoms resolved within several hours after
removal from exposure. A review of the data on human
exposures to phosphide fumigants identifies both pesticide applicators and individuals in the vicinity of
application to be at risk of accidental exposure and
injury from phosphine inhalation. More recent reports
have identified risks of phosphine gas inhalation in
association with the clandestine production of methamphetamine. Toxicodynamic effects of phosphine result
from the inhibition of cytochrome c oxidase and subsequent generation of reactive oxygen species. There remain unanswered questions relating to the toxicokinetics
of phosphine, as well as the assessment of human
exposure utilizing biomarkers. As initial signs and
symptoms of intoxication from phosphine gas may be
nonspecific and transient, there is a need for improved
recognition of the potential hazards associated with
phosphide fumigants and phosphine gas. Human &
Experimental Toxicology (2005) 24, 27 /33
Key words: environmental; epidemiology; fumigant; human;
occupational; phosphide; phosphine; poisoning; toxicodynamics;
toxicokinetics; toxicology
Introduction
Aluminium phosphide is a pesticide registered in
the USA and many other countries for the indoor
fumigation of agricultural commodities, animal
feeds, processed foods and structural as well as
outdoor pest control. The chemical is usually
formulated in pellets, granules or as a dust. Upon
contact with moisture in the environment, aluminium phosphide undergoes a chemical reaction
yielding phosphine gas, which is the active pesticidal component (Figure 1). In addition to these
chemical properties, phosphine may spontaneously
ignite in the presence of oxygen at concentrations
above a threshold limit range of 0.48 /1.9% (v/v).1
Phosphine gas has been variably described as
having a garlic or fishy odour, although exposures
to toxicologically relevant concentrations of phosphine can occur in the absence of obvious odour
detection.2 In the USA, the occupational Permissi*Correspondence: Daniel L Sudakin, Department of Environmental and Molecular Toxicology, Oregon State University, 333
Weniger, Corvallis, OR 97331-6502, USA
E-mail: sudakind@ace.orst.edu
Received 7 August 2004; revised 18 November 2004; accepted
22 November 2004
– 2005 Edward Arnold (Publishers) Ltd
ble Exposure Limit (PEL) for phosphine gas is
0.3 ppm.
Exposure to aluminium phosphide is a relatively
common cause of poisoning from agricultural chemical exposures in many countries.3 5 The risks
of major morbidity and mortality associated with
both accidental and intentional exposure to aluminium phosphide fumigants have been well
described.6 9 Despite these risks, intoxication from
phosphine inhalation can be difficult to confirm
and is frequently a diagnosis of exclusion when
reliable biomarkers of exposure and environmental
measurements are not available.10 Risks from phosphide fumigants may increase in the future, as
they are considered an alternative to the use of
methyl bromide, which is currently being phased
out of use as a fumigant in many countries throughout the world. The purpose of this article is to
present a case of suspected occupational exposure
to phosphine gas in a manufacturing facility for
phosphide fumigants, and to update the available
information on the epidemiology and clinical toxicology of accidental human exposures to aluminium phosphide and phosphine. Emphasis is
10.1191/0960327105ht496oa
Exposure to aluminium phosphide and phosphine gas
DL Sudakin
28
OH
moisture
Al
P
+
aluminum phosphide
3 H2O
HO
+
Al
OH
PH3
phosphine
Figure 1 Aluminium phosphide and liberation of phosphine gas.
placed on the need for improved recognition of
individuals at risk of occupational exposure.
Case report
A 42-year-old male had been employed at a manufacturing facility for aluminium phosphide fumigants for over 14 years. His work involved rotation
through several different steps in the manufacturing
process. This process included mixing of aluminium phosphide with ammonium carbonate, tumbling of the mixture, transferring the product to a
hopper, and subsequently adding talc and zinc to
generate a pellet formulation. The worker described
workplace safety concerns including air filters that
frequently became clogged with dust generated
through the manufacturing process, infrequent monitoring and documentation of phosphine gas concentrations, poor compliance with the use of
required respiratory protective gear, and previous
incidents of hoppers that had exploded in the
workplace (Figure 2).
Figure 2 Storage container for aluminium phosphide, which
had previously exploded.
On a day when the worker was having difficulty
removing the solid product during the blending
process, he acutely developed symptoms of chest
pain, shortness of breath, weakness, dizziness, disorientation and nausea with an episode of vomiting.
He did not experience abdominal pain or dyspepsia.
The worker was not wearing respiratory protection
at the time, and did not recall noticing an odour. He
was taken to the company physician, who noted
the worker was alert and responsive with a normal
respiratory rate, but appeared pale, sweaty and
acutely ill. On initial examination, the heart
rate was described as very slow with distant
heart sounds. The initial blood pressure was
78/58 mmHg, and a rhythm strip indicated a junctional bradycardia (58 beats/min). He was transported via ambulance to an emergency room, and it
was suspected that he was having a myocardial
infarction.
An initial ECG showed normal sinus rhythm
with nonspecific ST and T-wave abnormalities. No
arrhythmias were apparent. Laboratory analyses
revealed an elevated creatine phosphokinase (CK
247 U/L), with a normal CK-MB index and a
normal troponin I. Other laboratory values, including a complete blood count, amylase, and renal
and liver function, were within normal limits.
Serum magnesium was not measured. Chest and
abdominal X-rays were unremarkable. The worker
had a history of gastro-oesophageal reflux disease
for which he was taking medication, but no
known prior history of cardiovascular disease, and
a recent exercise stress test, which was unremarkable. He was admitted to the hospital with a
diagnosis of acute chest pain, ruling out unstable
angina.
His clinical condition improved rapidly while in
the emergency room, and his symptoms resolved
over the next 6 hours. He did not develop arrhythmias or other clinical or laboratory signs of cardiac
injury while under observation. A repeat ECG
showed no significant change from the previous
study. Consultation by a gastroenterology specialist
revealed no evidence that the episode was gastrointestinal in origin. He was subsequently discharged
to home the next day. He returned to the duties of
his job, reporting changes in workplace safety
procedures. These included improved engineering
controls, routine monitoring for phosphine gas
and appropriate use of respiratory protective equipment. The worker reported that an investigation to
determine concentrations of phosphine gas in his
immediate work area was not conducted on the date
that he became acutely ill.
Exposure to aluminium phosphide and phosphine gas
DL Sudakin
29
Epidemiology of exposure to phosphide
fumigants and phosphine gas
The epidemiology of occupational and environmental exposure to phosphine gas in association with
phosphide fumigants has been reviewed by
the National Institute of Occupational Safety and
Health (NIOSH).11 Relevant findings in a 10-year
study of 205 symptomatic exposures included the
observation that 75% of cases occurred among
individuals who were not directly handling or
applying the fumigants. In 63% of cases among
applicators, and 45% of cases among nonapplicators, symptomatic exposure was reported to have
occurred from the normal handling of phosphide
fumigants (consistent with the product labelling).
In this case series, approximately 25% of exposures to aluminium phosphide among applicators
occurred in the context of a misapplication (handling violations).11 There were no reported occupational cases occurring among individuals involved
in the manufacturing process of phosphide fumigants in this series.
Another epidemiological study investigated
health endpoints among Indian workers engaged in
fumigation of stored grains.12 The mean duration of
employment among these workers was 11.1 years,
and workplace concentrations of phosphine gas
ranged from 0.17 to 2.11 parts per million (ppm)
during the period of investigation. In this study,
workers did not use facemasks, gloves or aprons as
personal protective equipment. The most frequently
reported symptoms reported immediately after completing fumigation activities included headache
(31.8%), dyspnoea (31.8%) and chest tightness
(27.3%). Physical examinations of these workers
were unremarkable, and no significant abnormalities were observed in tests of motor and sensory
nerve conduction.12
Outside of the workplace, phosphide fumigants
are frequently implicated in association with epidemiological reports of accidental morbidity and
mortality. A three-year (1999 /2001) analysis of
childhood poisonings in India found that 9% of all
cases resulted from exposure to agricultural pesticides, and aluminium phosphide fumigants were
the most frequently implicated classification
(29.67% of cases). Most of these cases involved
ingestion pathways of exposure resulting from improper storage of fumigants.3 Medical outcomes
were not reported in this study. In another longitudinal, retrospective review of acute poisoning
deaths in northern India, aluminium phosphide
fumigants were identified as the most commonly
implicated poison associated with fatalities (65% of
4
cases). In this investigation, the incidence of cases
resulting in death from aluminium phosphide increased during the period of observation (1972 /
1997). This study did not provide further analysis
of demographics or circumstances surrounding exposures resulting in fatalities.
Morbidity and mortality have also been reported
from phosphine inhalation in association with the
in-transit fumigation of ships and railways.13,14 In
one such report, two children and 29 of 31 adults
aboard a grain freighter developed acute and severe
symptoms of headache, nausea, vomiting and shortness of breath when phosphine gas escaped from a
cargo hold and was transmitted to forward areas of
the vessel. One child died after this exposure, and
another child had evidence of myocardial injury as
evidenced by abnormal ECG, echocardiography and
transient elevation of creatine phosphokinase.14
A review of more recent epidemiological reports
demonstrates that occupational and environmental
exposure to phosphine may also occur from scenarios that do not involve phosphide fumigants.
Case reports of inhalation exposure to phosphine
gas have been described in association with the
clandestine synthesis of methamphetamine, as
phosphine can be produced from phosphorous
acid that is formed when iodine and red phosphorus are combined in aqueous media. WillersRusso reported three fatalities from acute inhalation
of phosphine gas, which occurred in a motel
room where methamphetamine was being synthesized.15 Burgess described a case of transient symptoms of dizziness, headache, cough and diarrhoea
in a law enforcement official who was investigating
a clandestine methamphetamine laboratory.16 In
this case, the affected individual was exposed
to phosphine gas at a concentration of 2.7 ppb for
20 /30 min.
Exposure assessment: phosphine gas
Epidemiological reports of accidental incidents
involving phosphide fumigants and phosphine
gas demonstrate the difficulties that can be encountered in predicting inhalation exposure. Industrial
hygiene studies provide further evidence of these
challenges. A study of aluminium phosphide fumigations in grain elevators reported considerable
temporal variation in the concentration of phosphine gas liberated in enclosed bins, with ambient
temperature and air movement conditions significantly influencing the concentrations.17 Ventilation
practices including the use of fans and aerating
windows were found to reduce the phosphine gas
concentrations to less than 0.3 ppm in most cases,
Exposure to aluminium phosphide and phosphine gas
DL Sudakin
30
although the potential for accumulation of phosphine gas to concentrations more than 0.3 ppm was
noted to occur in worker areas after weekends, when
windows and other ventilation systems were normally closed or not operating.17
Earlier environmental monitoring studies conducted during grain fumigations have measured
concentrations of phosphine gas up to 52 ppm,18 a
level which exceeds the immediately dangerous to
life and health (IDLH) value of 50 ppm established
by the NIOSH. A minimum set of respiratory
protective measures has been recommended by
NIOSH, although the implementation of effective
engineering controls is considered the primary goal
and means to prevent worker exposure to phosphine
gas from phosphide fumigations.11
Toxicology of phosphine
The clinical toxicology of aluminium phosphide
and phosphine gas have been previously reviewed.19 Phosphine, a nucleophile which acts as
a strong reducing agent, is capable of interacting
with and inhibiting critical cellular enzymes involved in metabolic processes. Early studies of
phosphine demonstrated specific inhibitory effects
on mitochondrial cytochrome c oxidase.20 Experimental and observational studies have subsequently
demonstrated that the inhibition of cytochrome c
oxidase and other enzymes leads to the generation of
superoxide radicals and cellular peroxides, and
subsequent cellular injury through lipid peroxidation and other oxidant mechanisms.21,22 Results of
animal studies suggest that glutathione, melatonin,
vitamin C, beta-carotene and possibly other antioxidants may play an important role in reducing the
effects of reactive oxidant species caused by phosphine.23,24 The four-hour inhalation LC50 of phosphine gas is 11 ppm (approximately 0.014 mg/L) in
animal (rat) studies, which places it in the highest
toxicity category (E.P.A. signal word ‘Danger’) for
acute inhalation exposure.25
Mutagenic effects resulting from oxidative damage
to DNA have been reported in vitro. 26 A cytogenetic
study of phosphide fumigant applicators reported a
significantly higher incidence of chromatid gaps
and deletions in comparison to controls.27 A more
recent investigation of genetic damage among phosphide fumigant applicators reported no significant
difference in multiple endpoints (fluorescence in
situ hybridization and the glycophorin A assay)
between exposed and control individuals, a finding
that may be partly explained by improved use of
personal protective equipment.28
Accidental or intentional ingestion of aluminium
phosphide results in the rapid onset of gastrointestinal signs and symptoms, including epigastric pain
and recurrent, profuse vomiting.19,29 Cardiovascular
manifestations of acute ingestion or inhalation
exposures include hypotension and bradycardia.19
Nonspecific ST-T wave changes on electrocardiogram have been frequently reported, as well as left
ventricular systolic dysfunction on echocardiogram
during the initial phases of human intoxication.30
Myocardial and skeletal muscle injury can occur as
a result of high level inhalation or ingestion pathways of exposure.31 Increased CK with a normal
CK-MB fraction has been previously reported.32
Pulmonary injury and oedema have been described
after ingestion of aluminium phosphide, as well as
from environmental and occupational exposure to
phosphine gas.33,34 Neurological manifestations
following acute exposure include headache and
dizziness,35 frequently accompanied by a normal
mental state.19 Acute renal and liver injury can also
develop.19,36 The prognosis from suicidal ingestion
of aluminium phosphide is poor. A case fatality rate
of 77.2% was reported in a case series of 408
patients.37
Very little information is available relating to the
toxicokinetics of phosphine in humans. In an
investigation of a series of patients with intoxication
from aluminium phosphide, indicators of oxidative
stress (malonyldialdehyde levels, superoxide dismutase and catalase activity) appeared to peak
within 48 hours of exposure, with normalization of
most indicators occurring by day 5.38 Reliable
biomarkers of exposure to phosphine are not readily
available,39 but one investigation reported a correlation of blood phosphine concentrations with clinical grades of toxicity in individuals with severe
intoxication.40
A bedside test has been described for the diagnosis of aluminium phosphide ingestion, using
gastric aspirates and paper strips impregnated
with silver nitrate.41 The test was found to be
positive in 100% of cases of aluminium phosphide
ingestion, and negative in all controls in one case
series.42 The same test was also investigated to
detect phosphine in the exhaled air of patients
with intoxication from aluminium phosphide
ingestion, and the results were positive in 50% of
cases.43
Clinical management of phosphine gas
exposure
The clinical management of intoxication from aluminium phosphide is supportive. The administra-
Exposure to aluminium phosphide and phosphine gas
DL Sudakin
31
tion of H2 receptor antagonists has been recommended after aluminium phosphide ingestion to
reduce the gastric acidity and prevent further
liberation of phosphine gas. As hypomagnesemia
is a frequent complication of acute intoxication from
phosphine gas exposure,42 and intracellular magnesium plays an important role as a co-factor in the
synthesis and activity of glutathione and other
antioxidants, the administration of intravenous
magnesium has been investigated in cases of aluminium phosphide poisoning. In an unblinded trial of
50 patients, individuals receiving repeated doses of
intravenous magnesium had significant improvement in indicators of oxidative stress (malonyldialdehyde, reduced glutathione) and a lower incidence
of mortality (20%) in comparison to control subjects
(44% mortality).43
More recently, the oral administration of the
anti-ischaemic drug trimetazidine, which works
through a metabolic mechanism of decreasing the
production of oxygen-derived free radicals and
stimulating the oxidative metabolism of glucose,44,45
was temporally associated with clinical improvement in a case report of occupational inhalation
exposure to phosphine gas from aluminium phosphide.46
Case discussion
While most of the epidemiological reports of occupational exposure to phosphide fumigants have
involved pesticide applicators, risks among workers
involved in the manufacturing of phosphide fumigants have not been previously described. In the
current case report, a worker acutely developed
severe symptoms in the course of their job duties
in the production of aluminium phosphide fumigants. They were not wearing respiratory protection
at the time the symptoms developed. Symptoms
consistent with acute inhalation to phosphine
gas included the sudden onset of chest pain, shortness of breath, weakness, dizziness, disorientation
and nausea. Signs consistent with overexposure
to phosphine included vomiting, hypotension, bradycardia and an abnormal elevation in the CK
(with a normal CK-MB). Although the worker
did not recall an odour at the time he developed symptoms, other studies have reported
the absence of detectable odours among workers
exposed to phosphine concentrations exceeding
50 ppm.2
A significant limitation in exposure assessment in
this case is that phosphine concentrations were
apparently not investigated at the time the worker
became symptomatic. The role that occupational
exposure to phosphine may have had in the aetiology of the worker’s symptoms was not immediately
considered or investigated by the treating physicians in this case. Based upon the worker’s occupation, however, acute inhalation exposure to
phosphine was plausible and the observed signs
and symptoms were consistent. The rapid resolution
of symptoms following removal from exposure and
the apparent ruling out of alternative explanations
provide additional evidence suggestive of acute
intoxication from phosphine gas.
Risks associated with phosphide fumigants have
recently been reassessed in the USA. In 1998, the US
E.P.A. completed a re-registration eligibility decision (RED) for aluminium phosphide fumigants.47
The risk assessment process identified concerns
with respect to handlers (applicators) performing
aeration and fumigation tasks without the use of
respiratory protective equipment. Similar concerns
were identified with respect to the potential risks of
nonapplicators (in the vicinity of the application).
A Memorandum of Agreement amending the aluminium phosphide RED was subsequently issued by
E.P.A., which outlined a series of provisions intended to mitigate risks.48 These provisions include
fumigant exposure monitoring studies, improved
training and education for applicators, the development of fumigation management plans, and plans
to review and determine whether current exposure
standards for phosphine should be lowered from
the current limit of 0.3 ppm. While these provisions were intended to reduce risks in the general
population, this case report suggests that workers
involved in the manufacture of aluminium phosphide fumigants should be considered individuals
at high risk of exposure.
Conclusions
Inhalation exposure to phosphine gas liberated from
aluminium phosphide fumigants presents risks of
major morbidity and mortality. The rapid progression to life-threatening symptoms and limited data
on the efficacy of therapeutic interventions pose
challenges to the clinical toxicologist. This case
report describes a scenario consistent with acute
intoxication from the inhalation of phosphine gas at
a manufacturing facility for phosphide fumigants,
and adds to the more recent literature demonstrating
that accidental inhalation of phosphine gas may
occur from processes other than phosphide fumigation. There is a growing need for improved awareness of these risks with an emphasis on recognition,
management and prevention.
Exposure to aluminium phosphide and phosphine gas
DL Sudakin
32
References
1 Kondo S, Tokuhashi K, Nagai H, Iwasaka M, Kaise M.
Spontaneous ignition limits of silane and phosphine.
Combustion Flame 1995; 101: 170.
2 Zaebst DD, Blade LM, Burroughs GE, Morelli-Schroth
P, Woodfin WJ. Phosphine exposures in grain elevators
during fumigations with aluminum phosphide. Appl
Ind Hyg 1988; 3: 146 /54.
3 Gupta SK, Peshin SS, Srivastava A, Kaleekal T. A study
of childhood poisoning at National Poisons Information Centre, All India Institute of Medical Sciences,
New Delhi. J Occup Health 2003; 45: 191 /96.
4 Singh D, Jit I, Tyagi S. Changing trends in acute
poisoning in Chandigarh zone: a 25-year autopsy
experience from a tertiary care hospital in northern
India. Am J Forensic Med Pathol 1999; 20: 203 /10.
5 Abder-Rahman HA, Battah AH, Ibraheem YM, Shomaf
MS, el Batainch N. Aluminum phosphide fatalities,
new local experience. Med Sci Law 2000; 40: 164 /68.
6 Deaths associated with exposure to fumigants in railroad cars / United States. Morb Mortal Wkly Rep 1994;
43: 489 /91.
7 Abder-Rahman HA, Battah AH, Ibraheem YM, Shomaf
MS, el Batainch N. Aluminum phosphide fatalities,
new local experience. Med Sci Law 2000; 40: 164 /68.
8 Anger F, Paysant F, Brousse F, Le N, I, Develay P,
Gaillard Y, Baert A, Le Gueut MA, Pepin G, Anger JP.
Fatal aluminum phosphide poisoning. J Anal Toxicol
2000; 24: 90 /92.
9 Popp W, Mentfewitz J, Götz R, Voshaar T. Phosphine
poisoning in a German office. Lancet 2002; 359: 1574.
10 Schoonbroodt D, Guffens P, Jousten P, Ingels J, Grodos
J. Acute phosphine poisoning? A case report and
review. Acta Clin Belg 1992; 47: 280 /84.
11 National Institute of Occupational Safety and Health.
NIOSH alert: preventing phosphine poisoning and
explosions during fumigation . Columbus, OH: NIOSH,
2003: 99 /126, 1 /16.
12 Misra UK, Bhargava SK, Nag D, Kidwai MM, Lal MM.
Occupational phosphine exposure in Indian workers.
Toxicol Lett 1988; 42: 257 /63.
13 Feldstein A, Heumann M, Barnett M. Fumigant intoxication during transport of grain by railroad. J Occup
Med 1991; 33: 64 /65.
14 Wilson R, Lovejoy FH, Jaeger RJ, Landrigan PL. Acute
phosphine poisoning aboard a grain freighter. Epidemiologic, clinical, and pathological findings. JAMA
1980; 244: 148 /50.
15 Willers-Russo LJ. Three fatalities involving phosphine
gas, produced as a result of methamphetamine manufacturing. J Forensic Sci 1999; 44: 647 /52.
16 Burgess JL. Phosphine exposure from a methamphetamine laboratory investigation. J Toxicol Clin Toxicol
2001; 39: 165 /68.
17 Reed C. Influence of environmental, structural, and
behavioral factors on the presence of phosphine in
worker areas during fumigations in grain elevators.
J Agric Saf Health 2001; 7: 21 /34.
18 Zaebst DD, Blade LM, Burroughs GE, Morelli-Schroth
P, Woodfin WJ. Phosphine exposures in grain elevators
during fumigations with aluminum phosphide. Appl
Ind Hyg 1988; 3: 146 /54.
19 Gupta S, Ahlawat SK. Aluminum phosphide poisoning / a review. J Toxicol Clin Toxicol 1995; 33: 19 /24.
20 Chefurka W, Kashi KP, Bond EJ. The effect of phosphine [gas toxic to insects] on electron transport in
mitochondria. Pestic Biochem Physiol 1976; 6: 65 /84.
21 Bolter CJ, Chefurka W. Extramitochondrial release of
hydrogen peroxide from insect and mouse liver mitochondria using the respiratory inhibitors phosphine,
myxothiazol, and antimycin and spectral analysis of
inhibited cytochromes. Arch Biochem Biophys 1990;
278: 65 /72.
22 Chugh SN, Arora V, Sharma A, Chugh K. Free radical
scavengers and lipid peroxidation in acute aluminium
phosphide poisoning. Indian J Med Res 1996; 104:
190 /93.
23 Hsu CH, Chi BC, Liu MY, Li JH, Chen CJ, Chen RY.
Phosphine-induced oxidative damage in rats: role of
glutathione. Toxicology 2002; 179: 1 /8.
24 Hsu CH, Han BC, Liu MY, Yeh CY, Casida JE.
Phosphine-induced oxidative damage in rats: attenuation by melatonin. Free Radic Biol Med 2000; 28: 636 /
42.
25 United States Environmental Protection Agency,
Office of Prevention Pesticides and Toxic Substances.
Reregistration Eligibility Decision: Aluminum and
Magnesium Phosphide. Washington, DC: US EPA,
1998.
26 Hsu CH, Quistad GB, Casida JE. Phosphine-induced
oxidative stress in Hepa 1c1c7 cells. Toxicol Sci 1998;
46: 204.
27 Garry VF, Nelson RL, Danzl TJ, Cervenka J, Krueger LA,
Griffith J, Whorton E. Human genotoxicity in phosphine-exposed fumigant applicators. Prog Clin Biol
Res 1990; 340C: 367 /76.
28 Tucker JD, Moore DH, Ramsey MJ, Kato P, Langlois RG,
Burroughs B, Long L, Garry VF. Multi-endpoint biological monitoring of phosphine workers. Mutat Res
2003; 536: 7 /14.
29 Singh S, Dilawari JB, Vashist R, Malhotra HS, Sharma
BK. Aluminium phosphide ingestion. Br Med J (Clin
Res Ed) 1985; 290: 1110 /11.
30 Gupta MS, Malik A, Sharma VK. Cardiovascular
manifestations in aluminium phosphide poisoning
with special reference to echocardiographic changes.
J Assoc Physicians India 1995; 43: 773 /80.
31 Khosla SN, Nand N, Kumar P, Trehan V. Muscle
involvement in aluminium phosphide poisoning.
J Assoc Physicians India 1988; 36: 289 /90.
32 Dueñas A, Pérez-Castrillon JL, Cobos MA, Herreros V.
Treatment of the cardiovascular manifestations of
phosphine poisoning with trimetazidine, a new antiischemic drug. Am J Emerg Med 1999; 17: 219 /20.
33 Chugh SN, Ram S, Mehta LK, Arora BB, Malhotra KC.
Adult respiratory distress syndrome following aluminium phosphide ingestion. Report of 4 cases. J Assoc
Physicians India 1989; 37: 271 /72.
34 Willers-Russo LJ. Three fatalities involving phosphine
gas, produced as a result of methamphetamine manufacturing. J Forensic Sci 1999; 44: 647 /52.
35 National Institute of Occupational Safety and Health.
NIOSH alert: preventing phosphine poisoning and
Exposure to aluminium phosphide and phosphine gas
DL Sudakin
33
36
37
38
39
40
41
42
explosions during fumigation. Columbus, OH: NIOSH,
2003: 99 /126, 1 /16.
Arora B, Punia RS, Kalra R, Chugh SN, Arora DR.
Histopathological changes in aluminium phosphide
poisoning. J Indian Med Assoc 1995; 93: 380 /81.
Chugh SN, Dushyant, Ram S, Arora B, Malhotra KC.
Incidence and outcome of aluminium phosphide
poisoning in a hospital study. Indian J Med Res
1991; 94: 232 /35.
Chugh SN, Arora V, Sharma A, Chugh K. Free radical
scavengers and lipid peroxidation in acute aluminium
phosphide poisoning. Indian J Med Res 1996; 104:
190 /93.
Singh S. Serial blood phosphine levels in aluminium
phosphide [ALP] poisoning. J Assoc Physicians India
1996; 44: 841 /42.
Chugh SN, Pal R, Singh V, Seth S. Serial blood
phosphine levels in acute aluminium phosphide
poisoning. J Assoc Physicians India 1996; 44: 184 /85.
Chugh SN, Ram S, Chugh K, Malhotra KC. Spot
diagnosis of aluminium phosphide ingestion: an
application of a simple test. J Assoc Physicians India
1989; 37: 219 /20.
Chugh SN, Kamar P, Sharma A, Chugh K, Mittal A,
Arora B. Magnesium status and parenteral magnesium
43
44
45
46
47
48
sulphate therapy in acute aluminum phosphide intoxication. Magnes Res 1994; 7: 289 /94.
Chugh SN, Kolley T, Kakkar R, Chugh K, Sharma A.
A critical evaluation of anti-peroxidant effect of
intravenous magnesium in acute aluminium phosphide poisoning. Magnes Res 1997; 10: 225 /30.
de Leiris J, Boucher F. Rationale for trimetazidine
administration in myocardial ischaemia-reperfusion
syndrome. Eur Heart J 1993; 14: 34 /40.
Lopaschuk GD. Treating ischemic heart disease by
pharmacologically improving cardiac energy metabolism. Am J Cardiol 1998; 82: 14K /17K.
Dueñas A, Pérez-Castrillon JL, Cobos MA, Herreros V.
Treatment of the cardiovascular manifestations of
phosphine poisoning with trimetazidine, a new antiischemic drug. Am J Emerg Med 1999; 17: 219 /20.
United States Environmental Protection Agency, Office
of Prevention Pesticides and Toxic Substances. Reregistration Eligibility Decision: Aluminum and Magnesium Phosphide. US EPA, 1998.
United States Environmental Protection Agency, Office
of Prevention Pesticides and Toxic Substances. Fact
Sheet on Memorandum of Agreement Amending Aluminum and Magnesium Phosphide RED. US EPA,
2001.