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    Published under the joint sponsorship of
    the United Nations Environment Programme,
    the International Labour Organisation,
    and the World Health Organization

    World Health Orgnization
    Geneva, 1988

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    1.1. Properties, analysis, and occurrence
    1.2. Effects on organisms in the environment
    1.3. Effects on animals
    1.4. Effects on man
    1.5. Evaluation


    2.1. Identity, physical and chemical properties
          2.1.1. Phosphine
          Physical and chemical properties
          Conversion factors
          2.1.2. Metal phosphides
    2.2. Analytical methods
          2.2.1. Gaseous phosphine
          Direct-indicating methods
          Absorptive or adsorptive sampling and analysis
          Continuous methods
          2.2.2. Residues
          2.2.3. Metal phosphides


    3.1. Natural occurrence
    3.2. Man-made sources
          3.2.1. Production levels and processes
          World production figures
          Manufacturing processes
          3.2.2. Uses


    4.1. Transport and distribution between media
          4.1.1. Air
          4.1.2. Soil
          4.1.3. Aquatic environment
          4.1.4. Vegetation, wildlife, and entry into the food chain
    4.2. Biotransformation
    4.3. Ultimate fate


    5.1. Environmental levels
          5.1.1. Air, water, and soil
          5.1.2. Food and feed
          Residue values
          Factors affecting residue levels
          5.1.3. Tobacco and consumer products
          5.1.4. Terrestrial and aquatic organisms

    5.2. General population exposure
          5.2.1. Access to phosphine and phosphides
          5.2.2. Residue exposure
          5.2.3. Subgroups at special risk
    5.3. Occupational exposure during manufacture, formulation, or use


    6.1. Insects
    6.2. Mammals
          6.2.1. Absorption
    6.3. Distribution
    6.4. Metabolic transformation
    6.5. Elimination and excretion
    6.6. Retention and turnover
    6.7. Reaction with body components


    7.1. Microorganisms
    7.2. Aquatic organisms
    7.3. Terrestrial organisms
          7.3.1. Insects and mites
          7.3.2. Birds
          7.3.3. Mammals
          Non-target species
    7.4. Plants
          7.4.1. Harvested plants
          7.4.2. Viable seeds and grain


    8.1. Single exposures
          8.1.1. Inhalation studies on phosphine
          8.1.2. Inhalation studies on zinc phosphide
          8.1.3. Oral studies on metal phosphides
          8.1.4. Dermal and other studies on metal phosphides
    8.2. Short-term exposures
          8.2.1. Inhalation exposure to phosphine
          8.2.2. Oral exposure to metal phosphides
          8.2.3. Dermal and other exposures
    8.3. Skin and eye irritation; sensitization
    8.4. Long-term exposure
    8.5. Reproduction, mutagenicity, and carcinogenicity
    8.6. Factors modifying toxicity; toxicity of metabolites
    8.7. Mechanisms of toxicity - mode of action


    9.1. Organoleptic effects
    9.2. General population exposure
          9.2.1. Phosphine

          9.2.2. Metal phosphides
    9.3. Occupational exposure


    10.1. Evaluation of human health risks
    10.2. Evaluation of effects on the environment
    10.3. Conclusions


    11.1. Gaps in knowledge
    11.2. Preventive measures
          11.2.1. Management
          11.2.2. Treatment of poisoning
         Inhalation of phosphine
         Ingestion of metal phosphides
          11.2.3. Leaks, spillages, residues, and empty containers
         Aluminium and magnesium phosphides
                           and their formulated preparations
         Zinc phosphide and preparations





Professor E.A. Bababunmi, Laboratory of Biomembrane Research,
   Department of Biochemistry, University of Ibadan, College
   of Medicine, Ibadan, Nigeria

Dr L. Badaeva, All Union Scientific Research Institute of
   Hygiene and Toxicology of Pesticides, Polymers and
   Plastics, Kiev, USSR

Dr J.R. Jackson, Medicine and Environmental Health, Monsanto
   Europe, Brussels, Belgium  (Rapporteur)

Dr C.N. Ong, Department of Social Medicine and Public Health,
   National University of Singapore, Kent Ridge, Singapore

Dr N.R. Price, United Kingdom Ministry of Agriculture,
   Fisheries and Food, Slough Laboratory, Berkshire, United

Dr V.A. Rao, Department of Toxicology, Haffkine Institute,
   Acharya Donde Marg, Bombay, India  (Vice-Chairman)

Dr Ch. Reichmuth, Stored Products Protection Institute, Federal
   Biological  Research  Centre  for Agriculture  and Forestry,
   Berlin (West)

Dr F.G.R. Reyes, School of Food Engineering, State University of
   Campinas, UNICAMP, Campinas, Sao Paulo, Brazil  (Chairman)


Dr E.M. Smith, International Programme on Chemical Safety,
   World Health Organization, Geneva, Switzerland  (Secretary)

Dr J.K. Chipman, Department of Biochemistry, University of
   Birmingham, Birmingham, United Kingdom  (Temporary Adviser)

Dr Thomas K.-W. Ng, Office of Occupational Health, World
   Health Organization, Geneva, Switzerland


    Every  effort has been  made to present  information in  the
criteria  documents  as  accurately as  possible  without unduly
delaying their publication.  In the interest of all users of the
environmental  health  criteria  documents, readers  are  kindly
requested  to communicate any errors  that may have occurred  to
the Manager of the International Programme on  Chemical  Safety,
World  Health Organization, Geneva,  Switzerland, in order  that
they  may  be  included in  corrigenda,  which  will  appear  in
subsequent volumes.

                          *    *    *

    A  detailed data profile  and a legal  file can be  obtained
from  the International Register of Potentially Toxic Chemicals,
Palais des Nations, 1211 Geneva 10, Switzerland  (Telephone  no.
988400 - 985850).


    A  WHO  Task  Group  on  Environmental  Health  Criteria for
Phosphine and Selected Metal Phosphides met in Geneva  on  17-21
November  1986.  Dr E.M. Smith  opened the meeting on  behalf of
the Director-General.  The Task Group reviewed and  revised  the
draft  criteria document and made an evaluation of the risks for
human  health and the environment from exposure to phosphine and
metal phosphides.

    The  original draft of this document was prepared by DR J.R.
JACKSON,  Department  of  Medicine and  Health Science, Monsanto
Europe, Brussels, Belgium.

    The contributions of all who helped in the  preparation  and
finalization of this document are gratefully acknowledged.

                           *   *   *

    Partial  financial  support  for  the  publication  of  this
criteria  document  was kindly  provided  by the  United  States
Department of Health and Human Services, through a contract from
the   National  Institute  of  Environmental   Health  Sciences,
Research   Triangle   Park,  North   Carolina,   USA  -   a  WHO
Collaborating Centre for Environmental Health Effects.


1.1.  Properties, Analysis, and Occurrence

    Phosphine,  or hydrogen phosphide, is a colourless gas which
is  odourless when pure, but the technical product usually has a
foul odour, described as "fishy" or "garlicky", because  of  the
presence  of  substituted  phosphines  and  diphosphine  (P2H4).
Other impurities may be methane, arsine, hydrogen, and nitrogen.
For  fumigation, it is produced  at the site by  hydrolysis of a
metal phosphide and supplied in cylinders either as  pure  phos-
phine  or diluted with nitrogen.   Aluminium, magnesium (trimag-
nesium  diphosphide), and zinc (trizinc diphosphide)  phosphides
are the most commonly used metal phosphides for this purpose.

    Phosphine   is  flammable  and  explosive  in  air  and  can
autoignite at ambient temperatures.  It is slightly  soluble  in
water  and soluble in  most organic solvents.   Metal phosphides
are usually powders of various colours, which hydrolyse in acids
to  yield phosphine and  metal salts.  Aluminium  and  magnesium
phosphides hydrolyse in water.

    Phosphine  in air can  be detected by  the discoloration  of
silver nitrate or indicator papers impregnated with mercury (II)
chloride,  and can be measured using indicator tubes or by flame
photometry,  infrared  spectroscopy,  mass spectrometry,  or gas
chromatography.   Samples can be  taken on solid  adsorbents and
desorbed  for analysis.  Various classical analytical techniques
are  available in  which phosphine  is trapped  by mercury  (II)

    Phosphine  residues  in foods  can  be measured  by nitrogen
purging and trapping the phosphine.  Phosphide residues  can  be
included  in the analysis by  extraction with silver nitrate  or
sulfuric  acid and measuring  the chromophore or  the  phosphine
contents of the head-space gas, respectively.

    Metal phosphides are most easily determined after hydrolysis
to  phosphine.  A method has  been described in which  magnesium
phosphide is converted to magnesium pyrophosphate, which is then

    Phosphine  may occur naturally in  the anaerobic degradation
of   phosphorus-containing  organic  matter,  such   as  in  the
production  of  marsh  gas.  Naturally-occurring  phosphides are
extremely  rare.  None have been  reported in the earth's  crust
but  an iron-nickel phosphide  (schreibersite) is found  in  all
iron meteorites.

    Phosphine  is  manufactured  by  the  hydrolysis  of   metal
phosphides, by the electrolysis of phosphorus in the presence of
hydrogen,  and by a  phosphorus-steam reaction.  It  is produced
incidentally  by the hydrolysis of impurities in calcium carbide
(in the production of ethyne (acetylene)), in  ferrosilicon  and
spheroidal   graphite   iron,   and  in   various  metallurgical
operations.  Metal phosphides can be prepared by  the  reduction

of  phosphates,  by  a direct  reaction  between  the metal  and
phosphorus  vapour or amorphous  phosphorus, or by  an  exchange
reaction between the metal and another metal phosphide.

    Phosphine is used in the synthesis of  organophosphines  and
organic  phosphonium derivatives and  as a dopant  in the  manu-
facture  of semiconductors in the electronics industry.  Formul-
ations  of aluminium or  magnesium phosphide are  available  for
fumigation in pest control.  Zinc phosphide is used as a rodent-
icide in the form of a powder or a paste containing 2.5 or 5% of
zinc phosphide, which is incorporated in bait at 1 part in 10.

    Phosphine in air reacts with HO x radicals and is removed by
this  mechanism with a half  time of 5 -  28 h depending on  the
conditions.   Phosphine in air is  slowly absorbed by soil  at a
rate that is dependent on surface effects and  the  permeability
of  the soil  matrix, and  is slower  in wet  conditions.   Zinc
phosphide  undergoes  negligible  hydrolysis  in  a  variety  of
surface  and  ocean  waters over  a  period  of 11  days, but is
oxidized  within about five  weeks in soils  with a 50%  or more
saturated  moisture content.  Significant hydrolysis only occurs
at  a pH value of 4 or less.  Aluminium and magnesium phosphides
are  rapidly hydrolysed in neutral  moist conditions.  Phosphine
and  zinc,  magnesium,  and aluminium  phosphides are inherently
degradable  and non-persistent in the environment.  The ultimate
fate  for  the phosphides  is  inorganic phosphate,  water,  and
metallic compounds.

    Phosphine is normally undetectable in air, water,  or  soil.
Residues in fumigated foods depend on the technique  of  fumiga-
tion,  but are normally low after aeration, except where a metal
phosphide fails to react completely.  In general,  residues  are
below the WHO/FAO recommended levels of 0.1 mg/kg (PH3)  for raw
cereals and below 0.01 mg/kg (PH3) for other stored products.

1.2.  Effects on Organisms in the Environment

    The  antimicrobial activity of phosphine varies depending on
the  microbial species, and the type and moisture content of the
product being fumigated.  Many microorganisms survive fumigation
at  exposures (concentration x time) that are  effective against

    The few studies available indicate that phosphine has little
effect  on growing  plants (e.g.,  sugar cane  and  lettuce)  at
effective pesticidal doses.  Germination of seeds was unaffected
by their fumigation with phosphine or by prior fumigation of the
soil  in  which  they were  planted,  except  when the  moisture
content  of the seed  exceeded 20%.  Lettuce  sustained substan-
tially less damage after fumigation with phosphine than  with  5
other fumigants.

    The  few data  available on  the effects  of  phosphine  and
phosphides  on aquatic organisms  suggest that, despite  its low
solubility, phosphine in solution can be acutely toxic.

    Generally,  insects,  a  principal target,  are susceptible,
though  the susceptibility at different stages of the life-cycle
varies  and  diapausing  larvae are  particularly tolerant.  The
threshold   for  adverse  effects  of   phosphine  to  Drosophila
 melanogaster is about 1.4 mg/m3 (1 ppm), which is similar to the
threshold  for acute inhalation  effects in mammals.   Resistant
strains of insects exist and are sometimes difficult to control.
The  mechanism of  resistance may  have a  metabolic basis  that
persists  throughout all stages  of metamorphosis, and  in  some
cases  has  been shown  to be a  process of active  exclusion of
phosphine  by energy-dependent processes.  In general, mites are
less sensitive than insects.

    Wild  birds and mammals  are similarly susceptible  to  both
phosphine  and phosphides.  Zinc phosphide  formulations vary in
acceptability as baits, and the relative efficacy  of  different
commercial  preparations may be a function of this.  Aversion to
zinc phosphide at 0.05% in the diet was demonstrated  in  Indian
gerbils.  Census studies have shown that, with  appropriate  use
of  bait  or  the application  of  aluminium  phosphide  to  the
entrance  of active burrows, elimination  of most or nearly  all
target  species  can  be  achieved  with  a  single application.
Ingested zinc phosphide is detectable in the intestine and liver
of  poisoned animals, but  not in the  muscle tissue.   Poisoned
animals are not toxic to carrion eaters.

1.3.  Effects on Animals

    In  mammals,  phosphine  is readily  absorbed by inhalation.
Aluminium  or magnesium phosphide  powder, if inhaled,  releases
phosphine for absorption on contact with the  moist  respiratory
epithelium.  Zinc phosphide would not hydrolyse rapidly  in  the
respiratory tract but might be absorbed as such and hydrolyse in
the  tissues.   The  acute dermal  LD50  for  zinc phosphide  in
rabbits  is  in  the range  of  2000  - 5000  mg/kg body weight,
suggesting little dermal absorption. Gastrointestinal absorption
of phosphine produced by the hydrolysis of ingested phosphide is
likely  and the  absorption of  zinc phosphide  itself  and  its
transport to the liver, where it can be detected for many hours,
has  been  demonstrated  in the rat and in a case of fatal human
poisoning.   Information regarding the distribution of phosphine
in  the  body has  been derived from  the clinical syndromes  of
poisoning,  which indicate that  it reaches the  central nervous
system, liver, and kidney.

    Absorbed phosphide is hydrolysed to phosphine or oxidized to
the  salts of  the oxyacids  of phosphorus.   Phosphine is  both
slowly  oxidized  to  oxyacids  and  excreted  unchanged  in the
expired  air.  Hypophosphite is the  principal urinary excretion
product.  Following an oral dose of zinc phosphide, phosphine in
the expired air had disappeared after 12 h and clinical symptoms
lasted  only  a  few hours.   This  suggests  that phosphine  is
eliminated  fairly rapidly.  On  the other hand,  the  phosphide
contents of the liver were higher after daily dosing  with  zinc
phosphide  than  after  a  single  dose,  suggesting  that liver
phosphide is not completely eliminated within 24 h.

    Studies  by  the inhalation  route  indicate that  both  the
concentration  and  duration  of exposure  are  important deter-
minants  of acute lethality and that different mammalian species
are  essentially  similar in  susceptibility.   The 4-h  LC50 of
phosphine in rats is about 15 mg/m3. The oral LD50 value of zinc
phosphide in wild Norwegian rats is 40.5 mg/kg body weight.

    Results  of  short-term  administration  indicate  that  the
effects  of phosphine exposure  cumulate with daily  exposure so
that after 6 days pretreatment, the survival time at  a  concen-
tration  of 681 mg/m3 was  reduced to one-third of  its value in
animals  without previous exposure.  Clinical  features of liver
and  kidney dysfunction were observed and all the parenchymatous
organs  were  affected  by congestion  and  oedema.  Neurohisto-
logical changes were seen in rats and less markedly  in  guinea-
pigs and cats.  Changes in various serum enzyme levels  at  very
low  levels of exposure  over a period  of 1.5 months  have been
reported. Short-term feeding studies on female rats administered
zinc  phosphide resulted in  mortality at concentrations  of 200
and  500  mg/kg  diet,  but  biological  effects,  qualitatively
similar  to  those  at higher  doses,  were  seen at  the lowest
dietary concentration of 50 mg/kg.

    There are no studies relating to long-term effects, carcino-
genicity,  or mutagenicity.  There  is no information  regarding
factors modifying toxicity in vertebrates or the toxicity of any
metabolites.  Information on biochemical effects is insufficient
to  explain the  mechanisms of  toxicity, in  either animals  or

1.4.  Effects on Man

    Because the odour of phosphine depends on  impurities  which
may  be removed by purification  or adsorption, odour cannot  be
relied on for warning of toxic concentrations.
    Ingestion   of   phosphides  may   cause  nausea,  vomiting,
diarrhoea,  retrosternal  and  abdominal pain,  tightness in the
chest  and  coughing, headache  and  dizziness.  In  more severe
cases  this may progress  to cardiovascular collapse,  pulmonary
oedema,  cyanosis and respiratory failure.   Pericarditis, renal
failure,  and  hepatic  damage including  jaundice,  may develop

    Symptoms may be delayed and death may occur up to  one  week
after    poisoning.    Pathological   findings   include   fatty
degeneration  and necrosis of the liver and pulmonary hyperaemia
and oedema.

    Inhalation  of  phosphine  or  phosphide  may  cause  severe
pulmonary  irritation.   Mild  exposure may  cause  only  mucous
membrane  irritation, with initial  symptoms mimicking an  upper
respiratory tract infection.  Other symptoms may include nausea,
vomiting,  diarrhoea,  headache,  fatigue, and  coughing, whilst
more severe symptoms may include ataxia, paraesthesia, intention
tremor,  diplopia, and jaundice.  Very severe cases may progress

to acute pulmonary oedema, cardiac arrhythmias, convulsions, and
coma.   Renal damage and leukopenia may also occur.  Exposure to
1400 mg/m3 (1000 ppm) for 30 min may be fatal.

    Death,  which may be sudden, usually occurs within four days
but   may   be  delayed  for  one  to  two  weeks.   Post-mortem
examinations  have  revealed  focal myocardial  infiltration and
necrosis,  pulmonary oedema and widespread  small vessel injury.
There  is no evidence  for cumulative effects  from intermittent
low-level exposure averaging 14 mg/m3 (10 ppm) or less.

    Chronic  poisoning  from  inhalation or  ingestion may cause
toothache, swelling of the jaw, necrosis of the mandible (phossy
jaw),   weight   loss,   weakness,  anaemia,   and   spontaneous

    Laboratory  findings  may  include abnormal  liver  function
tests, acidosis, increased blood urea and bilirubin, haematuria,
and   proteinuria.   Other  diagnostic  studies  should  include
electrocardiogram,  sputum,  and  differential white  blood cell

    Occasional  cases  of  accidental exposure  of  the  general
population  to  phosphine  have  occurred  in  the   region   of
fumigation  operations  and  on  board  ships  carrying  cargoes
capable of releasing phosphine.  There have been many  cases  of
accidental   or  suicidal  ingestion  of  phosphide  pesticides.
Lethal  doses vary, but most fatal cases have ingested more than
20  g  zinc  phosphide, and  most  of  those who  recovered  had
ingested  less  than  20  g  phosphide.   Pulmonary  oedema  and
congestion  and  necrosis  of the  liver  and  kidneys  are  the
principal pathological features in fatal cases.  There have been
occasional  cases of fatal  occupational exposure to  phosphine,
some of which have involved repeated exposures.

    Various  reports of adverse effects of occupational exposure
at normal operational levels have been published, but in no case
has  the  description  of exposure  or  the  control group  been
adequate  to draw definite conclusions regarding the possibility
of  the  adverse  effects of  phosphine  at  the higher  current
occupational exposure limits.

1.5.  Evaluation

    Phosphine  and metal phosphides are toxic.  They have a very
limited  distribution in the environment.   Proper standards and
procedures in their use prevent harmful effects.  No significant
global  effects on the environment have resulted from the use of
phosphine or phosphides.


2.1.  Identity, Physical and Chemical Properties

2.1.1.  Phosphine  Identity

Chemical structure:           H

Molecular formula:            PH3

Common synonyms:              hydrogen     phosphide,     phosphorus
                              trihydride,   phosphoretted  hydrogen,

CAS registry number:          7803-51-2  Physical and chemical properties

    Pure  phosphine is a  colourless gas at  ambient temperature
and pressure. Its relative molecular mass is 34.

    The  principal physical properties of phosphine are given in
Table  1 (Lowe,  1971).  The  chemistry of  phosphine  has  been
extensively reviewed (Fluck, 1973).

    Phosphine is odourless when pure, at least up to  a  concen-
tration of 282 mg/m3 (200 ppm), which is a highly  toxic  level.
The  odour of  technical phosphine  depends on  the presence  of
odoriferous  impurities and their  concentrations and the  odour
threshold is usually in the range 0.14 - 7  mg/m3  (Netherlands,
1984).  The odour factors can easily be removed  from  phosphine
(Dumas & Bond, 1974).

    Pure phosphine has an autoignition temperature of 38 °C but,
because   of   the   presence  of   other   phosphorus  hydrides
(particularly  diphosphine) as impurities, the technical product
often  ignites spontaneously at room  temperature (ACGIH, 1986).
Phosphine  forms explosive mixtures  with air at  concentrations
greater than 1.8%.

    Phosphine  has intense ultraviolet  absorption in the  185 -
250 nm (1850 - 2500 Å) region.  It dissociates to phosphorus and
hydrogen in contact with hot surfaces in the absence  of  oxygen
(Lowe, 1971).

    Oxidation  of phosphine involves a branching chain reaction.
In  air, the  upper and  lower explosion  limits depend  on  the
temperature,  pressure,  and  proportions of  phosphine, oxygen,

inert  gases and water  vapour present, and  also on the  ultra-
violet   irradiation.    In  aqueous   solutions,  oxidation  of
phosphine results in the production of hypophosphorous acid.

Table 1.  Physical properties of phosphine and some phosphidesa
                        Phosphine   Trizinc       Aluminium     Magnesium
                                    diphosphide   phosphide     phosphide
Formula                   PH3         Zn3P2         AlP           Mg3P2
Physical state            gas         solid         solid         solid
Colour                    none        grey          grey/yellow   grey
Melting point (°C)        -133.5      sublimes      > 1350b       > 750
Boiling point (°C)        -87.4          -             -            -
Spontaneous ignition
 temperature (°C)         38d            -             -            -
Lower explosive           1.8%           -              -          -
Upper explosive           unknown        -              -          -
Vapour density (air = 1)  1.17           -              -           -
Density (temp °C)                     4.55 (13)   2.85 (25)        2.1
a  From: Lowe (1971) and Wilson (1971).
b  Some authorities give a temperature in excess of 2000 °C.
c  In   air,  depending  on  presence   of  other  gases  and   ultraviolet
d  The  spontaneous ignition behaviour  of phosphine is  very unpredictable
   and  though  this  figure is  quoted,  its  validity will  depend on the
   conditions of measurement.
e  From: Anon. (1936).

    An   important  reaction  of   phosphine  is  with   metals,
especially with copper or copper-containing alloys, which causes
severe corrosion.  The reaction is enhanced in the  presence  of
ammonia   (which  is  given   off  with  phosphine   during  the
decomposition  of some fumigation tablets or pellets) and in the
presence  of  moisture  and salt.   Copper-containing equipment,
especially  electrical  apparatus,  may be  severely  damaged by
exposure to phosphine during fumigation.

    Bond  et  al.  (1984) reported  a  systematic  study on  the
corrosion  of metals by  phosphine using a  specially  developed
method  in which the reaction of phosphine was determined by its
depletion  from an enclosed  space.  The authors  confirmed  the
positive effects of phosphine concentration, oxygen and relative
humidity  on the rate of  corrosion.  The rate of  reaction with
copper exceeded by a factor of ten or more the rates of reaction
with  brass, silver, steel, aluminium, galvanized steel (various
galvanizing   processes),   fine  gold,   nickel,  lead  solder,
platinum,  and  iron  powder.   Eighteen  carat  gold  jewellery
reacted at one-eighth of the rate of copper.  The  corrosion  of
copper appears to be similar to that produced by phosphoric acid
and  can  be  reduced by  coating  the  copper with  a saturated
solution of sodium carbonate (1/3 rate)  or,  more  effectively,
with a saturated solution of potassium dichromate  (1/44  rate).

The  type  of polymeric  spray  used to  moisture-proof ignition
systems on internal combustion engines was also  effective  (1/7

Table 2.  Solubility of phosphine in water and organic solvents
                      Temperature (°C)   Solubilitya
Water                 17                 0.26
                      24                 0.24
Acetic acid           20                 3.19
Acetone               22.4               4.45
Aniline               22                 2.8
Benzene               22                 7.26
Carbon disulphide     21                 10.25
Carbon tetrachloride  20.5               4.19
Cyclohexane           18.5               7.47
Toluene               22.5               7.15
Trifluoroacetic acid  26                 15.9
a  Solubility  is measured  by the  volume of  phosphine 
   (measured  at  the temperature  of the study and at 1 
   atmosphere pressure) dissolved in one volume of solvent 
   under a partial pressure of 1 atmosphere.  From:  Lowe 

    Phosphine  dissolves in water  to form a  neutral  solution.
Solubility  is little affected  by the pH.   Dissolved phosphine
reacts  with hydrogen ions to form the phosphonium ion - (PH4)+.
Its solubility in water at different temperatures and in various
organic solvents is given in Table 2.

    The  technical  product  can  contain  impurities  including
higher  phosphines  (e.g.,  up  to  5%  diphosphine,  P2H4)  and
substituted   phosphines,   which   are  responsible   for   the
characteristic  foul odour of phosphine which is often described
as "fishy" or "garlicky" (Fluck, 1976) (section 9.1).  Depending
on the method of manufacture, other impurities can  be  methane,
arsine,  hydrogen,  and  nitrogen.  Phosphine  is often produced
directly, when required, by the hydrolysis of  metal  phosphides
or  phosphonium iodide; it  may also be  supplied compressed  in
cylinders either pure or in various concentrations in nitrogen.  Conversion factors

    At 20 °C, 1 ppm = 1.41 mg/m3; 1 mg/m3 = 0.71 ppm.
              1 ppm (as P) = 1.1 ppm (as PH3).

2.1.2.  Metal phosphides

    The metal phosphides dealt with in this document are trizinc
diphosphide  (zinc  phosphide),  aluminium phosphide,  and  tri-
magnesium diphosphide (magnesium phosphide).

    The  principal  physical  and chemical  properties  of zinc,
magnesium,  and  aluminium  phosphides  are  given  in  Table  1
(Wilson, 1971).

    Many  metals  have  one  or  more  phosphides  that  can  be
synthesized   and  have  been  characterized,  but  few  are  of
commercial importance.  The properties of tricalcium diphosphide
(Ca3P2)  are  similar  to  those  of  trimagnesium  diphosphide.
Tricalcium  diphosphide also reacts with excess white phosphorus
to form calcium monophosphide (CaP)  which, in turn, reacts with
water to form diphosphine by the reaction 2CaP + 4H2O = 2Ca(OH)2
+  P2H4.  Zinc diphosphide is  formed when phosphorus vapour  in
nitrogen  is passed over  zinc at 700 °C.   Trizinc  diphosphide
(Zn3P2,  1314-84-7, relative molecular  mass = 258.1),  commonly
referred  to  as zinc  phosphide, is used  as a rodenticide  and
fumigant because of its reaction with acid to release phosphine.
As a rodenticide, the acid in the stomach causes the hydrolysis.
For  fumigation,  the  acid has  to  be  supplied.   Since  they
hydrolyse  in neutral moist  conditions, aluminium or  magnesium
phosphide are preferred as fumigants.

    Aluminium  phosphide  (AlP,  20859-73-8, relative  molecular
mass  = 57.96)  reacts  with water to  release phosphine.   This
reaction may be incomplete, possibly owing to the formation of a
protective   layer  of  aluminium  hydroxide   on  the  surface.
Aluminium  phosphide  has  been used  as  a  rodenticide  and  a
fumigant.  It is the only compound of aluminium  and  phosphorus
(Wilson, 1971; Van Wazer, 1982).

    Trimagnesium   diphosphide   (Mg3P2,  12057-74-8,   relative
molecular mass = 134.87), commonly known as magnesium phosphide,
is used as a pesticide and fumigant.

    Zinc   phosphide  is  available  in  bulk,  typically  to  a
specification of at least 80% Zn3P2, and as pastes containing 5%
or 2.5% for use as a rodenticide by mixing in  bait.   Aluminium
and magnesium phosphides are available as a number of commercial
formulations.   Aluminium phosphide formulations usually contain
approximately  57%  active  ingredient and  those  of  magnesium
phosphide  34% active ingredient.   Some registered trade  names
and presentations are:

    Aluminium phosphide

    Celphide (tablets)
    Celphine (tablets)
    Celphos (tablets)
    Delicia Gastoxin
    Detia Gas-Ex-B (bags)
    Detia Gas-Ex-P (pellets)
    Detia Gas-Ex-T (tablets)
    "L" fume (tablets)
    Phosfume (pellets and tablets)
    Phostek (pellets and tablets)
    Phostoxin (pellets, tablets, "prepacs", rounds, strips)
    Quickfos (pellets and tablets)
    Zedesa (bags, pellets, tablets)

    Magnesium phosphide

    Detiaphos (pellets)
    Mag-disc (plates)
    Magtoxin (pellets, tablets, rounds)

    Phostoxin  (strip)  formulations  are designed  to produce a
controlled  release of phosphine to achieve efficient fumigation
with  low  operator  risks.   Some  include  other   ingredients
designed  to  reduce fire  hazards.   Depending on  the  storage
conditions,  the  composition  of  metal  phosphides  and  their
formulations may change over time by hydrolysis and oxidation.

    Metal  phosphides  are  analysed by  assaying  the phosphine
liberated  by acid hydrolysis.  After this preparatory step, the
procedure  is the same as for gaseous phosphine (Bontoyan, 1981;
Terzic, 1981; Worthing & Walker, 1983).

2.2.  Analytical Methods

2.2.1.  Gaseous phosphine

    Work-place  air monitoring and  fumigation control demand  a
measurement  range from about 0.04 µg/m3  to more than the lower
explosion  limit of about 25 000 mg/m3.   Thus, methods covering
concentrations   differing  by  six  orders   of  magnitude  are

    Techniques  are  available  that: (a)  directly indicate the
concentration  in a grab sample or time-weighted average sample;
(b)  adsorb or absorb phosphine  from a known volume  of air for
subsequent  analysis directly or by desorption and gas analysis;
and  (c) give a  continuous record of  time-dependent concentra-
tions.  Some methods reviewed by Verstuyft (1978) are  given  in
Table 3.

Table 3.  Methods of sampling and analysisa
Method                                                  Range                Efficiency   Interference
                                                ppm           mg/m3

Silver nitrate (0.1 N) impregnated paper        0.05 - 8.0    9.07 - 11.3    90%

Ethanolic mercuric chloride                     0.05 - 3.0    0.07 - 4.2                  NH3

Acidic potassium permanganate (0.1 N) impinger                0.01 - 0.05    100%         H3S

Silver diethyldithiocarbamate (0.5%) bubbler    0.6 - 18      0.85 - 25      54 - 86.2%   H2S,AsH3, SbH3

Mercuric chloride (0.5%) aqueous bubbler        10 - 28       14  - 28                    AsH3

Toluene impinger                                                             41.5%

Mercuric chloride (0.1%) conductance cell       0.05 - 2.5    0.07 - 3.5     88.0%        SO2, H2S, AsH3,

Silver nitrate impregnated silica gel           0.05 - 4.1    0.07 - 5.8     95%          H2A, AsH3

Auric chloride impregnated silica gel           0.01 - 1000   0.014 - 1 400  100%         AsH3, SbH3

Ethanolic mercuric chloride (0.1%)                            0.0006         88 - 100%    AsH3,SO2,HCN,

Mercuric cyanide impregnated silica gel         0.014 - 1.18  0.02 - 1.7     80%

Table 3 (contd.)
Methodb                                                Sensitivity

Bendix phosphorus method/sulfur monitor      ns
HNU photoionization detector                 0.1 - 100 ppm    0.14 - 140 mg/m3
Gas chromatography - FID. 3% TCP             ns               
Gas chromatography - Therm. 4.5% QF-1        2 ppt            3 pg/m3
Gas chromatography - FPD. 3% Carbowax        0.5 ppt          0.7 pg/m3
Gas chromatography - Coulson                 500 ppt          0.7 µg/m3
Gas chromatography - TC. porous beads        10 ppm           14 mg/m3
Gas chromatography - Therm. 30% Apiezon      50 ppb           70 µg/m3
Gas chromatography - FID. PPD. beta-ioni-    20 ppb           30 µg/m3
 zation Poropak Q
Colorimetric - ammonium molybdate 720 nm                      10 mg/litre
Colorimetric ammonium molybdate 880 nm                        10 mg/litre
Colorimetric silver DDC 465 nm               0.05 ppm         70 µg/m3
Colorimetric silver sulfide 470 nm           0.02 ppm         30 µg/m3
a  From: Verstuyft (1978).
b  DDC - diethyldithiocarbamate.
   FID = flame ionization detector.
   FPD = flame photometric detector.
   Therm = thermal detector.

   ns = not stated. Direct-indicating methods

    Phosphine  can be detected by filter papers impregnated with
a  mixture of  silver nitrate  and mercury  (II) chloride.   The
method  can be made semi-quantitative  by appropriate configura-
tion  and measurement of stain-length (Brandon, 1983)  or colour
comparison  (Hughes  &  Jones,  1963).   Kashi  &  Muthu  (1975)
described a simple and sensitive method for detecting phosphine,
using paper strips impregnated with dimethyl yellow, cresol red,
and  mercury (II)   chloride in  methanol.   It is  claimed that
these  paper  strips  have a  better  shelf-life  and  are  more
sensitive  than  paper  strips impregnated  with dimethyl yellow
alone,  or cresol red  plus mercury (II)  chloride.  The  strips
need  not be kept  in air-tight containers  or under  controlled
conditions of temperature and humidity.

    Direct-indicating  detector tubes are commercially available
for  spot  sampling  (using  syringes  and  grab-samplers)   and
personal  monitoring  of  occupational exposure  (using portable
pumps).  Leesch (1982) compared the accuracy of various pump (5)
and  detector tube (7)  combinations.  Means of  measured values
for  test  concentrations  varied from  59  to  256%  of  actual
concentrations  over the whole range  of pump/tube combinations.
Pumps  and tubes  from the  same manufacturer  gave mean  values
varying from 85 to 214% of the actual values.   Measurements  at
low levels of phosphine in the range 2.8 - 7 mg/m3 (2 -  5  ppm)

with  matched  pumps  and  tubes  from  the  same  manufacturers
resulted  in mean values of  133%, 130%, and 128%.   Using tubes
from   three  manufacturer's  and   the  pump  from   only   one
manufacturer gave mean values of 120%, 101%, and 90%.   In  most
cases,   the   techniques  over-estimated   the  concentrations.
Clearly,  inaccuracies  of  individual measurements  are greater
than  those  of these  mean values and  care is required  in the
choice of pumps and detector tubes, in their calibration, and in
the interpretation of results obtained with them.

    Other  direct-indicating  tubes  of  lower  sensitivity  are
available   for   the   measurement  of   the  higher  phosphine
concentrations   used   in   fumigation.  Classical   analytical
techniques,  such as oxidation to phosphate and the formation of
the  phosphomolybdate  complex  have been  specially  applied to
fumigants (Kao, 1981).  Shaheen et al. (1983) recently described
the  use of  indicator tubes  as passive  dosimeters  to  record
concentration x time  product  integrals.  The  stain-length was
closely,  but not linearly,  related to the concentration x time
product in the range 0 - 1400 mg x days/m3.  Absorptive or adsorptive sampling and analysis

    Gas  chromatography  is the  most  sensitive method  for the
determination    of  the  phosphine  content   of  air  samples.
Usually, samples are desorbed from a solid absorbent coated with
mercury (II)  cyanide, although samples  taken in syringes,  gas
bags, or tonometers can be used. Microcoulometric and thermionic
detectors have detection limits of 5000 and 20 pg, respectively.
The  limit  for  flame photometric  and  argon  and helium  beta
ionization  detectors is 5  pg and that  for mass  spectrometry,
1 ng.   Photoionization detection is also  commonly used.  Flame
photometry  combines both sensitivity and  stability (Verstuyft,

    Using   a  gas  chromatograph  equipped   with  a  nitrogen/
phosphorus-selective  detector, Vinsjansen & Thrane  (1978) were
able to detect phosphine in the environment at  a  concentration
of 0.04 µg/m3.

    Other  techniques  for  estimating phosphine  in air involve
entrapping  phosphine by adsorption or  reaction with subsequent
analysis  of the  desorbed or  reacted sample.   In a  classical
method  (Furman, 1962), air containing phosphine is reacted with
mercury  (II) chloride, followed  by the addition  of  potassium
iodide and then excess standard iodine solution.  Back-titration
of  the excess iodine with  thiosulfate is used to  quantify the

    Of  the solid sorbents, acid-washed charcoal and silica gels
coated   with   silver   nitrate  and   potassium   permanganate
effectively  collect phosphine but quantitative  release has not
been  achieved.   Mercury (II)  cyanide  on silica  gel collects
phosphine quantitatively and holds 80% of the phosphine  over  2
weeks storage. The phosphine is released for gas chromatographic
analysis  by treatment with alkaline sodium borohydride solution

(Barrett  &  Dillon,  1977) or  is  oxidized  (using a  hot acid
permanganate solution) to phosphate, which is measured using the
phosphomolybdate  colorimetric  technique (US  NIOSH, 1979).  It
should  be noted that  many commercially available  sorbents are
unsuitable (Dumas & Bond, 1981).

    Liquid  impingers/bubblers containing a variety of solutions
can be used to collect and react phosphine for quantification by
colorimetry/spectrophotometry,  by conductance, or  by potentio-
metric  titration.   Classical  colorimetric techniques  are the
development of the red-orange complex with silver diethyldithio-
carbamate,  which can be measured at 465 nm, or the oxidation by
permanganate  to phosphate which is  reacted with a solution  of
ammonium molybdate in concentrated sulfuric acid, extracted with
toluene-isobutanol,  reduced with tin (II) chloride and measured
as the phosphomolybdate complex at 625 nm (US NIOSH, 1979).  The
first  method suffers from  arsine interference and  the  second
also  measures  any  phosphorus  species  that  are  oxidized to
phosphate by oxalic acid/permanganate treatment.

    The  quantity  of phosphine  bubbled  through a  solution of
mercury (II) chloride and reacting:

                PH3 + 3HgCl2 = P(HgCl)3 + 3HCl

can be measured by the change in electrical conductivity using a
conductance  cell or by potentiometric titration of the HCl with
NaOH (Verstuyft, 1978).  Continuous methods

    There  are directly indicating continuous  samplers in which
phosphine-containing   gas  is  passed  through   a  paper  tape
impregnated  with  a  silver nitrate-containing  mixture,  which
develops a colour related to the phosphine  concentration.   The
tape  can subsequently be  passed through a  reader-recorder  to
produce  a concentration versus  time plot (McMahon  &  Fiorese,
1983).   Other continuous monitors  draw air at  a metered  rate
through  detectors  using  either  flame  photometry  or  photo-
ionization.   The  detection  limit of  infrared spectroscopy is
about  0.4 mg/m3 (0.3 ppm)  but this is barely  sensitive enough
for  monitoring  occupational  exposure (Webley  et  al., 1981).
Continuous direct estimation of phosphine can also be made using
the  property of chemiluminescence  in ozone and  measuring  the
emission at 550 - 560 nm using a photomultiplier tube (Boubal et
al.,  1981).  A portable  quadrupole mass spectrometer  has been
used (Arnold & Robbiano, 1974).

2.2.2.  Residues

    Fumigated foodstuffs may contain gaseous phosphine (adsorbed
and interstitial) and residual aluminium or magnesium phosphide.
Different  techniques  for  the determination  of  residues  may
measure the phosphine or the phosphide residues.

    Interstitial  and  adsorbed  phosphine  can  be  purged   by
nitrogen  and trapped in reagents  for classical analysis or  on
adsorbents  for chromatographic analysis (Dumas,  1978; Nowicki,
1978; Saeed & Abu-Tabanja, 1984).

    Total phosphine and phosphide is measured by  extraction  of
the  fumigated stored product  with silver nitrate  (Rangaswamy,
1984; Rangaswamy & Muthu, 1985), or with sulfuric acid (Nowicki,
1978;  Saeed & Abu-Tabanja, 1984).   The silver nitrate forms  a
chromophore, which is measured spectrophotometrically at 400 nm.
Following  sulfuric  acid  extraction,  headspace  gas  can   be
analysed spectrophotometrically for phosphine.

    Saeed  & Abu-Tabanja (1984) reported substantial differences
between  the purge-and-trap method and the sulfuric acid method.
Some of these differences may have been due to the  presence  of
powdered  aluminium phosphide in the  sample, but some may  have
been  due to incomplete desorption during purging.  The sulfuric
acid  method was preferred because it also measures the capacity
of the product to release phosphine and this is of  more  biolo-
gical significance than the measurement of free phosphine only.

    Robinson   (1972)   reported  the   measurement  by  neutron
activation  analysis of phosphorus-containing residues in filter
paper fumigated with PhostoxinR and demonstrated a net  gain  in
phosphorus content.

    Robison   &  Hilton  (1971)  described   the  estimation  of
phosphine/phosphide residues in zinc phosphide-treated sugarcane
by  extraction in sealed flasks  into a mixture of  aqueous acid
and  toluene  followed by  the  gas chromatographic  analysis of

2.2.3.  Metal phosphides

    Hydrolysis  of metal phosphides with acids yields phosphine,
which can be measured by any of the methods  already  described.
Terzic  (1981)  has  described a  method  in  which the  evolved
phosphine  is  absorbed  in  silver  nitrate  to   form   silver
phosphide,  which is oxidized to  silver phosphate, precipitated
as  magnesium ammonium phosphate,  and converted by  ignition to
magnesium  pyrophosphate, which is weighed.  A single conversion
factor applied to this weight gives the quantity of phosphide in
the sample.


3.1.  Natural Occurrence

    Phosphine is extremely rare in nature. It occurs transiently
in  marsh  gas  and other  sites  of  anaerobic  degradation  of
phosphorus-containing  matter, and the equilibrium  of reactions
in  which  it participates  favour  its oxidation  (Ciba, 1978).
Although  phosphorus could be expected  to occur naturally as  a
phosphide, the only phosphide in the earth's crust is  found  in
iron meteorites as the mineral schreibersite (Fe,Ni)3P, in which
cobalt and copper may also be found (Van Wazer, 1961).

3.2.  Man-Made Sources

3.2.1.  Production levels and processes

    Apart  from  natural sources,  atmospheric phosphine results
from  emissions and effluents from industrial processes and from
the use of phosphides as rodenticides and fumigants.  Unexpected
focal  release of phosphine may occur due to the action of water
on   phosphides  present  as   impurities  in  some   industrial
materials.    Amounts  of  phosphate  arising  from  atmospheric
phosphine  are insignificant in  comparison with the  amounts of
phosphate  added  to  the environment  from sewage, agricultural
run-off, and industrial and urban effluents.   World production figures

    It  is difficult to  quantify the production  of  phosphine,
since much of it is manufactured and used in relation to another
process.   Though some phosphine is supplied in cylinders, it is
often produced, as and when required, by hydrolysis of  a  metal
phosphide. Phosphine is also produced as a by-product or evolved
incidentally in various industrial processes.

    A  main use of phosphine  is as a dopant  in the electronics
industry.   A total of 42  electronics companies used 6  million
litres  of phosphine gas  mixtures in various  concentrations in
1979,  probably  equivalent  to  some  300 000  litres  of  pure
phosphine (LaDou, 1983).  In 1981, 90% of speciality  gases  for
the  electronics  industry  were produced  by  six manufacturers
(LaDou, 1983).The annual growth rate for the use of  dopants  by
the  electronics industry has been estimated to be 30% per annum
(SRI, 1982).  By contrast, volumes more than twice this  may  be
produced  and used as a chemical intermediate in a single plant,
and  even greater  amounts are  used for  fumigation  of  stored
products.   For example, in the  Federal Republic of Germany  in
1975,  37 000 kg (approximately 28 million litres)  of phosphine
were  used for  fumigation, though  it decreased  to  10 000  kg
(approximately  7.5 million litres) in  1977 as a result  of the
introduction of alternatives (Noack & Reichmuth, 1982a).  Manufacturing processes

    Phosphine  is  manufactured  by the  hydrolysis of aluminium
phosphide  or magnesium-aluminium phosphide, or  by the electro-
lysis  of phosphorus in the presence of nascent hydrogen (Boenig
et  al., 1982).  It is formed as a co-product in the manufacture
of  hypophosphites  by the  reaction  of white  phosphorus  with
alkali  where  conditions  can  be  established  so   that   the
phosphorus-steam   reaction  yields  phosphine.    Phosphine  is
produced  as  a  by-product  in  the  manufacture  of acetylene,
through  the  hydrolysis of  calcium  carbide, if  this contains
calcium  phosphide as  an impurity.   It is  also  evolved  from
phosphorus  furnaces  (Al'zhanov  et al.,  1983),  impurities in
ferrosilicon  alloy  (Anon.,  1956;  Lutzmann  et  al.,   1963),
machining  of  spheroidal  graphite iron  (Bowker, 1958; Mathew,
1961),  steel  pickling  (Vdovenko  et  al.,  1984),  and  other
metallurgical   operations  (Habashi  &  Ismail,   1975).   Zinc
phosphide has been prepared by reducing trizinc  phosphate  with
hydrogen  at 600° C, by passing  phosphorus vapour over zinc  at
400 °C, or by direct reaction between amorphous  phosphorus  and
powdered zinc under pressure or heat.  Aluminium  phosphide  and
magnesium  phosphide are produced in similar ways or by exchange
reactions  between  aluminium  or magnesium  and  a  heavy-metal
phosphide (Wilson, 1971).

3.2.2.  Uses

  A  ternary compound, magnesium  aluminium phosphide, in  which
aluminium  and magnesium are present in the ratio by weight 1:3,
is  used in  sea flares  and as  an intermediate  for the  local
formation of phosphine by hydrolysis.

    As  a  chemical  intermediate,  phosphine  is  used  in  the
synthesis    of   organophosphines   and   organic   phosphonium
derivatives.   Alkyl  phosphines  may  be  made  by   additional
reactions  across  an  olefinic  double  bond.   Using  Grignard
reactions, both aryl and alkyl phosphines can be made  from  the
appropriate alkyl or aryl halide and PCl3.  Organophosphines are
used  in  oil-additive  and pharmaceutical  applications.  Phos-
phonium compounds are made by the addition of P-H bonds across a
carbonyl function with acid catalysis. For example, the reaction
of  phosphine with formaldehyde, in the presence of hydrochloric
or  sulfuric  acid, forms  the  corresponding salt  of tetrakis-
(hydroxymethyl)-phosphonium which is employed in the manufacture
of  polymers  used in  the  flame-retardant treatment  of cotton

    As  a  fumigant in  pest  control, phosphine  is  invariably
produced  at  the  site of  fumigation  by  the hydrolysis  of a
phosphide,  usually of aluminium or  magnesium.  As a dopant  in
the  electronics industry, phosphine is  used in high purity  at
low concentrations in nitrogen.

    Zinc  phosphide is used principally in the form of a 2.5% or
5% paste as a rodenticide incorporated in food (10%) as  a  bait
(WHO/FAO, 1976).  There are other formulations in which powdered

zinc  phosphide is incorporated,  possibly with a  zinc salt  to
inhibit  phosphine  formation before  use,  and histamine,  or a
histamine  releaser, to stimulate acid  secretion (and therefore
phosphine production) in the stomach of rodents taking the bait.
One  formulation includes a binder and is encapsulated in a form
that enables it to be included with grain as bait (Degesch GmbH,
1978).   Aluminium and magnesium  phosphides are used  in powder
form  or  in  formulations as  a  source  of phosphine  for  the
fumigation of storage facilities and stored products, to prevent
spoilage  by  a  wide  range  of  pests.   In general,  for  the
satisfactory  hydrolysis  of  the phosphide,  the material being
fumigated should have a moisture content of 10% or more.


4.1.  Transport and Distribution Between Media

4.1.1.  Air

    Frank & Rippen (1986) studied the disappearance of phosphine
from  air released following the aeration of fumigated premises.
The  most important chemical  reactions are with the  HO x radi-
cals, which are usually present in abundance in  the  atmosphere
due  to the reaction of ozone with water, a reaction enhanced by
impurities such as NOx:

                H2O + O3 +2  e - -> 2 HO x  + 02

    The following reactions of HO x  and phosphine may occur:

                 PH3 + HO x  -> H2O + PH2 x 

                   PH3 + HO x   ->   HOP x  H3

    This reaction is dependent on phosphine concentration and is
very  rapid with a reaction rate constant at room temperature of
about 1.5 x 10-11 cm3/mol x sec   (Fritz et al., 1982;  Becker  et
al.,  1984).   Direct  reactions with  ozone  are quantitatively
unimportant,  since  reaction  with HO x  occurs   before  PH3 can
reach the ozone-rich upper atmosphere. With the usual concentra-
tions of HO x ,   the half-life of phosphine in air is about 28 h.
Sunshine  increases  the  HO x  concentration  and  may reduce the
half-life to less than 5 h. Direct photolysis cannot be expected
with  phosphine (Calvert & Pitts, 1966).  The eventual oxidation
product of phosphine will be phosphorus oxyacids  and  inorganic
phosphate,  which  will  be  deposited  and  contribute  to  the
nutritive environment of soils and surface waters.

    Hilton  &  Robison  (1972)  studied  the  disappearance   of
phosphine from dry tubes sealed by a rubber membrane   and  from
similar tubes containing a small quantity of  water.   Phosphine
completely  disappeared from the dry  tubes in 40 days,  but the
presence of water in the others reduced the rate  of  disappear-
ance.   However, possible losses  through, or by  adsorption on,
the  membrane were not quantified  and no information was  given
regarding illumination of the tubes.

4.1.2.  Soil

    Hilton  & Robison (1972)  introduced phosphine at  1.4  g/m3
(1000  ppm) (as P)  in the headspace of tubes containing 3 types
of  soil  at  5 moisture  levels,  0%,  25%, 50%,  75%, and 100%
saturation.   It  was  not stated  whether  the  soils had  been
sterilized.   Phosphine disappeared within 18 days from all air-
dried  soils, whereas up to 40 days was necessary for disappear-
ance  from  moisture-saturated soils.   Quantities of phosphorus
recoverable  as phosphate from the soils after incubation for 40
days varied widely with different soil types and  reached  about
70%  of total phosphine  in a slightly  acidic soil,  containing

12% -  15% organic matter  content at 25%  moisture  saturation.
Variation  in  phosphate  recovery probably  reflected  rates of
diffusion  of phosphine into  the soil matrix  as a function  of
moisture  content, as well as  differences in the efficiency  of
different  soils with different  moisture contents as  oxidizing
substrates for phosphine.  Clearly, in time, soils are  able  to
entrap the phosphine in the air in contact with them and oxidize
it to orthophosphate.

    Hilton & Robison (1972) studied the fate of  zinc  phosphide
and  phosphine in the  soil-water environment.  The  results  of
preliminary  experiments showed that phosphine  was undetectable
in  headspace  gases  over  soil  containing  zinc  phosphide at
1.4 mg/m3  and 14 mg/m3 (1 and 10 ppm) (as PH3).  Zinc phosphide
was  added at 1000 ppm (as P)  to each of 3 types of soil at 0%,
25%, 50%, 75%, and 100% water saturation in sealed bottles which
were incubated at 27 - 28 °C for up to 34 days.  Headspace gases
were  sampled periodically and the  appearance and disappearance
of  phosphine followed.  At the  end of the phosphine  evolution
period,  acetic  acid  was added  to  the  samples to  hydrolyse
phosphide  to  phosphine  with minimum  conversion to phosphate.
The headspace was analysed for phosphine after heating for  3  h
and  cooling.   It  was then  flushed  with  nitrogen to  remove
phosphine,  and sulfuric acid was  added to the soil  to extract
the  phosphate.   The  amount  of  phosphine  in  the  headspace
increased  with increasing moisture content up to 50%.  The data
were  sufficient to estimate  the extent of  hydrolysis of  zinc
phosphide to phosphine.  After 34 days of  incubation,  residual
phosphide was detectable only in the dry (about 35% of original)
and  25% saturated (about 10%  of original) soils.  Over  80% of
the phosphide phosphorus was recovered as phosphate,  except  in
the case of dry soil samples.

4.1.3.  Aquatic environment

    The hydrolysis of zinc phosphide was negligible in a variety
of surface waters, tap water, and ocean water over periods of up
to 11 days.  Only in a buffered solution at pH 4 did significant
hydrolysis  take place (Hilton  & Robison, 1972).   The  authors
concluded that zinc phosphide released or carried  into  streams
or ocean water would not decompose rapidly.  Bottom or suspended
sediments would be likely to decompose zinc phosphide  with  the
formation  of phosphine or  phosphoric acid under  anaerobic and
aerobic conditions, respectively.

4.1.4.  Vegetation, wildlife, and entry into the food chain

    Robison  &  Hilton  (1971)  studied  phosphine  residues  in
sugarcane in  vitro using 32PH3.  About 30% of the 32PH3 reacted
irreversibly to form water-soluble compounds of phosphorus while
another  10% remained irreversibly bound  to the fibre.  It  was
suggested  that  the  water-soluble  compounds  were  phosphorus
oxyacids  and a portion of  the acids may have  formed insoluble
iron or aluminium salts in the fibre.

    Effects  on  viable  seeds, (section  6.4.3)  suggest little
effect on plant metabolism.

    The  only significant exposure  of wildlife to  phosphine or
metal  phosphides is through  their use as  pesticides; domestic
animals  may also  be accidentally  exposed in  this way.   Zinc
phosphide  baits are known to  be highly palatable for  rodents.
Acceptability  of  bait by  non-target  species depends  on  the
presentation  (Janda, 1973) and the precise location in relation
to  natural  feeding  sites (Chentsova,  1972).   Persistence of
phosphine  or phosphides in the carcasses of poisoned animals is
low  and  their  carcasses are  not  toxic  when eaten  by other
animals (Kozhemyakin et al., 1971; Schitoskey, 1975).

    Various  studies  have been  undertaken  on the  effects  of
feeding  fumigated  diet  to  experimental  animals.   Kadkol  &
Jayaraj  (1967)  reported  the  effects  of  feeding  phosphine-
fumigated  rice  to albino  rats for 12  weeks.  The only  dose-
related  effects  were  slight  increases  in  liver  and kidney
weights in male rats.  Hackenberg (1972) reported a study on the
effects on Wistar rats (30 male and 30 female in both  test  and
control groups) of a standard laboratory chow treated for  72  h
with  PhostoxinR uniformly distributed in  the food at 48  mg/kg
for the first 16 weeks and thereafter at 90 mg/kg (corresponding
to  10  times  the  recommended  treatment  level).    Following
treatment,  food was mixed and aerated for 1 h before determina-
ation  of phosphine,  which was  found to  be in  the region  of
1 mg/kg food, including any residues of pellets.  The methods of
administration and storage of food were probably responsible for
further  losses  of phosphine  after  the aeration  period.   No
differences  attributable  to  diet were  observed in behaviour,
development,  body weights, food  consumption,  or in  blood and
urine composition (at any stage in the study), and in  gross  or
microscopic pathology between test and control animals.

    Cabrol  Telle et al. (1985) undertook a similar study of the
effects of feeding a phosphine-fumigated test diet to 30 Sprague
Dawley  rats of both sexes for 2 years, with a control group fed
an  identical but non-fumigated control diet.  The test diet had
been  fumigated by storage in phosphine at 2820 mg/m3 (2000 ppm)
for  at least 6 months.  Just before consumption, it was aerated
for  48 h and supplemented  with a balanced vitamin  preparation
(also  added to the  non-fumigated control diet).   The  average
residue  level in  the fumigated  diet was  less than  5  mg/kg.
There  were  no  differences  between  test  and  control groups
attributable  to the consumption of a fumigated diet in terms of
weight  gain,  food consumption,  plasma chemistry, haematology,
urinalysis,  behaviour, growth, survival, organ  weights, histo-
pathology, tumour incidence, or carcass analysis.

    It  is unlikely,  therefore, that  the use  of phosphine  or
phosphides  results in  food residues  that are  of any  toxico-
logical significance.

4.2.  Biotransformation

    There  have  been no  studies  on the  biotransformation  of
phosphine  or metal phosphides.  Energy   considerations suggest
that  phosphine  is  liable  to  be  oxidized  to  phosphate  in
biological  systems  (Ciba, 1978).   There  is no  suggestion of
bioaccumulation or biomagnification.

4.3.  Ultimate Fate

    The ultimate fate of phosphine and the phosphide  moiety  of
metal phosphides is the formation of phosphate.

    Disposal  of phosphide-bearing wastes  is regulated in  many
countries.   Effluent  phosphine  is  usually  burned  and   the
resultant  gases can be scrubbed to remove phosphorus oxides and
oxy-acids  before discharge into the atmosphere.  Zinc phosphide
formulations  and  baits  in  some  countries  are  regulated as
hazardous wastes, for instance when their concentration  exceeds
10%  (US EPA, 1983).   Deep burial  is the  preferred method  of

    IRPTC (1985) gives the following recommendations:

Aluminium phosphide

    "Allow  it to react  slowly with moisture  out in the  open,
taking  precautions to see that the poisonous gas (phosphine) is


    "Surplus  gas or leaking cylinders  can be vented slowly  to
air  in a safe,  open area or  gas can be  burnt off  through  a
suitable burner in a fume cupboard".


a   It  should be  added that  precautions should  be  taken  to
    ensure  that the area is  inaccessible to children and  ani-
    mals. The IRPTC comments "Phosphine gas creates no permanent
    environmental  hazard because it is  eventually converted to
    harmless  phosphoric  acid  and water".   An  alternative is
    admixture with an inert dry diluent and burning at a temper-
    ature  greater  than  1000 °C with  effluent  gas scrubbing.
    These recommendations also apply to magnesium phosphide.


5.1.  Environmental Levels

5.1.1.  Air, water, and soil

    Phosphine  and metal phosphides  have only been  detected in
the general environment in relation to the recent use  of  metal
phosphides  in  pest  control and  in  relation  to a  number of
industrial activities.

    Arendt  et al. (1979) studied open-air concentrations in the
vicinity of a silo at successive stages during  fumigation  with
phosphine and aeration.  Within 20 m of the silo  wall,  concen-
trations  reached  a  peak of  3  mg/m3  (2.15 ppm)  during  the
fumigation phase and averaged 0.37 mg/m3 (0.26 ppm)  during  the
aeration  phase, but the maximum value after 3 h of aeration was
0.06  mg/m3 (0.04 ppm).  At distances greater than 20 m from the
silo,  the concentration was at  all times less than  0.05 mg/m3
(0.035  ppm).  Measurements at 7 locations from < 5 to 60 m from
the silo, during aeration, showed that the highest concentration
20  -  30 min  after the start  of aeration was  0.1 mg/m3 (0.08
ppm), while other values were about half of this or less.  Seven
hours  after the commencement  of aeration, concentrations  were
uniformly less than 0.014 mg/m3 (0.01 ppm).

    Reichmuth  et  al.  (1981) reported  similar  results.  They
found that open air concentrations immediately adjacent  to  the
outer  walls  of  buildings under  phosphine  fumigation reached
280  mg/m3 (200 ppm (v/v)), but at a distance of > 10 m from the
buildings,   all  concentrations  except  one   were  less  than
0.14 mg/m3 (0.1 ppm (v/v)).  However, there are isolated reports
of  persons  in  the  neighbourhood  of  fumigated  stores being
affected by phosphine (Gessner, 1937; Hallerman & Primela, 1959;
Sayvetz,  1982); in the  2 earlier reports,  effects were  fatal
(section 9.2).

    These results indicate that fumigation operations contribute
only  locally and transiently to atmospheric phosphine exposure.
The  volumes released in industrial operations (section
are  much smaller  and are  therefore of  less  significance  in
relation  to atmospheric concentrations, except at the immediate
work station.

5.1.2.  Food and feed  Residue values

    Because  of  the techniques  of  analysis used,  residues of
phosphine  or metal phosphides are usually measured together and
reported as total phosphine or phosphorus.  The results indicate
that  residues in fumigated foods  are negligible at 0.01  mg/kg
(0.01  ppm)  or  less (Dieterich  et  al.,  1967).  Urga  (1983)
reported  residue levels in a variety of stored grains or pulses
(minimum  moisture  content 7.6%)  that  had been  fumigated  by
inserting PhostoxinR at 3 tablets per tonne under  PVC  sheeting

for  3 - 8 days,  followed by a minimum  of 2 months'  aeration.
Phosphine  was measured by  bromine oxidation and  the  phospho-
molybdate  colorimetric  method.   Average  phosphine   residues
measured  as phosphorus in different stored grains or pulses are
shown in Table 4.

Table 4.  Average PH3 residues (as phosphorus)a
                  Number of     mg/kg
                  samples       average (range)
Wheat             15            0.05 (0.01-0.08)

Chick-peas        9             0.07 (0.02-0.12)

Barley            3             0.11

Maize             12            0.06 (0.01-0.11)

Sorghum           3             0.11
a  From: Urga (1983).

    Cabrol  Telle  et  al.  (1985)  (section 4.1.4)  found  that
residue   levels  after  prolonged  fumigation   at  2820  mg/m3
(2000  ppm)  were on  average 0.005 mg/kg  (0.005 ppm), but  the
phosphine  was  apparently  not  produced  from  mixing  a metal
phosphide  in  the  diet.  Hackenberg  (1972)  mixed  PhostoxinR
pellets  with  basic  diet  and  determined  residues   included
hydrolysis  of unreacted phosphide to  phosphine.  Residues were
generally under 0.75 mg PH3/kg feed.  Since the  fumigation  was
at 10 times the recommended rate, this result is comparable with
a  residue level  of less  than 0.1  mg/kg (0.1  ppm) at  normal
doses.  Samples of 2 of the batches of feed contained exception-
ally  high levels of 1.3  and 7.5 mg PH3/kg  feed, respectively,
presumably  as a  result of  residual phosphide  in the  samples
selected.  Singh et al. (1983) fumigated pulses  with  PhosfumeR
tablets  at the recommended dosage (2 tablets/tonne) and also at
2  and 4 times the  recommended dosage.  After fumigation  for 5
days,  phosphine residues decreased  exponentially with a  half-
life that depended on the type of pulse and the fumigation dose;
the  half-lives varied from  0.66 to 1.33  days.  In each  case,
residues  fell  below  the limit  of  detection  of 0.001  mg/kg
(0.001 ppm)  in less than 3 days at normal fumigation rates, and
in less than 6 days at 4-fold fumigation rates.

    Breyer  (1973) described field  studies using magnesium  and
aluminium  phosphide formulations as the source of phosphine for
the  treatment of wheat.  After 12 days exposure at 17 °C with a
concentration  of  6  g  phosphine/tonne,  the  wheat  contained
0.009 mg  phosphine/kg in the  case of magnesium  phosphide  and
0.012 mg/kg for aluminium phosphide.

    Residues  in  wheat, millet,  milled  rice, soya  beans, and
azuki  beans were studied after exposure to 5640 mg phosphine/m3
(4000  ppm) at 25 °C (Sato  & Suwanai, 1974).  After  12 days of

fumigation,  the residue levels were 0.46, 1.16, 0.34, 0.18, and
0.24 mg phosphine/kg, respectively.

    When   wheat   was  fumigated   with   phosphine  at   5  mg
phosphine/kg,  the residue level  after 4 days  of aeration  was
0.2 µg/kg   (0.2 ppb);  after 220  days of  aeration, the  level
dropped to 0.004  µg/kg (0.004 ppb) (Dumas, 1986).

    Phosphine  levels in Iraqi  dates fell rapidly  within 24  h
after  fumigation, but residues persisted  for at least 9  days.
Higher   residue  levels  were   found  with  storage   at   low
temperature.  For example, more than 1 mg  phosphine/kg  (1 ppm)
could  still be detected after  10 days in dates  stored at 4 °C
(Alomar & Al-Bassomy, 1984).  Factors affecting residue levels

    The factors affecting phosphine residues in hazel nuts, soya
beans,   and   wheat  that   had  been  fumigated   at  20.5  mg
phosphine/litre,  for periods  of 1  and 14  days, were  studied
(Noack  et al., 1984a).  Fumigated  food was then aerated  for 5
weeks  in a layer about 20 mm deep in a wire basket, open to the
air  at 70%  relative humidity  and at  temperatures of  -18 °C,
+5 °C,  +20 °C, and +35 °C.   Residue levels were  studied as  a
function  of  fumigation  duration and  aeration temperature and
duration.   Residues decreased approximately  exponentially with
time, more rapidly at higher temperatures and with  the  shorter
fumigation  period.  Residues were much more persistent in hazel
nuts  than in  wheat, with  intermediate levels  in soya  beans.
Temperature dependence was much less marked with hazel nuts than
with the other 2 foods.  Residue levels immediately at  the  end
of fumigation were not much higher after 14 days  of  fumigation
than  after 1 day,  presumably because equilibrium  was achieved
within  the shorter fumigation period.   Concentrations in wheat
and  soya  beans after  3 days aeration  or more were  about 2.5
times  higher when fumigated for 14 days than when fumigated for
1  day.  For hazel  nuts, the corresponding  ratio was about  5.
Times  for phosphine residues to  reach 0.1 mg/kg (0.1  ppm) and
0.01  mg/kg (0.01 ppm) are given in Table 5 (Noack et al., 1983,

    The  shorter the period of  fumigation, the lower the  dose,
and  the higher the storage  temperature, the more rapid  is the
decomposition of phosphine.  Crops with high contents of fat and
protein  appear to retain a higher level of phosphine than those
with  a high water  content.  The residue  level for hazel  nuts
fumigated at 20.5 mg phosphine/litre for 14 days was 15.2 mg/kg,
whereas for wheat similarly fumigated only 0.6  mg  phosphine/kg
was detected (Noack et al., 1983).

    A  further study described  in the same  report showed  that
after fumigation for 10 days (5.6 mg phosphine/litre) and active
ventilation  at  8,  50, or  100  litres/h  for 12  days  during
aeration, residue levels were independent of airflow.

Table 5.  Approximate time necessary for phosphine residues to reach
0.14 mg/kg and 0.01 mg/kg in different stored products at 
various storage temperatures and durations of fumigationa
Food type   Fumigation    Target    Time to reach residue 
            (20.5 mg      residue       level (days)         
            pH3/litre)    level           Temperature (°C)   
            duration      mg/kg    -18   +5     +20    +35

Hazel nuts    1           0.1      35+   35+    35+    20
                          0.0      35+   35+    35+    35+
              14          0.1      35+   35+    35+    35+
                          0.01     35+   35+    35+    35+

Soya beans    1           0.1      35+   10     4      3
                          0.01     35+   35+    9      6
              14          0.1      35+   35+    18     5
                          0.01     35+   35+    35+    16

Wheat         1           0.1      20    < 1    < 1    < 1
                          0.01     35+   25     4      3
              14          0.1      35+   15     7      2
                          0.01     35+   35+    28     8
a  Adapted from: Noack et al. (1984a).

    The results indicate that the decrease in phosphine residues
is limited by the rate of diffusion within the  food  substance,
the  rate of desorption from  its surface, or chemical  decompo-
sition, rather than by interstitial diffusion; the rate-limiting
process is temperature dependent.

    Noack et al. (1984a,b) were able to describe  the  behaviour
of  phosphine  residues  in semi-empirical  mathematical  models
which  were in  good agreement  with experimental  data.   In  a
further  study (Noack & Wohlgemuth,  1985), the effects of  non-
constant  phosphine  concentrations on  fumigation residues were
examined.   There was a  correlation between the  final residues
and  the concentration of  phosphine used but  during fumigation
concentrations  rose  to  a  peak  then  declined.   Residues in
samples  of foodstuffs removed  from fumigation at  a particular
concentration in the rising phase decreased more rapidly than in
samples  removed from fumigation  at the same  concentration in
the declining phase. Residue levels in samples of food fumigated
at  constant concentration reached a maximum later than the time
at which the maximum fumigation concentration had been achieved.
These  results could be explained  on the basis of  the sorption
and  diffusion  of  phosphine  and  the  authors  concluded that
residues  are minimized by  fumigation at low  concentrations (a
few hundred mg/m3) over a long period (2 - 3 weeks).

    Robison  &  Hilton  (1971) measured  phosphine  residues  in
sugarcane  harvested  from  fields  treated  4  times  with zinc
phosphide as a rodenticide at 5.6, 11.2, or 56 kg/ha.  Sugarcane

was analysed for phosphine after 7 and 110 days using extraction
by  aqueous acid and  toluene and gas  chromatographic analysis.
In  general, residue levels were less than 0.01 mg/kg (0.01 ppm)
and  in  no  case did the levels exceed 0.1 mg/kg (0.1 ppm).  At
harvest,  110  days  after  application,  sugarcane  from  a wet
location did not contain any residues of phosphine, whereas that
from   a   dry  location  still  contained  up  to  0.032  mg/kg
(0.032 ppm) (highest application).

    In a study by Robinson & Bond (1970), 32P-labelled phosphine
derived   from   labelled   aluminium  phosphide   was  used  to
investigate  the presence of phosphorus residues after treatment
of  wheat and flour.  The radioactive residue in wheat and flour
could  not be  removed by  thorough aeration  or by  heating  at
baking  temperature.  It was shown  to be largely water  soluble
and  paper  chromatography  identified  the  main  products   as
hypophosphite and phosphite. It was concluded that the oxidation
of  phosphine to the lower  oxyacids of phosphorus was  mainly a
surface  phenomenon  and  that, in  the  normal  course  of  air
oxidation,  all  residues  would eventually  appear  as   ortho-
phosphate.   Deposition of oxidation products  of phosphine also
occurred on glass and other surfaces.

    Laboratory  studies by Disney  & Fowler (1972a)  showed that
wheat  exposed to phosphine  levels (3 mg/litre)  several  times
higher  than  those  normally used,  at  25 °C  for 5  days (10%
moisture   content)  and  14  days   (19.7%  moisture  content),
contained residue levels varying from 1.7 mg/m3 (1.2 ppm) in the
first case to 25.9 mg/m3 (18.4 ppm) in the second, demonstrating
the important effect of water content as well as exposure period
in  determining residues.  Autoradiography of  sections of whole
grain showed that most of the radioactivity was present  in  the
outer  layers and  crease, and  that 70%  of the  residues  were
extractable with hot water.  Tkachuk (1971, 1972)  showed  that,
in wheat, flax, and rapeseed, approximately 50% of the phosphine
formed  non-phosphine residues, which were  distributed in wheat
in  the bran (85%), endosperm (14%), and germ fractions.  Eleven
percent  of the residues were  water soluble and appeared  to be
hypophosphite and pyrophosphate. The remainder may have included
insoluble aluminium salts.  It was suggested that this  did  not
represent   the  behaviour  of  non-radioactive  phosphine,  but
further studies confirmed the isotopic studies (Disney & Fowler,
1972b; WHO/FAO, 1972).  The adsorbed non-phosphide residues were
oxyacids  of  phosphorus  and of  no  toxicological significance
(Robinson, 1972; US EPA, 1986).

    Some  national  and international  standards and recommenda-
tions  for  phosphine residues  in food and  feeds are given  in
Table 6.

Table 6.  Various national and international standards for phosphine
residues in food
Organization         Commodity                       Level of
(reference)                                          phosphine   
                                                     ppm   mg/kg
Joint FAO/WHO Food Standards Programme Codes Alimentarius Commission
Codex Alimentarius   Maximum Residue Limits (MRL)
                     Cereal grains                         0.1
                     Flour and other  milled cereal        0.01
                     products, dried foods, fruit
                     and vegetables, spices, cocoa
                     beans, nuts, peanuts and
                     breakfast cereals
cited in             Raw cereals, soy beans,         0.1   0.1
US EPA (1986)        processed foods, animal feeds

Government of        Whole food grains               0.05  0.05
India: Department
of Health (1976)
(cited by Smugh      Milled food grains              0.01  0.01
et al. (1983))

US EPA (1985a)       Tolerances for residues         0.1   0.1
                     applicable to either aluminium
                     or magnesium phosphide:
                     almonds, barley, cashews,
                     cocoa beans, coffee beans,
                     corn, cottonseed, dates,
                     filberts, millet, nuts (Brazil,
                     pistachio), oats, peanuts,
                     pecans, popcorn, rice, rye,
                     flower seed, sesame seed,
                     sorghum, soybeans, sunflower
                     Tolerances for residues of      0.1   0.1
                     aluminium phosphide:
                     vegetables (seed and pod,
                     except soybeans)
                     Walnuts, wheat                  0.01  0.01
                     Tolerances for residues of      0.01  0.01
                     magnesium phosphide:
                     avocados, bananas, Chinese
                     cabbage, egg-plants,
                     endive (escavole)
                     grapefruit, kumquats, lemons,
                     lettuce, limes, mangoes, mush-
                     rooms, oranges, papayas,

Table 6. (contd.)
Organization         Commodity                       Level of
(reference)                                          phosphine   
                                                     ppm   mg/kg

                     peppers, persimons, pimentos,
                     plantains, salsify tops,
                     tangelos, tangerines, tomatoes

Kagan (1985)         Cereals                         0.01  0.01

5.1.3.  Tobacco and consumer products

    Residues  of phosphine in fumigated tobacco were reported to
be not greater than 8.3 µg/kg (8.3 ppb) (Childs et al.,  1969;  Kuhn
et  al., 1971).  Experimental  fumigation of tobacco  with  32P-
phosphine  similarly led to residual 32P-phosphorus of less than
5  mg/kg  (5  ppm) (Underwood,  1972).   However,  this may  not
qualitatively  simulate the residues found in practice since the
32P-phosphorus  contained  in  tobacco was  predominantly in the
form  of  phosphate  (which  is  a  normal  constituent).   This
contrasts  with  the results  of a similar  study (Kuhn et  al.,
1971)  where  the majority  of  residual 32P-phosphorus  was  as
phosphine   and   approximately   25%  was   non-volatile.    In
Underwood's  study, fumigated tobacco  was made into  cigarettes
that  were smoked in a  smoking machine and the  ash, mainstream
smoke,  and butt  analysed for  32P.  The  32P was  found to  be
confined  to the ash as  phosphate.  Winks (1970) reported  that
tablet   and  pellet  residues   from  tobacco  fumigated   with
PhostoxinR  contained 3.4% and 2.9%,  respectively, of unreacted
aluminium  phosphide.  According to subjective evaluation of the
fumigated  leaf  after aeration  for 2 days  there were no  off-
odours or the odour of phosphine.

5.1.4.  Terrestrial and aquatic organisms

    Phosphine   or  phosphides  have   only  been  reported   in
terrestrial or aquatic organisms due to deliberate or accidental
administration of phosphine or phosphides.

    Muscle  tissue of rabbits  and chickens poisoned  with  zinc
phosphide  did not contain  detectable residues (Kozhemyakin  et
al.,  1971; Bubien  et al.,  1974).  Intestines  and  liver  may
contain phosphides (Bubien et al., 1974; Meredith, 1981) but the
whole  carcass  of  a kangaroo  rat  killed  by a  dose  of zinc
phosphide  was not toxic to  the kit fox, despite  the fact that
the amount ingested by the rat was 3 times the  amount  expected
to  be lethal for  the fox, on  a body weight  and LD50 of  zinc
phosphide  for the fox (Schitoskey, 1975).  Rats, cats, and mice
fed  for  30  days on  meat  from  the carcasses  of rabbits and
chickens  killed with zinc phosphide  did not show any  specific
toxic effects (Kozhemyakin et al., 1971).

5.2.  General Population Exposure

5.2.1.  Access to phosphine and phosphides

    Zinc  phosphide  pastes,  though legally  restricted in many
countries,   are  available  without  restriction   for  use  as
rodenticides  in others,  and there  are many  reports of  their
ingestion  in suicide cases.  Magnesium  and aluminium phosphide
formulations are also restricted and not normally  available  to
the  general public.  In most countries, there is strict control
of  fumigation  to prevent  public  exposure to  phosphine,  and
guidelines  for safe fumigation are  available.  These measures,
combined with negligible ambient air concentrations, effectively
limit exposure.

5.2.2.  Residue exposure

    Residue levels in fumigated foods are generally regulated at
0.1  mg/kg (0.1 ppm) or  sometimes 0.01 mg/kg (0.01 ppm).   Even
among  populations whose diet is mainly derived from stored pro-
ducts,  the daily intake would be unlikely to exceed 0.1 mg/day,
even  if the phosphine  or phosphides survived  cooking.   Under
most  circumstances  daily intakes  would  be several  orders of
magnitude  lower than this, because of lower residues, the small
fractions  of the diet that  have been fumigated, and  losses of
fumigant in storage and food preparation.

5.2.3.  Subgroups at special risk

    No  subgroups of the general population have been identified
to  be at special risk  from phosphine or phosphides  except for
children, who might find and eat bait containing phosphides.

5.3.  Occupational Exposure During Manufacture, Formulation, or Use

    Occupational   exposure  can  be  divided   into  4  general
categories:  (a) workers producing phosphine and phosphides; (b)
workers in operations that can release phosphine, e.g., welding,
metallurgy,  semi-conductors  (c)  fumigators  and  pest-control
operatives;  and (d) transport  workers, e.g., drivers,  seamen.
Both  the exposure  patterns and  the potential  for control  of
exposure differ from case to case.

    Exposure  to phosphine and  phosphorus oxides, which  occurs
during  the manufacture of metal phosphides, varies according to
the method of manufacture.  High levels of exposure may occur in
the direct methods involving the reaction of red phosphorus with
powdered  metal.   Freshly  produced powdered  phosphides evolve
phosphine  at fairly high  rates initially, producing  warehouse
concentrations ranging from 0.4 to 1.6 mg/m3 (0.3 -  1.13  ppm).
Concentrations of 2.5 and 4 mg/m3 (1.8 and 2.9  ppm),  necessit-
ating  the  use of  personal  respiratory protection,  have been
reported in production areas (Jackson & Elias, in press).

    The  use of zinc  phosphide in the  preparation of  poisoned
bait   would  not  be  associated   with  significant  phosphine
exposure,  because of the stability of zinc phosphide in neutral
media.   There is no literature  regarding occupational exposure
to phosphine during the formulation of preparations of aluminium
phosphide for use in fumigation.  Jones et al.  (1964)  reported
that atmospheric levels to which operatives were  exposed  while
adding tablets of formulated aluminium phosphide to  wheat  were
undetectable. Levels encountered when stores were re-entered for
loading or turning were much higher, ranging from 18 to 35 mg/m3
(13 - 25 ppm).  In the USA, an estimated one million workers are
at  risk of inadvertent exposure.  Ten thousand of these workers
are  engaged  in  the  grain  freight  trades  where  accidental
exposure is a considerable hazard (US NIOSH, 1977).

    Exposure  to  phosphine  has  also  been  described  in  the
operation  of  acetylene  generators (Harger  &  Spolyar, 1958);
exposure to a level of 11 mg/m3 for up to 2 h per day  has  been
estimated.    Exposure  to  phosphine  can  also  occur  in  the
production   of   phosphorus   (Beloskurskaya,  1978),   in  the
conversion of white phosphorus to red phosphorus where levels of
up  to 0.5  mg/m3 (0.35  ppm) were  found (Jackson  & Elias,  in
press), and also in steel pickling (Vdovenko et al., 1984).

    The  carriage of ferrosilicon  as a badly  ventilated cargo,
particularly  in barges, can  release phosphine accidentally  by
the  action of water on calcium phosphide, one of the impurities
present.   The transport of ferrosilicon  requires precautionary
measures  to prevent dangerous  emissions of phosphine  (Hunter,
1978).   High ship-board concentrations  of 1.4 -  3 mg/m3 (1  -
2 ppm)  in living quarters  and about 8.5  mg/m3 (6 ppm)  in the
hold  were  reported  in  a  vessel  transporting   ferrosilicon
(Lutzmann,  1963) and  a case  of fatal  poisoning in  the  same
environment  was  reported by   Ziemer,  (1963).  Jones  et  al.
(1964)  reported phosphine concentrations of 5 - 13 mg/m3 (3.7 -
9  ppm) in  the holds  of ships  transporting  fumigated  wheat.
Phosphine  fumigation of agricultural commodities  on board ship
during  transit is common practice  in some parts of  the world.
Countries  that import grain normally accept fumigation en route
and some nations require such treatment (Davis,  1986).   Guide-
lines  for safe fumigation practice have been established by the
United  Nations International Maritime Organization  (IMO, 1980)
and include the regular monitoring of air in the living quarters
to  ensure  that there  is no hazard  for crew members  from the
accumulation of phosphine.

    Many  metals  contain  phosphorus  in  small  amounts,   and
phosphine  can  be  generated  in  a  variety  of  metallurgical
processes.  Cole & Bennett (1950) reported the presence of about
4  mg phosphine/m3 in the immediate vicinity of magnesium powder
after  its  manufacture  from  bulk  metal  containing  0.0038 -
0.0093%  phosphorus.  Ferrosilicon alloys in  contact with water
form  phosphine in amounts  that vary with  the silicon  content
(which  correlates  with the  phosphide  levels) so  that alloys
containing  30  -  60%  silicon  can  release  10 -  230  litres
phosphine   per  tonne  (Delomenie,  1933).   Concentrations  of

phosphine  close to the  tool cutting edge  in the machining  of
spheroidal  graphite iron were reported by Mathew (1961) to vary
between 0.01 and 6.5 mg/m3 (0.01 and 4.6  ppm).   Concentrations
in  the  breathing zone  ranged from 0.01  to 1.3 mg/m3  (0.01 -
0.95 ppm)  and the average was  0.9 mg/m3 (0.65 ppm).   Earlier,
Bowker  (1958)  had  reported  similar  results  and  found that
phosphine  concentrations  fell  from 8.5  mg/m3  (6  ppm) at  a
distance  of  1  cm from  the  tool  to slightly  over  1  mg/m3
(0.8 ppm) at 8 cm from the tool.

    Although  phosphine  is  used extensively  in semi-conductor
manufacture,  there  are  no published  figures for occupational
exposure  in this industry.  Since  installations are invariably
modern   and  phosphine  is  used  under  precise  and  strictly
controlled  conditions,  frequently  diluted with  inert  gases,
exposure  of  workers is  not likely to  be high.  There  are no
published   data  relating  to  exposure  to  phosphine  in  the
synthesis of organophosphine or phosphonium derivatives.

    Some  recommended occupational exposure limits for phosphine
in various countries are given in Table 7.
Table 7.  Occupational exposure limits for phosphine in various countries
Country         Legal   mg/m3   Comments     Source
Australia       Reca    0.4     TLV TWAc     Approved occupational health
                                             guide threshold limit values

Belgium         Recb    0.4     TLV          Threshold limit values (1978)

Bulgaria        Reg     0.1     MPCc         Official journal, 88 (1971)

Czechoslovakia  Reg     0.1     MAC TWA      Hygienicke predpisy
                        0.2     MAC Ceiling  Ministerstva zdravotnictvi
                                value        CSR/Hygienic regulations of
                                             Ministry  of  Health of  CSR, 58
                                             Uprava No. 7/1985 Vest. Mz SSR
                                             Reg. V Ciast.24/1985 ZB/
                                             Regulation of Ministry of Health
                                             of SSR No. 7/1985 Reg. In
                                             Section 24/1985 ZB

Finland         Reg     0.1     MPC TWA      Luftfoereningar paa Arbets-
                                             platsen  (Air pollutants at the
                                             workplace) (1982)

German          Reg     0.1     TWA          Maximale zulässige
Democratic              0.3     STELc        Konzentrationen Gesundheits-
Republic                                     gefärdender Stoffe in der Luft
                                             am Arbeitsplatz (Maximum
                                             allowable concentrations of
                                             noxious substances in the
                                             Atmosphere (1983)

Table 7 (contd).
Country         Legal   mg/m3   Comments     Source
Germany,        Rec     0.15    8-h TWA      Deutsche Forschungsgemein-
Federal                 0.3     5-min STEL   schaft, "Maximale Arbeits-
Republic of                                  platzkonzentrationen",
                                             xxi, 16, (1985)
                                             German Association for
                                             Research, "Maximum Workplace
                                             xxi, 16, (1985)

Italy           Rec     0.4     8-h TWA      Valori limitati ponderati
                                             (Threshold limit values) (1978)

Hungary                 0.1                  ILO (1980)

Netherlands     Rec     0.4     TWA          Nationale MAC-Lijst
                        1.5     STEL         (National MAC-List) (1985)

Poland          Reg     0.1     Ceiling      Ordinance of the Minister of
                                value        Labour, Wages & Social Affairs
                                             22 Dec. (1982)

Romania         Reg     0.2     TWA          Ordinance of the Ministry
                        0.5     Ceiling      of Health, 60 (1975)

Sweden          Reg     0.4     1-day TWA    Arbetarskyddsstyrelsens
                                             Foerfattiningssamling, (1984,
                                             1985)  10 (1984)

Switzerland     Reg     0.15    TWA          Zulässige werte in Arbeitsplatz
                                             (permitted values in the
                                             workplace (1984))

United          Rec     0.4     8-h TWA      Health and Safety Executive
Kingdom                 1.0     10-min TWA   EH40/85 (1985)

USA             Rec     0.4     TWA          ACGIH (1986)
                        1.0     STEL         ACGIH (1986)
                                             US CFR (1981)

USSR            Reg     0.1     Ceiling      Gosndarstrennyi Standart
                                value        SSSR/State Standard of USSR,
                                             12.1.005 (1976)

Yugoslavia      Reg     0.1     MAC TWA      Ordinance, 24-3698/1 (1971)
a  Rec. = Recommendation.
b  Reg. = Registered regulatory requirement.
c  TLV = Threshold limit value.
   TWA = Time-weighted average.
   MPC = Maximum permitted concentration.
   MAC = Maximum allowable concentration.
   STEL = Short-term exposure limit.

6.1.  Insects

    Uptake of phosphine by insects is rapid in the  presence  of
oxygen,  but little  absorption occurs  in low  or  zero  oxygen
atmospheres,  and  the  insecticide potential  is  thus reduced.
Over  100 mg phosphine/kg body weight may be absorbed by insects
at  high  dosage  rates, and  some  insects  continue to  absorb
phosphine  for long periods, even after knock down (Bond et al.,
1969).  Phosphine taken up by insects is not removed by ventila-
tion of volatile phosphine derivatives or phosphine  itself  but
is apparently excreted slowly (Price et al., 1983).  Most of the
32P,  derived from 32PH3,  taken up by  insects is found  in the
soluble  fraction  of  the cells  (Robinson  &  Bond, 1970);  in
deproteinized  tissue extracts, the radiolabel is present mainly
as hypophosphite and orthophosphate (Price et al., 1982).

6.2.  Mammals

    There have been no formal studies of the  toxicokinetics  of
phosphine and metal phosphides in mammals.

6.2.1.  Absorption  Inhalation

    Because  systemic toxic effects  are detectable after  short
exposures  to very low atmospheric  concentrations of phosphine,
inhaled phosphine is generally considered to be readily absorbed
through  the  lungs.   Hydrolysis  suggests  that  aluminium  or
magnesium  phosphides  deposited on  the  moist surfaces  of the
respiratory  tract would release  absorbable phosphine but  zinc
phosphide,   which  hydrolyses  significantly  only  under  acid
conditions,  would  be  stable  for  some  time.   However,  the
transfer  of  a  proportion of  inhaled  zinc  phosphide to  the
intestinal  tract by the  lung particulate clearance  mechanisms
would  permit hydrolysis to phosphine by gastric acid as well as
absorption  of  the  zinc  phosphide.   The  lungs  also  absorb
particulates and, as it is known that zinc phosphide is absorbed
intact  from the gut  (Meredith, 1981), inhaled  zinc  phosphide
dust  might be absorbed directly  via the respiratory tract  and
then hydrolysed in the tissues.  Dermal

    An acute dermal LD50 for zinc phosphide in rabbits  (2000  -
5000  mg/kg body weight) has  been reported, but no  details are
available.   Hydrolysis of aluminium and magnesium phosphides on
the skin would lead to the evolution of gaseous phosphine, which
could  then be absorbed by inhalation, but this is unlikely with
zinc  phosphide, and the LD50 result suggests toxicity by dermal
absorption  (US EPA, 1983).   In general, dermal  absorption  of
phosphine and metal phosphides is insignificant.  Oral

    The  oral route is not relevant to the absorption of gaseous
phosphine.   Ingestion of zinc  phosphide results in  detectable
amounts  of  acid-hydrolysable phosphide  in  the liver  of rats
(Curry  et  al.,  1959;  Meredith,  1981).   Human  ingestion of
tablets containing aluminium phosphide yielded evidence of acid-
hydrolysable phosphide in blood and liver (Chan et  al.,  1983).
These  results indicate that  metal phosphides can  be  absorbed
directly.  Meredith (1981) showed that when zinc  phosphide  was
administered  to  rats  by gavage  in  corn  oil,  the  fraction
recovered  as phosphine from  the air of  the metabolic  chamber
increased with the dose administered up to about 25% at  a  dose
of 4 mg/rat (approximately 20 mg/kg).  The possibility that this
phosphine derived directly from the alimentary canal and not via
systemic  absorption  and  subsequent exhalation  could  not  be
excluded.  For comparison,  in vitro hydrolysis of zinc phosphide
for  12 h yielded 7.1%  as phosphine at pH  4 and 38.8% at  pH 2
and,  unless  there is  some  special enzymic  mechanism, acidic
gastric  conditions afford the only opportunity for such a level
of  hydrolysis.  The efficacy of zinc phosphide as a rodenticide
depends on the absorption of phosphide or phosphine  after  oral
administration.   Meredith (1981) also showed that about 4 times
as  much phosphide  was recoverable  from the  liver  when  zinc
phosphide  was administered in  corn oil rather  than in  water,
suggesting greater absorption of unhydrolysed material.
    McGirr  (1953)  speculated that  commercially available zinc
phosphide  might consist  of 2  fractions that  are attacked  at
different rates in the gastrointestinal tract.  This  was  based
on  the  fact that  phosphine is produced  rapidly and yet  zinc
phosphide  is recoverable from  the liver of  poisoned  animals.
However, this did not consider the possibility that  storage  in
fat  might lead to a  fraction of the zinc  phosphide being more
slowly  hydrolysed  and  thus more  readily  absorbed  unchanged
(Meredith, 1981).

6.3.  Distribution

    Inhaled phosphine produces neurological and hepatic symptoms
suggesting  that it reaches the nervous system and liver (Childs
& Coates, 1971).  Ingested phosphides have been shown  to  reach
the  liver  and blood  in rats and  human beings (Curry  et al.,
1959;  Meredith, 1981; Chan et  al., 1983).  On the  other hand,
muscle tissue of animals poisoned with supralethal doses of zinc
phosphide  did  not contain  detectable  levels of  phosphine or
phosphide  and did not  produce toxic effects  when fed to  test
animals  (Kozhemyakin et al., 1971; Bubien et al., 1974).  Curry
et  al.  (1959)  reported  the  presence  of   acid-hydrolysable
phosphide  in the kidney as well as in the liver of a fatal case
of zinc phosphide poisoning.

6.4.  Metabolic Transformation

    Metal phosphides are hydrolysed to phosphine and the corres-
ponding metal cation (Van Wazer, 1982).  In rats, phosphine that
is  not excreted in the  expired air is oxidized  and appears in

the urine, chiefly as hypophosphite and phosphite (Curry et al.,
1959;  Meredith,  1981).   Meredith  (1981)  also  reported   an
unidentified  metabolite, detectable by paper chromatography and
distinct  from pyrophosphate and  metaphosphate.  The fact  that
(a) phosphine is incompletely oxidized; and (b)  the  proportion
of  an administered dose that is eliminated as expired phosphine
increases with the dose suggests that the oxidative  pathway  is

6.5.  Elimination and Excretion

    Meredith  (1981)  administered  zinc phosphide  suspended in
corn oil, by gavage, to Wistar rats (body  weight  approximately
200 g)  and measured the phosphine concentrations in a metabolic
chamber over the following 12 h.  After doses of 0.5, 1,  2,  3,
and 4 mg, the proportions of the administered doses as phosphine
in  air were 1.5%, 1.7%,  3.2%, 15.6%, and 23.5%,  respectively,
but  some or much of this could have been derived from faeces or
intestinal  gas rather than by absorption and exhalation.  Paper
chromatographic estimation of hypophosphite and phosphite in the
urine  of  rats  dosed  with  zinc  phosphide  showed  gradients
positively  correlated  with dose,  but  the proportion  of  the
administered dose excreted was not quantified.  Hypophosphite is
the principal urinary excretion product (Curry et al., 1959).

6.6.  Retention and Turnover

    Virtually all the phosphine in the air of metabolic chambers
housing  Wistar  rats, dosed  orally  with zinc  phosphide,  had
disappeared  after  12  h  (Meredith,  1981),  and  this  period
corresponds  with the duration of  symptoms following sub-lethal
doses of zinc phosphide.  The same author determined  the  acid-
hydrolysable  phosphide in the liver of single rats given a diet
containing 15 mg zinc phosphide/kg diet.  The liver of a rat fed
for  15 days contained nearly twice as much as that of a rat fed
for 7 days.  However, this limited study cannot be considered to
provide evidence for accumulation of metal phosphides.

6.7.  Reaction with Body Components

    Phosphine  reacts  with  some  haem-  and  copper-containing
proteins in  vitro.   Insect cytochrome c oxidase is reduced and
not  reoxidizable in air  (Rajak, 1971).  Mammalian  haemoglobin
does  not  react with  phosphine in the  absence of oxygen,  but
oxyhaemoglobin is converted through Fe3+-containing compounds to
a  verdichromogen-like material (Trimborn & Klimmer, 1962).  The
nature of the reaction between phosphine and these  proteins  is
uncertain,  but  oxyhaemoglobin is  denatured  and a  variety of
enzymes are inhibited by reaction with phosphine.


7.1.  Microorganisms

    Ruschel  & Da  Costa (1966)  treated seeds  of  French  bean
( Phaseolum   vulgaris L.)  with  aluminium  phosphide,  using  3
PhostoxinR  tablets/m3.   Treated  and untreated  control seeds,
inoculated  with a pure culture of the nitrogen-fixing bacterium
 Rhizobium   phaseoli,  were sown  in pots containing  sandy soil
(pH  4.5) and maintained  under greenhouse conditions.   Plants,
sampled  during the flowering  period, showed no  differences in
the numbers of nodules formed by the bacteria.

    Natarajan  & Bagyaraj (1984) reported  laboratory studies on
the effects of phosphine fumigation (100 mg/litre for 15 days at
an  unspecified  temperature)  on  the  microbial  load  (fungi,
bacteria,  and actinomycetes) of  blackgram and fieldbean  seeds
with  different moisture contents.  Total  microbial populations
were  estimated using the dilution plate technique.  Results are
given in Table 8.  It was concluded that phosphine was effective
on  actinomycetes.  The  effects of  phosphine on  each type  of
microorganism  depended  on  the  seed  type  and  the  moisture

Table 8.  Microbial loada per g seedsb
               Moisture    Fungi     Bacteria    Actinomycetes
               level (%)   (x100)    (x1000)     (x100)

Control        8           11.54     25.86       0.41
               12.5        51.96     267.20      0.30
               15          61.92     358.80      0.35

Phosphine-     8           .95       13.89       0.33
fumigated      12.5        1.16      34.23       0.06
               15          .88       69.71       0.00


Control        8.6         1.80      21.86       0.82
               12.5        3.79      35.77       0.38
               15          5.29      67.68       0.27

Phosphine-     8.6         1.32      6.17        0.22
fumigated      12.5        1.02      12.13       0.29
               15          .60       18.10       0.20
a  Microbial counts after 15 days fumigation at 100 mg 
b  From: Natarajan & Bagyaraj (1984).

    Lück  et  al.  (1984)  reported  the  effects  of  phosphine
fumigation  over 6 days with  variable concentrations equivalent
to  at least 85 mg x h/litre    on microorganisms in a  variety of
dairy  products.  There were no differences in bacterial, yeast,

or  mould  counts  between fumigated  products and non-fumigated
control products handled similarly but without fumigation.

    The  data  of  Rolulich  &  Menser  (1970)  (section 6.4.3),
indicate that phosphine damages and inhibits the respiration and
growth of microflora in moist stored wheat grains.

7.2.  Aquatic Organisms

    An  LC50 for phosphine for  the frog from a  30-min exposure
was  reported  to  be 0.56  mg/litre.   The  LC50 for  a  15-min
exposure  was  0.84  mg/litre (WHO/FAO,  1980).   The  aluminium
phosphide  formulation known as Detia PelletsR is reported to be
highly  toxic for  the bluegill  sunfish, with  a 96-h  LC50  of
0.178 mg/m3 (0.126 ppm) (Freyberg, 1979).

7.3.  Terrestrial Organisms

7.3.1.  Insects and mites

    Insects  are  a  major target  organism  of  phosphine as  a

    In  practice, fumigation is  carried out by  the distributed
insertion  of  formulated  aluminium phosphide  tablets into the
bulk  of the stored  product, so that  the phosphine evolved  by
hydrolysis with the moisture content of the  product  percolates
the bulk and is retained by the gas-tight design of the store or
the  use of an  impermeable covering.  Typically,  the phosphine
concentration rises to a maximum and then decays over  a  longer
period.  The phosphine dose is often described in terms  of  the
duration  of exposure and estimate  of concentrations or by  the
concentration x time  product.  This is calculated from the area
under the curve of concentration versus time Ct x dt or, approx-
imately, sigma (Ct x It), where Ct is the concentration at time t
and  It is the interval over which Ct is a sufficiently accurate
measure of the actual concentration.

    Because   the  susceptibility  to  phosphine   of  different
developmental  stages varies, it  is possible that  some indivi-
duals  will be at a  less susceptible stage at  the time of  the
peak   phosphine  concentration  and  may   survive  fumigation.
Moreover,  acclimatization may occur with rising concentrations.
The  dose  or  concentration that  is  lethal  for a  particular
species is therefore a complicated function of the concentration
and its time-course (Reichmuth, 1985).  Laboratory fumigation at
constant concentrations is not a sound basis for the calculation
of  doses for practical fumigation (Reichmuth, 1986).  Moreover,
the effects  of  any  concentration x time     product  will  be
influenced by the temperature and other aspects of  the  gaseous
environment,  such as the partial  pressure of oxygen which  may
fall  to a low level  in stores of metabolically  active pulses.
It  has been shown that  insects are tolerant to  phosphine in a
nitrogen-  or oxygen-deficient atmosphere (Kashi,  1981a,b).  By
influencing  the  rate  of  hydrolysis  of  the  phosphide,  the

relative  humidity  or  moisture content  affects the concentra-
tion x time   course  and  thus  independently   influences  the
toxicity for pests.

    In  spite  of the  complexity  of these  relationships,  the
concentration x time  product  is  frequently calculated  as  an
index  of  the  dose.  However, though the  concentration x time
product is related to mortality with some insecticides, there is
a  deviation  with phosphine.   Longer  exposures are  much more
effective  in  achieving  control  than  shorter  ones  with the
equivalent  concentration x time    product  (Hole et  al.,  1976;
Kashi,  1982; Winks, 1984,  1985).  Winks (1985)  suggested that
part  of  the  explanation of  the  relative  tolerance to  high
dosages  was  narcosis,  which reduced  absorption to sub-lethal
doses, but his experimental data neither confirmed  nor  refuted
his hypothesis.

    In  addition  to  these  uncertainties  in  determining  the
effectiveness  of fumigation, there is considerable variation in
susceptibility to phosphine among target organisms.  Grain mites
are  tolerant  (Bowley  &  Bell,  1981)  to   concentration x time
products 2 or 3 orders of magnitude greater than those effective
for many insect species.  Hole (1981) reported that 3 strains of
 Sitophilus granarius  and  Rhyzopertha  dominica  were relatively
tolerant compared with 3 other species of  Coleoptera.   The data
also  indicated considerable variation between  strains within a
species (Table 9).

    Adu & Muthu (1985) reported a 6-fold variation in  the  LC95
values   for  different  life  cycle   stages  of  Callosobruchus
 chinensis  L. with  the  susceptibility of  developmental stages
decreasing in the order: larva > adult > pupa >  egg.   However,
Bell et al. (1984) found that the eggs  of  Trogoderma  granarium
were   much more  susceptible than  the larva  and Winks  (1981)
found that the early pupae of  Tribolium castaneum  were substan-
tially more tolerant than the larvae.

    Larvae  of many  species can  enter a  state  of  suppressed
development known as diapause, so that the insects  can  survive
under  unfavourable conditions.  Cox  et al. (1984)  found  that
diapause  increased  tolerance to  phosphine  in the  larvae  of
 Ephestia     kühniella.     Diapausing   larvae    of  Trogoderma
 granarium  survived a 5-day exposure to  a  concentration x time
product  of 164 mg x h/litre, while laboratory stock larvae were
killed  by a 4-day  exposure to 120 mg x h/litre  (Bell et  al.,

Table 9. Concentration x time products of phosphine for 100% mortality and
maximum survived doses (MSD) for various numbers of strains of 7 
species of stored-product Coleopteraa
Species               Number   Stage   Temper-  RH   LDhi(mort %)  MSDb
                                       ature    (%)  (mg x h/      (mg x h/
                                       (°C)          litre)        litre)
 Sitophilus granarius  8        all     25       70   46 (100)      22
                      3        all     25       70   > 46 (100)    46

 Sitophilus zeamais    5        all     25       70   46 (100)      22
                      5        all     25       70   > 46 (100)    46

 Sitophilus oryzae     1        all     25       70   22 (100)      9
                      6        all     25       70   46 (100)      22
                      4        all     25       70   > 46 (100)    46

 Rhyzopertha dominica  5        all     25       70   9 (100)       < 9
                      4        all     25       70   22 (100)      9
                      1        all     25       70   46 (100)      22

 Oryzaephilus          7        all     25       70   > 4 (100)     > 4

 Tribolium castaneum   17       all     25       70   9 (100)       4
                      9        all     25       70   > 9 (100)     9

 Tribolium confusum    3        all     25       70   > 22 (100)    > 22
                      1        all     25       70   > 9 (100)     > 9
a  From: Hole (1981).
b  Maximum phosphine concentrations were about 0.28 mg/litre and  the  dose
   varied  with the duration of  the exposure period.  In  many cases, 100%
   lethality was not achieved at the highest dose used.
    A  further variant in the  response of insects to  phosphine
has  been the development  of resistant strains  (Champ &  Dyte,
1976). Attia (1984) found that phosphine resistance in  Tribolium
 castaneum and  Rhyzopertha   dominica was   sometimes  coincident
with,  but  not  otherwise related  to,  resistance  to 6  other
insecticides.   The  phosphine-resistant strains  had resistance
factors  of about  5 and  10, respectively.   Nakakita  &  Winks
(1981)  reported  that  ratios of  LC50  and  LC99.9 values  for
various stages of resistant and susceptible strains of  Tribolium
 castaneum  varied from 0.1 to about 6. In general, all stages of
a  resistant species have a higher tolerance than the equivalent
stage   of  the  susceptible  strain,   suggesting  a  metabolic
difference  persisting  through  metamorphosis.   Price   (1984)
reported  that adult insects of a resistant strain absorbed much
less  radioactive phosphine than their  susceptible counterparts
and  retained  normal  respiratory activity.   Living  resistant
insects  absorbed  less phosphine  than  dead insects,  and  the
author  concluded that the  active exclusion of  phosphine as  a
possible mechanism for resistance was supported by the data.

    Noack  & Reichmuth (1981) determined a toxic threshold value
for  phosphine  in  Drosophila  melanogaster  of about 1.4  mg/m3
(1 ppm)  in air, using  the criterion of  a statistically  just-
significant increase in mortality rate.  The value  obtained  is
comparable  to the threshold  for toxicity in  human beings  and
other mammals.

    Lethal  doses of phosphine  for a variety  of stored-product
pests are given in Tables 9, 10, and 11.  Childs (1972) reported
that all stages of the cigarette beetle were killed  by  fumiga-
tion  with  phosphine  at  concentrations  that  never  exceeded
500 ppm  (< 33.6 mg x h/litre)    for 48 h,  in field tests  using
transport   containers   at   an  unspecified   temperature  and

    Winks  (1970)  inoculated  tobacco bales  with  the  tobacco
beetle  Lasioderma serricorne  and  studied  the mortality  after
phosphine  fumigation  (20 tablets  PhostoxinR/28 m3).  Tempera-
tures  ranged from 11 to 25 °C and the relative humidity from 65
to  82%.  Peak concentrations  were about 300  mg/m3.  Mortality
was  assessed after a 7-day  recovery period, and the  number of
progeny  from eggs laid during  fumigation was assessed 8  weeks
after  fumigation.  Mortality was 100% and the number of progeny
was 0.2% compared with unfumigated controls.

7.3.2.  Birds

    Ikeda (1971) studied the lethality of zinc phosphide for the
quail and reported an oral LD50 of 35 mg/kg body  weight;  there
was  a reduction  in egg  laying at  3.5  mg/kg.   Shivanandappa
(1979) found that the acute oral LD50 and LD90 of zinc phosphide
in  poultry were  25 and  31 mg/kg  body  weight,  respectively.
Treatment of chickens with encapsulated doses of 14,  21,  31.5,
or 47.2 mg/kg body weight, daily for 4 weeks, resulted in deaths
at  all doses.  Mortality was 12% at the lowest dose and 100% at
the  highest  dose,  where death  occurred  within  6 -  18 h of
administration  of the first dose.   Hill et al. (1975)  studied
the  effects of zinc  phosphide administered in  the diet for  5
days to mallard ducks.  The dosing period was followed by 3 days
of   untreated  feed.   The  zinc   phosphide  concentration  of
1285 mg/kg diet was calculated to produce 50% mortality.  Though
the acute oral LD50 for most avian species is generally  in  the
range  of 20 - 100 mg zinc phosphide/kg body weight, it has been
reported that chickens fed 12 - 16 mg/kg body  weight  displayed
toxic  symptoms,  including  reduced  red-cell  counts,  reduced
haemoglobin  concentration,  and  leukocytosis, 1  - 1.5 h after
dosing  (Kozhemyakin  et al.,  1971).   Baxland &  Gordon (1945)
administered  oral doses of  zinc phosphide ranging  from 15  to
400 mg/kg body weight to single domestic hens of 2 species.  All
the  birds receiving more than  30 mg/kg body weight  died while
those receiving 20 mg/kg or less survived.

Table 10.  Concentration x time products for high and 50% lethality for 
different stages of common insect pests under specified conditions
Species         Stage         Temper-  Relative  Time  LDhi(mort %)     LD50       Reference
                              ature    humidity  (h)   (mg x h/litre)   (mg x         
                              (°C)     (%)                              h/litre)
 Trogoderma      DPa larva     20       60        120   75.0 (100)       -          Bell et al. (1984)
                egg           20       60        72    50.0 (100)       -          Bell et al. (1984)
                egg           20       60        48    22.6 (100)       -          Bell et al. (1984)

 Callosobruchus  egg           25-27    70-75     24    3.127 (95)       0.0708     Adu & Muthu (1985)
  chinensis L.   larva         25-27    70-75     24    0.556 (95)       0.1622     Adu & Muthu (1985)
                pupa          25-27    70-75     24    2.542 (95)       0.684      Adu & Muthu (1985)
                adult         25-27    70-75     24    0.823 (95)       0.240      Adu & Muthu (1985)

 Rhyzopertha     adult         27       65        20    0.5 (99.9)       0.126      Attia & Greening (1981)

 Tribolium       adult         27       65        20    0.32 (99.9)      0.166      Attia & Greening (1981)

 Tribolium       adult         27       65        20    0.58 (99.9)      0.26       Attia & Greening (1981)

 Ephestia        DP larva      10       70        < 20  79.6b  (100)    29-42      Cox et al. (1984)

 Tribolium   Sc  15-day larva  25       ns        6     0.52 (99.9)      0.17       Nakakita & Winks (1981)
  castaneum  Rd  15-day larva  25       ns        6     2.57 (99.9)      0.34       Nakakita & Winks (1981)
            S   20-day larva  25       ns        6     0.29 (99.9)      0.13       Nakakita & Winks (1981)
            R   20-day larva  25       ns        6     0.74 (99.9)      0.18       Nakakita & Winks (1981)
            S   pre-pupa      25       ns        6     0.74 (99.9)      0.17       Nakakita & Winks (1981)
            R   pre-pupa      25       ns        6     4.22 (99.9)      0.33       Nakakita & Winks (1981)
            S   early pupa    25       ns        6     11.94 (99.9)     4.2        Nakakita & Winks (1981)
            R   early pupa    25       ns        6          -           -          Nakakita & Winks (1981)
            S   mid-pupa      25       ns        6          -           0.69       Nakakita & Winks (1981)
            R   mid-pupa      25       ns        6          -           21.0       Nakakita & Winks (1981)
            S   late pupa     25       ns        6     1.12 (99.9)      0.09       Nakakita & Winks (1981)
            R   late pupa     25       ns        6     0.80 (99.9)      0.438      Nakakita & Winks (1981)

Table 10. (contd.)
Species         Stage         Temper-  Relative  Time  LDhi(mort %)     LD50       Reference
                              ature    humidity  (h)   (mg x h/litre)   (mg x         
                              (°C)     (%)                              h/litre)

 Trichoplusia    egg           24       ns        2     0.56 (100)       -          Leesch (1984)
 ni Hübner      larva         24       ns        0.67  0.28 (100)       -          Leesch (1984)
                pupa          24       ns        2     0.56 (100)       -          Leesch (1984)
a  Diapausing.
b  Approximate values.
c  Sensitive strain.
d  Resistant strain.
ns = not stated.
Table 11.  Concentration x time   products for 100% mortality and maximum
survived doses (MSD) for three species of grain-infesting mitea
Species       Stage  Temper- Relative  Time   LDhi(mort %)  MSD
                     ature   humidity  (days) (mg x h/      (mg x h/
                     (°C)    (%)              litre)        litre)
 Tyrophagus    adult  10      60-70     21     450 (100)     190

 Acurus siro   adult  10      60-70     14     310 (100)     150

 Glycyphagus   adult  10      60-70     14     310 (100)     150
a  From: Bowley & Bell (1981).

    Klimmer (1969) exposed 3 turkeys to phosphine at  a  concen-
tration  of 211  mg/m3 and  6 hens  at 224  mg/m3  in  an  acute
inhalation  study.  The turkeys exhibited  apathy, restlessness,
dyspnoea, and tonic-clonic convulsions, and died after  68,  74,
and  80 min, respectively.  When examined, organs were congested
with  oxygenated blood.  Hens exhibited tonic-clonic convulsions
and died after an average of 59 min (range, 50 - 64 min).  Their
organs were also congested with oxygenated blood.

7.3.3.  Mammals  Non-target species

    The  acute oral LD50  of zinc phosphide  in the kit  fox was
calculated  to be 93 mg/kg body weight (Schitoskey, 1975).  Dogs
(which  may also be a target species) were reported to be killed
by  a dose of 100  mg zinc phosphide/kg body  weight when fasted
for 24 h, but not when fed (Aminzhanov, 1972).

    The  acute  toxicity of  zinc  phosphide for  large domestic
animals was reported by Fitzpatrick et al. (1955).  Single doses
were  administered by capsule, stomach  tube, or mixed with  the
feed.  Deaths occurred as shown in Table 12.

    McGirr   (1953)  quoted  unpublished  work   by  Fitzpatrick
indicating  that  the dose  of  zinc phosphide  producing  toxic
effects  in cats  and dogs  lies between  20 and  40 mg/kg  body
Table 12.  Mortality of domestic mammals given single oral doses 
of zinc phosphide by capsule, stomach tube, or mixed with the feed
Dose (mg/kg            Mortality           
body weight) Cow   Goat  Sheep   Pig   Total   
20           0/1   1/2   -       0/3   1/6
30           -     -     0/1     0/3   0/4
40           1/1   0/1   1/2     1/2   3/6
50           -     -     -       0/1   0/1
60           -     1/1   1/1     1/2   3/4  Rodents

    The results of acceptance studies of 4  commercially  avail-
able wax baits containing zinc phosphide on Norwegian  rats  and
house  mice were reported by  Marshall (1981).  Each animal  was
offered the bait and a palatable non-toxic  alternative.   While
one  bait achieved an acceptance of 48.8% with 100% mortality in
rats and 38.5% acceptance with 100% mortality in mice, the other
baits achieved less than 6.5% acceptance and mortality rates did
not  exceed  50%.  Gill  & Redfern (1983)   reported 1 day  "no-
choice"  feeding tests, using standard procedures, which studied
the  effects  of zinc  phosphide  administered to  Shaw's gerbil
 (Meriones   shawi)  at 10,  20, 30, 40,  or 50 g/kg  diet (EPPO,
1975).  There was very little reduction in average food consump-
tion  at 40 and  50 g/kg diet  and none at  10, 20, and  30 g/kg
diet.  Zinc phosphide at 10 g/kg resulted in 20%  mortality  but
dietary  concentrations of 20  - 50 g/kg  resulted in 70  - 100%
mortality.   In palatability tests, consumption of both poisoned
(zinc  phosphide at 20 or 50 g/kg) and plain baits was very low,
presumably  because the poison acted rapidly and interfered with
feeding.   Survival of 8/10  animals given zinc  phosphide  bait
(20 g/kg) and 2/10 given 50 g/kg may indicate that these animals
could  detect the poison  and avoided consuming  a lethal  dose.
Similar results were reported at doses of 40 and 50 g/kg for the
golden  hamster ( Mesocricetus auratus  Waterhouse)  (Bradfield &
Gill, 1984).  Sridhara (1983), in a study on the  Indian  gerbil
( Tatera  indica  cuvieri  Waterhouse),  reported that  phosphide
incorporated in ragi (Eleusine  coracana),  a preferred food, at
0.5 g/kg induced aversion to this and enhanced  the  consumption
of maize  (Zea  mais)   offered as an  alternative.   Administra-
tion  of sub-lethally baited food  on the fifth day  only of the
study  also induced  aversion to  the same  food baited  with  a
different  poison,  and  to  a  new  food  substituted  for  the
preferred  food.  However,  it was  not reported  how  long  the
animals that had been given the poisoned preferred food on day 5
exhibited subsequent aversion to the same unpoisoned food.  This
makes it difficult to evaluate the study.

    Field  census studies have  been carried out  to assess  the
effects  of  rodenticide  use.  Traps  are  set  and the  rodent
population  assessed by the number  of each species trapped  per
100  traps per 24  h.  The rodenticide  is administered and  the
traps again set and the numbers captured are compared with those
of  the earlier study  to yield a  percentage figure for  rodent
control.   Advani (1983)  reported 90 - 95% overall control both
in  winter  (wheat, vegetable,  and  oil-seed crops)  and summer
(millet  crop)  with  zinc phosphide  administered,  after  pre-
baiting,  at  20  g/kg for  one  day  at the  entrance to active
burrows  and  the  administration  of  aluminium  phosphide   at
1.5 g/burrow followed by sealing with moist earth. Chopra (1984)
undertook  a similar study  on aluminium phosphide  in rice  and
wheat  fields with 3 species  in which the following  percentage
control rates were found (Table 13).

Table 13.  Control rates (%) for 3 species in 2 crops 
achieved by aluminium phosphidea
Species                   Rice fields    Wheat fields
 Rattus meltada            85.88          75

 Bandicota bengalensis     63.33          50

 Mus species               100            91.8
a  From: Chopra (1983).

    Zinc  phosphide dose-response data were  reported for Shaw's
gerbil   (Meriones  shawi)  (Gill & Redfern, 1983) and the golden
hamster  (Mesocricetus   auratus Waterhouse) (Bradfield  & Gill,
1984).   Zinc  phosphide  was administered  in no-choice feeding
tests at 10, 20, 30, 40, or 50 g/kg diet according to a standard
protocol (EPPO, 1975).  Their mortality data showed an irregular
relationship  for the gerbil (100% mortality at 20 g/kg diet but
90%  at  50  g/kg diet),  probably  as  a result  of small study
numbers.   For the hamster,  there was a  dose-related mortality
with 100% at 50 g/kg diet.

    An LD50 of zinc phosphide for the black-tail prairie dog has
been reported to be 18 mg/kg body weight (Tietjen, 1976).

7.4.  Plants

    The  threshold  concentration  of  phosphine  in  air  for a
harmful effect on growing lettuce (chosen as  a  representative,
highly  sensitive species) was  determined by Noack  & Reichmuth
(1982b)  to  be between  3 and 8  mg/m3.  There were  no adverse
effects  on the germination of watercress seeds in soil that had
been treated for 3 days with air containing either 20 or 1400 mg
phosphine/m3;   in   fact,  the   high  phosphine  concentration
stimulated the growth of watercress plants.

7.4.1.  Harvested plants

    Leesch  (1984) studied the damage to harvested fresh iceberg
lettuce  14  days  after  fumigation  with  various   fumigants,
including  phosphine, at 4.4 °C  without air circulation  and at
24 °C  both  with and  without  air circulation.   Three lettuce
heads  were exposed  to phosphine  at each  of 3  concentrations
(0.28, 0.56, and 0.83 mg/litre) for each of 3 periods  (16,  24,
and 48 h).  Lettuce heads were then stored at 4.4 °C in a sealed
bag made of 1 mm polythene.  An ordinal 5-point scale  was  used
to rate damage to the lettuce heads and an index  calculated  by
dividing the sum of the scores for each of the 3 lettuces by the
sum  of the scores of 3 unfumigated control lettuces.  There was
no   clear  dose-effect  relationship  between   the  concentra-
tion x time    product and the damage index.  Damage was slight to
moderate after fumigation at 24 °C with circulation, but without
circulation  (both at 4.4 and 24 °C)  damage was generally rated
as  "none",  though one  excursion  into the  "slight"  category

occurred.   This level  of damage  was small  compared with  the
damage  resulting  from  5 other  fumigants.   Only acetaldehyde
produced  similar slight damage.   However, the comparisons  are
not  clear  because of  the  arithmetic manipulation  of ordinal

7.4.2.  Viable seeds and grain

    Natarajan & Bagyaraj (1984) studied the effects of phosphine
on the viability of blackgram and fieldbean seeds and found that
it did not have any effects on seed germination.

    Effects on viable seeds of leguminous plants were studied by
Singh et al. (1983) who reported the effects on stored pulses of
phosphine fumigation for 5 days.  Phosphine residues  at  normal
fumigation levels (2 tablets of PhosfumeR per  tonne)  decreased
to  below the detection  limit of 1.5 µg/kg   after 3 or  4 days
aeration.  Standard germination tests carried out immediately at
the  end of fumigation  revealed no impairment  of  germination,
even  with pulses  fumigated at  4 times  the recommended  dose.
These  results  suggest that  stored  pulses are  not  adversely
affected  by  exposure  to  phosphine  or  formulated  aluminium

    Ahmad (1976) studied seeds of 11 edible legumes and measured
the moisture content and the germination rate of  control  seeds
and  of seeds fumigated for 7 days at 21 ± 5 °C using PhostoxinR
at  a rate  equivalent to  approximately 3  tablets/m3, about  4
times the recommended dosage.  After fumigation, test seeds were
aerated  for 3 days.  No  differences in germination rates  were

    Zutshi (1966) cited earlier work on the effects of phosphine
fumigation on seed germination and reported the results of germ-
ination tests on paddy, wheat, maize, bhindi,  brinjal,  tomato,
and onion seeds.  Three lots of each type of seed were fumigated
with PhostoxinR at doses equivalent to 12 or 18 mg/kg for 7 days
followed by 24 h aeration.  After 30 days air-tight storage, one
lot was given a second fumigation for 7 days, and a  second  lot
was  stored for 90 days in air-tight jars.  In no case was there
any reduction in germination rate.

    Kamel et al. (1973, 1974) reported that one variety of wheat
(Giza  155) was susceptible to phosphine fumigation (PhostoxinR,
2.5  tablets/m3)  over 72  h with a  germination rate that  fell
rapidly with the number of fumigations.

    The  effects of phosphine  on the biochemical  reactions  in
wheat  grain  of different  moisture  contents, which  had  been
fumigated with 10 mg phosphine/litre at 20 °C for 5  days,  were
studied  (Rohrlich  &  Menser, 1970).   Germination of fumigated
grain  with a 30% moisture content was totally inhibited, it was
reduced  with a 25% moisture  content, and was unaltered  with a
20%  content.  Phosphine reduced the respiration of wheat partly
by  damaging  the  microflora present.   Activity  of  glutamate

decarboxylase  was  reduced  by  phosphine,  when  the  moisture
content was 18% or more.  The activity of glutamate-oxaloacetate
transaminase was not significantly changed compared with that in
untreated  grain.   The  enzymes hexokinase,  aldolase,  glycer-
aldehyde-3-phosphate  dehydrogenase,  and  pyruvate  kinase  had
nearly  constant activity throughout  all the studies.   Alcohol
dehydrogenase  activity was reduced to  zero within 7 days  as a
result  of phosphine exposure of the grain at a moisture content
of  more than 24%.  Catalase activity in wheat (moisture content
about 15%) was reduced by about 20% after a 2-week  exposure  to
phosphine  fumigation.   Phosphine treatment  markedly inhibited
respiration  and  growth  of  microorganisms  in  wheat  with  a
moisture  content up to 20%,  thereby protecting the grain  from
microbial damage.  In grain with a moisture content  of  between
18  and 27%,  the amount  of adenosine  triphosphate  (ATP)  was
reduced by phosphine fumigation, but adenosine diphosphate (ADP)
was  not, indicating that  the respiratory activity  in  treated
grain was markedly reduced.


    This section deals with studies of effects  on  experimental
animals.   Studies related  to the  field use  of phosphine  and
phosphides  as  a  fumigant  or  rodenticide  are  discussed  in
section 6.

8.1.  Single Exposures

8.1.1.  Inhalation studies on phosphine

        The  effects of phosphine on a kitten, a puppy, rabbits
and  a guinea-pig exposed to concentrations that proved fatal in
a  matter  of  hours were  described  in  1890  (Schulz,  1890).
Meissner  (1924) reported observations on rabbits in which expo-
sure to 70 mg phosphine/m3 (50 ppm) for 10 min did  not  produce
any symptoms, but exposure to 140 mg/m3 (100 ppm) was  fatal  in
2.5  - 3 h, and  700 mg/m3 (500 ppm)  was fatal in 25  - 30 min.
Rats survived exposure to 80 and 800 mg/m3 for 4 and 1  h,  res-
pectively;  cats survived exposure to 240 mg/m3 for 2 h; guinea-
pigs  did not survive 2 h exposure to 400 mg/m3 (Rebmann, 1933).

    Klimmer (1969) investigated the effects of single inhalation
exposures  on cats, rabbits, rats, and guinea-pigs.  The concen-
trations  varied from 35 to  564 mg/m3.  The symptoms  described
were  similar to those described in section 8.2.1 for short-term
studies.  Death was attributed to respiratory paralysis followed
by cardiac arrest.

    The  Pesticide  Registration  Standards for  both  aluminium
phosphide  and magnesium phosphide (US EPA, 1981, 1982) tabulate
the  survival times for all  these studies and there  is a clear
relationship,  independent of species, between concentration and
survival  time.  This is illustrated in Fig 1.  The relationship
approximates to C x t1.43 = 200 000, where C is  the  concentra-
tion of phosphine measured in mg/m3 and t is the time  to  death
in minutes.

    Waritz  & Brown (1975) determined a 4-h LC50 (95% confidence
limits)  for phosphine in male Charles River-CD rats of 15 (11 -
21)  mg/m3 (11 (8.1 -  15) ppm).  Using CFT-Wistar  female rats,
Muthu  et  al.  (1980)  calculated  LC50  and  LC95  values  for
phosphine, produced by hydrolysis of aluminium phosphide, on the
basis of concentration x time   products. The LC50 (95% confidence
limits)  was 220 (180 -  270) mg x h/m3,   corresponding to  a 4-h
LC50 of 55 mg/m3.  However, the exposure durations  were  longer
than  4 h,  and there  is evidence  that the  concentration x time
product is not a good index of lethality in insects.   The  LC95
was  420 (260 - 670)  mg x h/m3.    These values were  obtained at
27 + 2 °C, whereas an LC50 value of 360 mg x h/m3   and an LC95 of
490 mg x h/m3 were obtained at about 26 °C.


    Neubert  &  Hoffmeister  (1960) investigated  the effects of
short-term exposures ranging from 460 to 2150 mg phosphine/m3 on
cellular  respiration  in  rats.  The  oxidation  of alpha-keto-
glutarate  in  liver  cells  was  inhibited,  but  not oxidative
phosphorylation.  Alpha-ketoglutarate oxidation was also reduced
in heart muscle, and phosphorylation was disrupted.  Survival of
groups of 8 rats at various concentrations  of  diphosphine-free
phosphine was studied with the following results (Table 14).

Table 14.  Survival times of 8 rats in different concentrations of
phosphine.  Concentration x time products calculated from 
the mid-point of the range of survival timesa
Concentration    Survival    Concentration x time
(mg/m3)          (min)       product (mg x min/m3)
4640             16 - 20     83 520

1000             50 - 70     60 000

320              150 - 200   56 000

100              400 - 600   50 000
a  From: Neubert & Hoffmeister (1960).
    If the use of the mid-point of the range of  survival  times
is  reasonable,  these  results indicate  that  the relationship
between   concentration   and   survival  time   is  not  simply
reciprocal,  and that the index of t is greater than 1, but less
than  the  value  of 1.43 derived from the data quoted by US EPA
(1981, 1982).

    Klimmer  (1969) determined lethal  concentration x time   pro-
ducts  for rats and  calculated, for example,  19 000  mg x min/m3
for a concentration of 287 mg/m3, but these results do not agree
with those calculated from the data of US EPA (1981,  1982)  nor
with  those of Neubert &  Hoffmeister (1960).  The value  of the
concentration x time    product, as a measure of phosphine dose in
mammals, is therefore open to question, as it is in insects.

8.1.2.  Inhalation studies on zinc phosphide

    The US National Pest Control Association submitted  a  value
of  19.6 mg/litre for an  inhalation LC50 of 10%  zinc phosphide
powder  in rats.  It  was not stated  whether the value  was for
pure  zinc  phosphide  or the  10%  dilution  and there  was  no
indication of exposure time (US EPA, 1983).

8.1.3.  Oral studies on metal phosphides

    In  a study on 35  rats of both sexes  administered doses of
20, 40, 50, or 80 mg/kg, Dieke & Richter (1946) reported an LD50
for  zinc phosphide  of 40.5 ± 2.9  mg/kg body  weight for  wild
Norway rats.  Schitoskey (1975) reported an LD50 for the kit fox
of  93  mg zinc  phosphide/kg  body weight.   Aminzhanov  (1972)
reported  that 100 mg/kg body weight of zinc phosphide was fatal
for  starved  dogs but  not for dogs  that were fed.   Ikimanova
(1977)  reported increased blood- and  urinary-porphyrin concen-
trations in rats dosed with zinc phosphide.   Other  authorities
refer to 27 mg/kg body weight for an acute oral LD50  value  for
94% pure zinc phosphide in rats (US EPA, 1983).

8.1.4.  Dermal and other studies on metal phosphides

    An  acute dermal LD50 of 2 000 - 5 000 mg/kg body weight for
zinc  phosphide (94% Zn3P2) in  rabbits was submitted by  the US
National Pest Control Association (US EPA, 1983).

8.2.  Short-term Exposures

8.2.1.  Inhalation exposure to phosphine

    Jokote (1904) determined cumulative survival times in inter-
mittent phosphine exposure as shown in Table 15.

Table 15.  Survival time for rabbits, cats, and guinea-pigs at 3
concentrations of phosphinea
                      Concentration of phosphine (mg/m3) 
                       14       35        140
Survival time (h)      16 - 30  8.5 - 12  2.5 - 3.5
(rabbits, cats, and 
a  From: Jokote (1904).

    Miller  (1940) exposed rabbits and  guinea-pigs for 4 h  per
day  to various concentrations  of phosphine.  At  28 mg/m3  (20
ppm),  both rabbits  and guinea-pigs  died during  or after  the
second  exposure.  At 14 mg/m3 (10 ppm), rabbits survived 7 - 14
successive  exposures, but at  12 mg/m3 (8.3  ppm), only 4  or 5
exposures.  In another study in the series, 2 rabbits  that  had
had five 4-h exposures to phosphine at 7 mg/m3 were accidentally
exposed  to 20 mg/m3  (14 ppm) on  the sixth day.   Both rabbits
died   during  this  exposure.    The  authors  concluded   that
pretreatment with sub-lethal concentrations of phosphine reduced
resistance to near-lethal concentrations.  At low concentrations
(up to 14 mg/m3), animals displayed no signs until about  1/2  h
before  death when they exhibited  diminished reactivity, became
stuporose   with   shallow   respiration,  and   died  in  coma.
Occasionally,  animals died following exposure, with symptoms of
pulmonary  oedema.  At 28 mg/m3  or more, all animals  exhibited
signs  of respiratory irritation  and died of  pulmonary oedema.
Pathological examination of the lungs revealed bronchiolitis and
atelectasis  of the lungs.  There was no evidence of haemolysis,
but   all  organs  were  hyperaemic.   The  liver  showed  fatty
infiltration  and there was  cloudy swelling of  kidney  tubular
cells.   After prolonged exposure, lungs  frequently contained a
brown  pigment  that  did  not  stain  with  Prussian  Blue  and
therefore was not iron-containing.

    Neubert & Hoffmeister (1960) exposed female Wistar  and  E-B
(inbred  strain) rats in  a 121-litre chamber  repeatedly for  6
days  to 681 mg/m3 phosphine  for 10 - 20  min per day.  On  the
seventh  day, they were exposed  until they died (22  - 35 min).
The  concentration x time    product  for lethality  after  6 days
pretreatment  (about 20 mg x min/litre)    was about one  third of
that  for a  first exposure  (48 -  87 mg x min/litre)    and  the
authors  concluded that the effects of exposure were cumulative,
rather than that the phosphine accumulated in the body.

    Klimmer  (1969)  exposed  cats,  guinea-pigs  and  rats   to
phosphine  concentrations of 1.4 and  3.5 mg/m3 (1 and  2.5 ppm)
for 4 - 6 h per day, 6 days a week, for a  total  of  more  than
800 h over a 24-week period without any clinical, laboratory, or
pathological  evidence of effects.   The liver function  in  the
cats, measured by bromosulphthalein (BSP) excretion, was normal.
In cats (3), guinea-pigs (3), and rats (10) exposed to phosphine
at  7  mg/m3 (5  ppm)  for 6  -  8 h  per  day, the  cats became
apathetic,  showing  anorexia  after  exposure,  but  exhibiting

thirst.    Later,   they   developed   unsteadiness,   vomiting,
agitation, dyspnoea, and apnoea, before cardiac arrest  after  a
total  of 35.5 -  45.5 h of  exposure.  The haemoglobin  concen-
tration  and erythrocyte count were reduced by 10 - 20% compared
with  initial  values, there  was  proteinuria and  delayed  BSP
excretion.   Post-mortem examination revealed congestion  of all
organs,  with oedema and focal emphysema and red pigmentation of
the  lungs.  The guinea-pigs  exhibited signs that  were similar
to, but more marked than, those in the cats, and 2  animals  had
asphyxial  convulsions.  Blood tests  showed no deviations  from
normal values, but the blood contained a brown  coloration  that
was not due to methaemoglobin, since spectroscopy  revealed  the
absorption  bands of oxyhaemoglobin only.   The guinea-pigs died
on  the  sixth day  after 24 h  - 32 h  cumulative exposure, and
post-mortem   examination  revealed  pulmonary  oedema  and  red
discolouration  and congestion of  other organs.  The  rats died
after 27 - 36 h cumulative exposure.  All  exhibited  congestion
of  organs,  3 had  pulmonary oedema and  7 had proteinuria.   A
second  series  of  exposures under  slightly  changed  exposure
conditions  at a different  time of year  produced qualitatively
similar  results. In both  series, neurohistological studies  in
rats  showed widening of the perivascular spaces, vacuolation of
the nuclei of ganglion cells, a reduction in the Purkinje cells,
and a glial reaction.  Similar, but less marked, changes without
glial reaction were seen in the cats and guinea-pigs.  There was
no control group in these studies, and certain  observations  in
exposed  animals were  dismissed on  the grounds  that they  had
previously been seen in unexposed animals.

    Waritz  &  Brown (1975)  exposed  Charles River-CD  rats  to
phosphine  for  4  h per day, for 12 days, at a concentration of
5.5  mg/m3  (0.163 µmol/litre).   The  rate  of weight  gain was
reduced during the exposure period.  Although the authors stated
that the rate returned to normal during a  14-day  post-exposure
observation period, their data indicate a uniformly reduced rate
of  weight  gain throughout  the  exposure and  recovery phases.
Post-mortem examination of rats, sacrificed both at the  end  of
the  exposure period  and at  the end  of the  recovery  period,
revealed no gross or microscopic abnormalities.

    The  effects  of  a 1.5-month  exposure  of  white  rats  to
phosphine  at concentrations of 0.05, 0.2, 1.5, and 8 mg/m3 were
reported by Pazynich et al. (1984).  There were changes in blood
cholinesterase,   peroxidase,  and  catalase  activity   and  in
phagocyte  behaviour.  The magnitude  of the changes  was large,
but  not generally dose-related.  On the basis of their results,
the authors recommended mean exposure limits for urban  air  for
exposure  durations of 24 h,  one month, and one  year of 0.004,
0.0015, and 0.001 mg/m3, respectively, with a ceiling  value  of
0.01  mg/m3, and  this recommendation  has been  adopted in  the

    In a study of the effects of phosphine on rats by inhalation
at  0.1 mg/m3 and 0.05  mg/m3, Atchabarov et al.  (1984) found a
reduction  in  total  plasma protein  without  a  change in  the
relative  proportions  of the  various  fractions, a  modest but

significant reduction in the glycoprotein A fraction  with  some
changes  in  the  relative  proportions  of  the  sub-fractions,
increased   plasma  bile  acids,   and  a  marked   increase  in
seromucoids.   Liver  glycogen,  lipids, and  cytochrome oxidase
levels were reduced.  Biochemical changes were  similar to those
in  a control group  treated with hydrogen  fluoride at a  known
toxic level.

8.2.2.  Oral exposure to metal phosphides

    Bai et al. (1980) reported a 13 week feeding study in female
weanling albino rats.  Zinc phosphide was mixed with the diet at
0 (control), 50 mg/kg (50 ppm), 100 mg/kg (100 ppm),  200  mg/kg
(200  ppm), and 500 mg/kg (500 ppm) w/w.  Deaths occurred at the
2 higher dosage regimes in 1/12 and 10/12 animals, respectively.
Food  intake and weight increase were reduced and dose-dependent
depilation  occurred at all  dosages.  The relative  weights  of
liver,  heart, brain,  and thyroid  were increased  at  200  and
500 mg/m3  and  the serum  zinc  and liver  alkaline phosphatase
levels  were increased at the  highest dose.  There was  a dose-
dependent  reduction  in  haemoglobin  concentration,  red  cell
count, and haematocrit.

    The  WHO/FAO Data Sheet on  Pesticides (No. 24) which  deals
with  zinc phosphide  (WHO/FAO, 1976)  cites a  study  in  which
300 mg  zinc  phosphide/kg  administered to  rats  produced  6/6
deaths  in the  second week  while 200  mg/kg  produced  reduced
weight  gain and 2/6 deaths.  Histopathological studies revealed
liver damage in the peripheral and central lobular areas and the
lungs were congested with haemorrhage or exudate in the alveolar

8.2.3.  Dermal and other exposures

    No reports are available on short-term studies involving the
dermal or other routes.

8.3.  Skin and Eye Irritation; Sensitization

    Zinc  phosphide powder moistened  with saline produced  mild
skin irritation in rabbits (Draize method) (Rao, 1986).a

8.4.  Long-Term Exposure

    No  long-term  studies  on  phosphine  or  metal  phosphides
exposure have been reported.

8.5.  Reproductive, Mutagenicity, and Carcinogenicity

    There  have been no long-term reproductive, mutagenicity, or
carcinogenicity studies on phosphine or metal phosphides.

a   Personal communication to the IPCS Task Group  on  Phosphine
    and Metal Phosphides.

8.6.  Factors Modifying Toxicity; Toxicity of Metabolites

    Aminzhanov  (1972)  reported  that 100  mg zinc phosphide/kg
body  weight was lethal for dogs starved for 24 h beforehand but
not for dogs that were fed.

    Phosphine  is not a  powerful reducing agent  and its  toxic
effects are unlikely to be associated with  chemical  reduction.
The recent discovery that phosphites and phosphorous acid have a
fungicidal  activity (Bompeix & Saindreman,  1984) suggests that
metabolites  of phosphine have biological  effects and therefore
might  contribute to its  toxicity.  However, this  contribution
can  only be small, since  phosphine is only slowly  oxidized to
hypophosphites  and phosphites and a maximum of about 40% of the
phosphide  dose  is recovered  as  these metabolites,  even with
small  doses.  Moreover, the toxicity of phosphites is much less
than  that of phosphides  (Schulz, 1887).  The  contribution  of
toxicity  of contaminants of  phosphine such as  diphosphides is

8.7.  Mechanisms of Toxicity - Mode of Action

    Studies  on  isolated  rat liver  showed  that mitochondrial
oxygen uptake was inhibited by phosphine (Nakakita et al., 1971)
and that this effect was due to the reaction of  phosphine  with
cytochrome  c and cytochrome c oxidase (Kashi & Chefurka, 1976).
Although  this  inhibitory in  vitro effect was  also  shown  in
insects,  it  was  found  that  insects  severely  poisoned with
phosphine  did  not suffer  any  inhibition of  their cytochrome
system (Price & Dance, 1983).  In the same report, phosphine was
found to inhibit insect catalase though this appeared to  be  an
indirect  effect  and  might have  been  a  result of  phosphine
toxicity rather than a cause.

    There  have not been any systematic studies on the mechanism
of   phosphine   toxicity.   Various   effects  on  intermediary
metabolism  have  been  described.   Ikimanova  (1977)  reported
increased  blood-  and  urinary-porphyrin concentrations,  which
were related to the dose of zinc phosphide and the  duration  of
treatment.   In a study  on rabbits, Minchev  & Dimitrov  (1970)
reported   changes  in  serum  glutamic-pyruvic   and  glutamic-
oxaloacetic  transaminases,  leucine  aminopeptidase,  aldolase,
alkaline  phosphatase and  albumin in  the first  24 h  of  zinc
phosphide  poisoning.  Dysfunction of hepatic fat metabolism was
also  observed.   Loss  of  cell  viability  and  cell  membrane
integrity   accounted  for  the  raised   hepatic  enzymes,  the
bronchiolitic effect, the cloudy swelling of renal tubular cells
and  the  occasionally  reported  haemorrhagic  lesions  in  the
myocardium.   There is no adequate explanation for the fact that
phosphine  does  not  cause  the  haemolysis  characteristic  of


9.1.  Organoleptic Effects

    The  odour of phosphine  depends on the  impurities it  con-
tains;  phosphine of high purity has no odour, even at 280 mg/m3
(Dumas & Bond, 1974; Fluck, 1976).  Phosphine  prepared  conven-
tionally, without purification, has a fishy or garlic-like odour
attributed  to impurities.  These may be adsorbed by stored pro-
ducts  during  fumigation with  resultant  loss of  odour,  even
though  phosphine remains at toxic concentrations (Bond & Dumas,
1967).  Amoore & Hautala (1983) reviewed the literature on odour
thresholds  and stated  that the  geometric mean  of all  the  6
reported  values for phosphine was 0.71 mg/m3 (0.51 ppm).  Fluck
(1976)  reported that thresholds for  phosphine at which 50%  or
more  of 10 persons  could positively identify  the odour  asso-
ciated  with phosphine differed according  to the source of  the
phosphine (Table 16).

Table 16.  Odour thresholds for phosphinea
Source                                  Odour thresholds for
                                        PH3 (mg/m3 converted
                                        from ppm)
Technical aluminium phosphide + H2SO4   0.14 - 0.28

Phosphorium iodide + aqueous hydroxide  2.8

Phostoxin + H2SO4                       0.014 - 0.028

(5 Å molecular seived)                  1.4 - 2.8

Phostoxin + H2SO4
a  From: Fluck (1976)

    Amoore & Hautala (1983) classified phosphine in safety class
D  in their classification because 20 - 50% of attentive persons
can  detect the  threshold limit  value (TLV)  (0.42  mg/m3)  by
smell.  However, the smell of phosphine cannot be relied  on  to
warn of toxic concentrations.

9.2.  General Population Exposure

9.2.1.  Phosphine

    There  is negligible exposure  of the general  population to
phosphine.  Gessner (1937) described an incident in which the 12
inhabitants  of an apartment house developed nausea and one died
when phosphine was emitted from an adjacent warehouse containing
bags of aluminium phosphide, which became damp.  Some passengers
on  ships and barges carrying  cargoes of ferrosilicon or  grain
under  fumigation have also been poisoned by phosphine (Harger &
Spolyar,  1958;  Netherlands,  1984).  Effects  were  similar to
acute occupational poisoning.

    Hallerman & Ribilla (1959) reported the deaths of  2  adults
and  a child living in a dwelling with a party wall to a granary
being  fumigated.   Symptoms  were  non-specific  and  insidious
initially  and illustrate the  risks of sustained  exposures  to
relatively  low concentrations (a  few mg phosphine/m3);  it was
estimated   that  the  concentration  in   the  bedroom  reached
1.2 mg/m3.   At  autopsy, there  was  congestion of  all organs.
Pulmonary oedema and focal emphysema were found in the lungs and
there was vacuolation in the liver.

9.2.2.  Metal phosphides

    Zinc  phosphide  baits  and formulated  aluminium  phosphide
pellets are widely used.  Occasional accidental, or more usually
suicidal,  exposure  to  metal phosphides  may  be  encountered.
Ingestion, the only easily toxic route, has almost  always  been
suicidal and the effects acute (Stephenson, 1967).

    Stephenson  (1967) reviewed 20 cases of acute zinc phosphide
poisoning  by ingestion (including  one treated by  himself)  in
which the approximate dose was recorded.  Ten cases  were  fatal
and  the doses ranged from  4.5 to 180 g;  6 cases had  ingested
20 g  or more.  In the 10 non-fatal cases, the doses ranged from
0.5 to  50 g with 7/10  ingesting less than 20  g.  In the  case
treated  by  the  author, clinical  features  included metabolic
acidosis, hypocalcaemic tetany, methaemalbuminaemia, and reduced
blood  coagulation  (thrombotest  28% of  normal).   Post-mortem
findings  included blood in  all the serous  cavities, pulmonary
congestion  and oedema, haemorrhagic  changes in the  intestinal
epithelium,  centrilobular  congestion  and necrosis  and yellow
discoloration  of the liver, and patchy necrosis of the proximal
convoluted tubules of the kidneys.

    An  unsuccessful  suicidal  attempt was  described  by  Zipf
(1967).  A 25-year-old man ingested 6 tablets of  PhostoxinR  in
water  (= 6 g phosphine).  Immediate symptoms were severe retro-
sternal  pain,  a  generalized burning  sensation, and vomiting.
There  was circulatory collapse necessitating  resuscitation and
he  was also treated  by gastric lavage  with potassium  perman-
ganate and magnesium sulfate. Subsequently, symptoms of cardiac,
cerebral,  and hepatic dysfunction appeared and there was severe
renal failure requiring haemodialysis.

9.3.  Occupational Exposure

    Cases of acute phosphine poisoning reported in  the  litera-
ture were reviewed by Harger & Spolyar (1958).  Fifty-nine cases
with 26 deaths had been recorded since 1900 (including Gessner's
(1937)  non-occupational cases).  In 6 out of 11 papers, cargoes
of  ferrosilicon were cited as  the source of phosphine  and, in
these  cases, the victims were passengers or crew members of the
ships or barges concerned.  Other cases involved the exposure of
welders  to calcium carbide and raw acetylene and of submariners
to  sodium  phosphide.   The  most  common  autopsy  finding was
congestion of the lungs with marked oedema.  The authors added a
case  of  their  own in  which  a  16-year-old  youth  operating

acetylene  generators died, probably  as a result  of  phosphine
exposure  at a level of about 11 mg/m3 (8 ppm) for 1 - 2 h daily
over a period of 6 weeks.  Arsine and hydrogen sulfide exposures
were considered to have been too low to have accounted  for  the
death.   Autopsy revealed acute  pulmonary oedema.  Other  cases
have  been described, all  of which exhibited  similar  features
(Ziemer, 1963; Furuno et al., 1976; & Netherlands, 1984).  Three
groups of symptoms of acute phosphine poisoning  were  described
by  Childs  &  Coates  (1971):  (a)  nervous  symptoms including
headache,  vertigo, tremors, and  unsteady gait, progressing  in
severe  cases  to  convulsions,  coma,  and  death;  (b) gastro-
intestinal symptoms include loss of appetite, thirst, nausea and
vomiting, diarrhoea, and severe epigastric pain; and (c) respir-
atory symptoms including a feeling of pressure and pain  in  the
chest as well as shortness of breath.  In addition, a sharp fall
in blood pressure was described as a characteristic, but seldom-
mentioned symptom.  Chronic effects include anaemia, bronchitis,
and  gastrointestinal, speech, and motor disturbances, but these
are by no means general.

    The toxic effects of phosphine are summarized in Table 17.

    The  IDLH (Immediately Dangerous to Life or Health) level is
282 mg/m3 (200 ppm) (US EPA, 1985b).

    Verga  & Belloni (1958) described a case of purpura ascribed
to  poisoning by phosphine.  The  platelet count was reduced  to
60 000/mm3; the red-cell count was also low at 3.1 x 106/mm3 and
the  haemoglobin concentration (Sahli) was  55%.  With recovery,
both  the red-cell and thrombocyte counts increased to 4.8 x 106
and  210 000/mm3, respectively, at  the end of  the  observation
period.   The electrolysis of phosphate  solutions being applied
to  metals  as  a corrosion  inhibitor  was  considered to  have
produced phosphine, but there was no measurement of the level of
exposure  and it  is possible  that the  exposure also  included
arsine,  which would account for the anaemia with a hyperplastic
erythroid  series  in the  marrow  biopsy.  While  haemolysis is
recognized  as a complication  of arsine poisoning,  purpura and
thrombocytopenia   are   not   widely  recognized   features  of
phosphine  poisoning,  though  Borodin et  al.  (1983) described
changes related to haemolysis (prolongation of clotting time and
reduced plasminogen levels) in workers exposed to a  variety  of
biocides  and disinfectants, including zinc phosphide.  However,
these changes could not be related specifically to  exposure  to

Table 17.  Toxic effects of phosphinea
Effect                                 Concentration 
                                      mg/m3       ppm
Rapidly fatal                         2800        2000

Death after 1/2 - 1 h                 560 - 840   400 - 600

Dangerous to life after 1/2 - 1 h     400 - 600   290 - 430

Serious effect after 1/2 - 1 h        140 - 260   100 - 190

No serious effects after 1/2 - 1 h    10          7
a  From: Childs & Coates (1971).

    In  1978, Beloskurskaya et al.  published the findings of  a
study  on 206  phosphorus workers,  which revealed  57 cases  of
toxic hepatitis. In 49 of these cases, there was stated to be no
other  apparent cause than occupational  exposure to phosphorus,
phosphine,  or phosphorus oxides.   No measurements of  exposure
were  reported.   Diagnostic  criteria  included  a  history  of
hypochondrial  pain,  clinical hepatomegaly,  and abnormal liver
function  tests  and  131I-Rose Bengal  scanning  and  clearance
studies.   Forty-six of the  57 cases had  additional  symptoms,
such  as  the  astheno-vegetative syndrome,  chronic  gastritis,
impotence,  toxic  encephalopathy,  toxic  cardiomyopathy,   and
respiratory disease.  There was no control group and no informa-
tion on alcohol consumption was provided.

    In  a  later  study, Wilson  et  al.  (1980)  described  the
symptoms of acute poisoning by phosphine as  headache,  fatigue,
nausea,   vomiting,   jaundice,  paraethesia,   ataxia,  tremor,
diplopia,  myocardial  infiltration  with  necrosis,   pulmonary
oedema, and myocardial and peripheral muscle damage.  Laboratory
results  indicated that there had been urinary tract involvement
(occult   blood)  and  levels  of  several  liver  enzymes  were
elevated.   Furthermore,  Roaldsnes (1982)  reported that metal-
workers  at a large shipyard  in Norway, drilling deep  holes in
spheroidal  graphite iron, became ill during work.  The symptoms
were  mostly nausea, dizziness, chest  tightness, dyspepsia, and
disturbances of smell and taste.  Measurement of  the  phosphine
concentration in the workers' breathing zone (with Dräger tubes)
showed  a phosphine concentration  of about 1.4  mg/m3 (1  ppm).
After  installing  local  exhaust ventilation  on  the  drilling
machines,  there  were  no  longer  any  measurable  amounts  of
phosphine,  and there were no complaints from the workers.  When
the  local exhaust ventilation was removed for technical reasons
5  years later, illness among the workers recurred.  Measurement
of phosphine levels just above the machines,  showed  concentra-
tions  of up to  56 - 70  mg/m3 (40 -  50 ppm).  When  the local
exhaust  ventilation was re-installed, the  phosphine concentra-
tions dropped to unmeasurable amounts, and no further  cases  of
illness were reported.  Addition of copper sulfate  solution  to
the  cutting  oil effectively  removed  the phosphine  gas,  but
resulted in problems of corrosion.

    Jackson  &  Elias  (in  press)  studied  liver  function and
gastrointestinal  symptoms  in:  (a) workers  exposed  to  white
phosphorus  at up to 5 times the occupational exposure limit and
also to some phosphine (0 - 0.5 mg/m3); (b) workers  exposed  to
phosphine alone (at up to 2.8 mg/m3, depending on  the  efficacy
and  use  of air-line  breathing  apparatus); and  (c)   gastro-
intestinal symptoms in a group of workers who were  not  exposed
to  either compound,  but who  worked the  same  shift  pattern.
Complaints to the factory medical department of gastrointestinal
symptoms  in  the  phosphine-exposed group,  in  the  phosphorus
exposed-group, and in the unexposed group were 1.51,  0.61,  and
0.24  per  man per  year,  respectively.  However,  the  alcohol
consumption  in  the  phosphine- and  phosphorus-exposed  groups
differed (289 and 154 ml per week, respectively).   The  alcohol
consumption was not estimated in the control group.  None of the
conventional  liver function tests reflected  the differences in
occupational  exposure or alcohol intake.  The phosphine-exposed
group  did have a  significantly raised post-prandial  bile acid
concentration,  but whether this reflected a difference in phos-
phine exposure or alcohol consumption could not be determined.


10.1.  Evaluation of Human Health Risks

    Phosphine  and metal phosphides are only focally distributed
in  the environment and exposure of large numbers of the general
population is unlikely.  The sources and uses of  phosphine  and
metal  phosphides are sufficiently  well established for  safety
techniques to be generally known, though it is  disturbing  that
shipboard poisonings are still occurring when the first case was
reported  over half a century ago.  The extensive world-wide use
of  metal  phosphides as  fumigant  sources and  as rodenticides
creates  the  hazard of  accidental  poisoning in  children  and
others  and provides a means  of suicide, unless the  supply and
use  of these materials is appropriately regulated.  There is no
evidence  of danger to the population from residues of phosphine
in fumigated foods or from residues of phosphides,  if  adequate
fumigation  and aeration techniques are  used.  Permitted limits
for  residues are in the range of 0.01 - 0.1 mg total phosphine/
kg.  There do not appear to be any deleterious effects  on  food
quality  as a result  of adequately undertaken  fumigation  with

    Published data on occupational exposure to phosphine in most
industries are not sufficient to evaluate the success of control
measures in  relation to occupational exposure limits.  There is
also  some  disagreement regarding  these  limits and  some data
suggest   that  an  occupational   exposure  limit  of   0.4  mg
phosphine/m3  is above the threshold for biological effects with
long-term exposure.  However, there are no studies  adequate  to
settle this question definitively.

    Major  accidental  release  of stored  phosphine  presents a
serious  explosion/fire hazard and an acute toxic hazard for man
and animals.

10.2.  Evaluation of Effects on the Environment

    Only very small amounts of phosphine and phosphides occur in
the  environment as  a result  of natural  processes  and  those
resulting from human activity are not persistent.

    Phosphine and phosphides are introduced into the environment
for  the  control  of pests,  for  which  they are  particularly
suitable,  because of their  efficacy, lack of  persistence, and
harmless decomposition products.

    Careful   positioning  of  bait  and  the  low  toxicity  of
carcasses for scavengers of poisoned animal targets minimize the
effects  of rodenticidal metal phosphides on non-target species.
Phosphine and phosphides are oxidized in the environment and the
final  product,  phosphate, is  normally  widely present  in the
natural  environment.   Phosphine  and phosphides  are only used
where  the  natural environment  is  already modified  by  human
activity and their environmental impact must be viewed  in  this

    Since  resistance to phosphine in insects does not appear to
reverse   in  the  absence   of  selective  pressures,   it   is
particularly  important to achieve effective  doses of phosphine
by  using  adequate  treatment  rates  and  good  practices.  In
practice,  the development of  resistance is more  of a  problem
than  the  effects  on  non-target  species.   Major  accidental
release  of  stored  phosphine  would  not  result  in long-term
environmental consequences.

10.3.  Conclusions

    In general, there is no risk to the public from the  use  of
phosphine  or phosphides, from emissions from fumigated products
or  spaces, from alloys,  industrial processes, or  residues  in
food, provided that proper fumigation, transport, and industrial
practices are used.

    While  phosphine  and  metal  phosphides  are  toxic,  their
extensive  use  in occupational  settings  has resulted  in  the
establishment  of  good  practice  guidelines.   If  these   are
followed,  there  is  a low  order  of  risk for  human  health.
However,  there  is  some  doubt  about  the   completeness   of
protection  afforded by the  higher occupational exposure  limit
(0.4 mg phosphine/m3).

    There  is no risk  of important environmental  effects  from
phosphine or metal phosphides.


11.1.  Gaps in Knowledge

1.  The principal area related to human health where information
is inadequate is concerned with occupational exposure levels and
their  safety.  There is a  need for an adequate  study of well-
being  and organ function  in exposed and  control  populations,
with  a complete description  of phosphine exposure,  concurrent
exposures  to  other chemicals  (which  should be  low), alcohol
consumption,  and smoking habits.  The establishment of exposure
levels that are free from any detectable effects would  help  to
determine agreed occupational exposure limits.

2.  It  would be  of assistance,  in this  regard, to  undertake
laboratory  studies to identify biological markers that are most
indicative of phosphine effects and reflect the suggested short-
term cumulative effects of repeated phosphine exposure.

3.  Further  research on the  mechanisms of action  of phosphine
and  phosphides will  assist in  the design  of good  fumigation
practice  and fumigation schedules, and  minimize the occurrence
of resistance in target organisms and associated problems.

4.  It  has been suggested that zinc phosphide may be relatively
persistent in aquatic sediments and there is a general  lack  of
aquatic toxicological data.  There is a need for research on the
levels  and persistence of zinc  phosphide in sediments and  for
further studies of its effects on aquatic organisms.

11.2.  Preventive Measures

11.2.1.  Management

    The  most important factor in the safe handling of phosphine
and metal phosphides, and in their formulation, is  proper  work

    Management  should identify these, provide  training for the
operatives, and ensure that the practices are carried out.

    Personal  protection  measures  recommended  to  reduce  the
likelihood  of absorption of phosphide  preparations include the
wearing of:

    (a)  synthetic rubber gloves;
    (b)  rubber boots;
    (c)  lightweight impervious overalls; and
    (d)  suitable eye protection.

    Adequate washing facilities should be available at all times
during  handling.   Eating,  drinking,  and  smoking  should  be
prohibited  during handling, and before  washing after handling.
The means to measure concentrations of phosphine in  air  should
be available and used to check atmospheric concentrations.  When
necessary,  respiratory protective equipment should be worn.  In

fumigation, each operator or other person liable to  be  exposed
to  the gas must be provided with an efficient means of respira-
tory  protection.   Persons  exposed to  magnesium  phosphide or
aluminium   phosphide  powders  (or  other   readily  hydrolysed
phosphides),  which may  give rise  to airborne  dust should  be
protected by respiratory protective equipment, effective against
gaseous phosphine, since hydrolysis of dust in the filter  of  a
dust  mask  or  respirator  may  give  rise  to  high  phosphine

11.2.2.  Treatment of poisoning    Inhalation of phosphine

    (a)  First Aid

    Remove  from exposure, keep at rest.  Rescuers should follow
full safety procedures.

    If  the patient is unconscious, place in semi-prone recovery
position or otherwise maintain the airway.

    If the patient is conscious but has difficulty in breathing,
treat  in  a  seated position  and  give  oxygen  if  available.
Otherwise, allow the patient to recline with the  legs  slightly

    If   breathing  stops,  immediately  ventilate  the  patient
artificially  (mouth-to-mouth/nose or mechanically  with oxygen,
if available).

    If  the  heart  stops, begin  cardiopulmonary  resuscitation

    (b)  Medical Treatment

1.  Give oxygen by mask if required; perform baseline  chest  X-
    ray and examine chest.  Treat shock conventionally.

2.  All patients should be observed for 48 - 72 h, as  onset  of
    pulmonary oedema may be delayed.

3.  If  respiratory distress is  severe, give steroids  (methyl-
    prednisolone  30  mg/kg,  or  equivalent,  intramuscularly),
    preferably within 4 h of exposure.
4.  If pulmonary oedema occurs, treat by positive and expiratory
    pressure ventilation.  Antibiotics should only be given if a
    secondary infection is present.

5.  Treat  any fits conventionally; give general supportive care
    with particular attention to fluid balance.

6.  Some  sources of exposure  to phosphine are  likely to  lead
    also  to exposure to  arsine, which has  haemolytic effects.
    Monitor  for haemoglobinaemia, haemoglobinuria, unconjugated
    hyperbilirubinaemia, and renal failure.

    In  general,  recovery  is  rapid  following  removal   from
exposure,  but  renal  damage  and  leukopenia  may  occur after
several days.    Ingestion of metal phosphides

    (a)  First aid

    Do not give milk, fats, or saline emetics by mouth.

    Give oxygen if there is respiratory distress.

    If first aiders are medically authorized to do so,  and  the
patient is conscious, induce vomiting.

    After  20  min  (or after  vomiting),  administer  activated
charcoal (50 g in water by mouth) if available.

    Obtain  medical  attention  as soon  as possible: preferably
send immediately to hospital.

    (b)  Medical treatment

1.  Consider  tracheal  intubation  and gastric  lavage  with 2%
    sodium  bicarbonate  solution  (to limit  hydrolysis of zinc

2.  Activated  charcoal or medicinal  liquid paraffin may  limit
    absorption  of  phosphine and  zinc phosphide, respectively,
    and may be administered by mouth or stomach tube.

3.  Monitor  and  support vital  functions, particularly hepatic
    and renal function.  Treat shock conventionally.

5.  Hepatic  and renal failure  should be treated  in specialist

11.2.3.  Leaks, spillages, residues, and empty containers    Phosphine

    Small leaks and residues of compressed gas can be discharged
slowly  to the atmosphere  in the open  air.  Larger  quantities
should be burned using an appropriate burner.  Aluminium and magnesium phosphides and their formulated

    Spillages  and residues in containers  will evolve phosphine
for several days by reaction with atmospheric moisture.  Respir-
atory  protective equipment will  be required by  those  dealing
with  them.  Even if atmospheric concentrations of phosphine are
initially   low,  they  may  rise  as  residues  are  disturbed.
Moderate  quantities should be  collected in a  secure place  to
protect  the public and wildlife,  and left in the  open air and
kept moist until hydrolysis is complete.

    Larger  amounts  should  be removed  to  a  deep pit,  at an
approved site, until phosphine evolution is complete.  Then they
can be buried.

    Residues  at the site of spillage should be washed away in a
large  quantity of water  and the area  kept secure and  aerated
until checked for zero gas concentration.

    Combustible  packages can be incinerated at high temperature
(>  1000 °C)  using proper facilities.  Containers should NOT be
cleaned for re-use, but should be disposed of by deep burial, at
an approved site, well away from habitation and where  there  is
no danger of contamination of water sources.    Zinc phosphide and preparations

    Zinc   phosphide  hydrolyses  only   slowly.   Nevertheless,
phosphine  may be evolved  and respiratory protective  equipment
should be available.

    Spillages  and residues in containers  should be incinerated
at high temperatures (> 1000 °C) or crushed and buried below the
topsoil  at an appropriate site.   Contaminated surface material
should be treated similarly or else the area should  be  secured
from public access until the gas concentration is zero.


    Phosphine  was  evaluated  in 1971  by  WHO  and FAO,  as  a
pesticide  residue  in food  (WHO/FAO,  1972).  A  tolerance  of
0.1 mg/kg  (0.1  ppm)  in raw  cereals  was  confirmed.  It  was
recommended  that the  tolerance of  0.01 mg/kg  (0.01  ppm)  in
flour,  other milled cereal  products, breakfast cereals,  dried
vegetables,  and  spices be  confirmed  and extended  to include
nuts,  groundnuts, dried fruit,  cocoa beans, and  other similar
foods, known to be fumigated with phosphine.

    The  use of zinc phosphide as a rodenticide in public health
was  reviewed by WHO in  1972.  It was concluded  that it was  a
generally effective compound and, while highly toxic to domestic
fowl, its safety record was good.  The use of zinc phosphide was
endorsed (WHO, 1973).


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on  the germination of certain cereal and vegetable seeds.  Bull.
 grain Technol., 4(4): 197-199.

    See Also:
       Toxicological Abbreviations