Paraquat
Paraquat
International Programme on Chemical Safety
Poisons Information Monograph 399
Chemical
1. NAME
1.1 Substance
Paraquat
1.2 Group
Bipyridilium herbicides
1.3 Synonyms
Paraquat dichloride;
Methyl viologen;
1.4 Identification numbers
1.4.1 CAS number
4685-147 (Cation)
1910-42-5 (Dichloride)
2074-50-2 (Dimethyl Sulphate)
1.4.2 Other numbers
UN 2781
2782
3016
3015
N.B. No Hazchem Code.
1.5 Main brand names/ Main trade names
Paraquat only Paraquat + Paraquat +
Diquat Urea Herbicides
Barclay Total(R) Actor(R) Anuron(R)
Crisquat(R) Dukatalon(R) Dexuron(R)
Cyclone(R) Opal(R) Gramocil(R)
Dextrone X(R) Pathclear(R)1,2 Gramonol(R)
Dragocson(R) PDQ(R) Gramuron(R)
Esgram(R) Preeglox L(R) Tota-Col(R)
Efoxon(R) Preglone(R)
Goldquat(R) 276 Seccatuto(R)
Gramoxone(R) Spray Seed(R)
Herbaxon(R) Weedol(R) 1
Herbikill(R)
Katalon(R)
Osaquat(R)
Parakill(R)
Pilarxone(R)
Plusquat(R)
Priquat(R)
R-Bix(R)
Scythe(R)
Speeder(R)
Speedway(R)
Starfire(R)
Sweep(R)
Total(R)
Weedless(R)
1 granular formulation
2 also includes simazine and amitrole
1.6 Main manufacturers, main importers
Comlets, Crystal, Kuo Ching, Pilarquim, Productos OSA,
Sanex, United Phosphorus, Sinon, Zeneca
2. SUMMARY
2.1 Main risks and target organs
The main risks are from deliberate ingestion and are
related to the dose ingested. Serious accidental/occupational
poisoning is comparatively rare, and when it does occur there
usually has been inappropriate handling of the product and/or
inadequate treatment especially of skin exposure.
The risk is largely dependent on route of exposure as well as
dose. The target organs are: lungs, kidneys, liver and
myocardium
a) Ingestion of large amounts result in multiple organ
failure and death.
b) Ingestion of modrate amounts result inrenal failure
and or massive pulmonary infiltration and fibrosis.
Fatalities are not uncommon.
c) The concentrated product is severely irritant and
local exposure can result in mucous membrane, skin and
eye damage.
d) Minor exposures
There are many incidents of minor exposure which cause
great alarm. These often concern properly diluted
household or professional preparations. For example a
child licking a stick used to mix the granules or
eating food that has been touched by contaminated
hands is unlikely to come to great harm. Skin and eye
exposure to these dilute solutions is also unlikely to
cause any sequelae.
2.2 Summary of clinical effects
Clinical effects are dose and route dependent. Ingestion
can cause a burning sensation in the mouth, nausea, vomiting,
abdominal pain and diarrhoea, occasionally bloody). Nearly
all products contain an emetic and if this has been ingested
vomiting may be severe and repeated. After some hours,
inflammation and ulceration of the mouth, throat and
gastrointestinal tract may occur.
Other effects
a) Ingestion
Low dose (<20 mg paraquat ion per Kg body wieght =
10mls of a 20 to 24% concentrate)
Patients are often asymptomatic or may develop
vomiting or diarrhoea. Complete recovery occurs but
there may be a transient impairment of lung function
tests.
Moderate dose (20 to 40 mg paraquat ion per Kg body
weight = 10 to 20 mLs of 20 to 24% concentrate)
Initially renal and hepatic dysfunction are common.
Mucosal damage may become apparent with sloughing of
the mucous membranes in the mouth. Dyspnoea may
develop after a few days in the more severe cases. By
about 10 days crepitations and radiological signs of
lung damage usually develop. Renal function often
returns to normal at this stage. Massive pulmonary
fibrosis manifested by progressive dyspnoea may cause
death between 2-4 weeks after ingestion.
High dose (> 40 mg paraquat ion per kg body weight =
20 mL of 20 to 24% concentrate)
Toxicity is much more severe and death occurs early
(24-48 hrs) from multiple organ failure. The initial
gastrointestinal symptoms are similar but very severe
with considerable fluid loss. Renal failure, cardiac
arrythmias, coma, convulsions, oesophageal perforation
and death soon follow.
b) Inhalation
Paraquat is not volatile but most liquid paraquat
formulations contain an unpleasant 'stenching agent'
which may occasionally cause feelings of nausea or
headaches. In typical spray applications the droplets
are too large to be inhaled into the lungs. Inhalation
of paraquat can result in a sore nose and throat as
well as possible nose bleeds but there are no reports
of serious systemic toxicity from inhalation. Contact
of the nasal mucosa with fingers contaminated with the
concentrate may also cause nose bleeds.
c) Eye
Concentrated paraquat splashes may cause severe eye
irritation which may result in extensive loss of
superficial areas of the corneal and conjunctival
epithelium, ulcerated areas are at risk from secondary
infection. Corneal oedema may persist for up to 3 to
4 weeks with temporary blurring of vision.
d) Skin
Paraquat, especially in concentrated forms, is
irritating to the skin and if contact is prolonged
skin damage may occur. In cases with extensive skin
damage systemic poisoning can occur due to absorption
of paraquat through damaged skin and may result in
severe toxicity or even death. Nail contact may
result in white spotting or in severe cases transverse
cracking dermatitis and nail atrophy. There are
however no other chronic affects described.
2.3 Diagnosis
The diagnosis is based on the history of exposure and
symptoms and signs such as vomiting, abdominal pain,
diarrhoea, anuria, dyspnea, liver dysfunction.
Blood and urine samples should be taken for paraquat analysis
(10 and 20 mLs respectively). A rapid urine spot test can
confirm the presence of paraquat. Then quantitative
measurement in the blood should be performed.The samples must
not be put into glass containers of any type as paraquat ion
is absorbed by glass. A plastic heparinized tube is suitable
for blood and a plastic sterile universal container is
suitable for urine.
Urea, creatinine and electrolytes
Full blood count
Liver function tests
Blood gases
Qualitative test for paraquat
Quantitative test analysis for paraquat
Chest X-ray, ECG
2.4 First-aid measures and management principles
First aid:
The immediate priority is to prevent any further absorption
of paraquat. In the first aid situation if the patient is
not already vomiting induce vomiting. Give ipecacuanha syrup
if it is available. Contaminated skin should be thoroughly
washed with water and soap. If the skin is damaged the
possibility of absorption be considered. Any contaminated
clothing should be removed immediately and should be washed
before reuse or burnt. The patient should immediately be
transferred to the nearest hospital.
Hospital management:
Aspirate gastric contents and perform gastric lavage and give
adsorbents.
An asorbent such as activated charcoal or Fuller's Earth
together with a purgative such as mannitol or sorbitol should
be administered. The dose of absorbent and purgative should
be repeated until the adsorbent can be seen in the stools or
the urine spot test becomes negative.
Paraquat adsorbents
In order of preference
Type Dose
1. Activated charcoal 100 gm
(child 2gm/Kg)
2. Fullers Earth 1 liter 15% aqueous
suspension & purgative
3. Bentonite 1 liter 7% aqueous
suspension & purgative
Gastrointestinal fluid losses should be replaced with normal
saline. Having instituted measures to prevent further
absorption and start fluid replacement, the diagnosis should
be confirmed by the "spot" test for paraquat and the
prognosis assessed by the measurement of plasma paraquat. In
view of the risk of renal failure the central venous pressure
should be monitored and used as guide to fluid replacement.
If paraquat level is very high and the prognosis hopeless
adequate pain relief and terminal care is appropriate.
Although oxygen is in general contraindicated it may be
administered to the dying patient with severe dyspnoea.
Profound acidosis should be corrected with intravenous sodium
bicarbonate. Dialysis may be required and the indications
are as in any another form of acute renal failure.
Purgatives may produce further fluid losses which should be
replaced with intravenous normal saline. Mouth ulceration
may produce severe pain which may be helped by symptomatic
treatments. If there is any possibility of oesophageal
perforation the patient should not be allowed to take
anything by mouth until perforation is excluded by endoscopy
or radiological studies. Secondary infection of mouth ulcers
should be treated with antibiotics.
Elimination techniques such as dialysis, forced diuresis, and
charcoal haemoperfusion are largely ineffective in removing
paraquat but prolonged haemoperfusion may be considered in
early cases where the blood concentration indicates
moderately poor outcome (see 10.5). The prevention of
pulmonary complications using cyclophosphamide and
dexamethasone has been advocated, but the effectiveness of
this regime has not as yet been proven. Broken skin should
be treated as for superficial burns after thorough cleansing.
Antibiotics may be required for secondary skin infection.
Contaminated eyes should be copiously irrigated with running
water for at least 15 minutes. An ophthalmic examination
should be carried out 24 hours after exposure, secondary
infection should be prevented with a topical antibiotic
Steroid creams will aid resolution of granulation tissue.
Lung transplantation has been tried but not alltogether
successful.
Management of fire and disposal
Paraquat is non flammable. If exposed to fire, keep
containers cool by spraying with water. Extinguish with dry
powder, chemical foam (preferably alcohol resistant) or water
sprays. Avoid if possible the use of water jets. Absorb
liquid spills with sand or earth, move the earth to safe
place then flush the area with water.
Disposal of contaminated adsorbents, containers, leftover
pesticide: these should be buried in an approved dump, or in
an area where there is no risk of injury to plants or of
contamination of surface or ground water.
Decontaminate empty containers with 10% sodium carbonate
(washing soda) solution, added at the rate of at last 1 liter
per 20 litre drum capacity. Swirl round to rinse the walls,
empty and add rinsings to sawdust, sand or earth. Puncture
the container to prevent reuse.
3. PHYSICO-CHEMICAL PROPERTIES
3.1 Origin of the substances
Paraquat is a synthetic product. It was first described
in 1882 by Weidel and Russo. In 1933, Michaelis and Hill
discovered its redox properties and called the compound
methyl viologen. The herbicidal properties of paraquat were
first described in 1958 and it became commercially available
in 1962.
3.2 Chemical structure
Chemical name:
1,1'-DIMETHYL-4',4'-BIPYRIDILIUM DICHLORIDE
Formula (C12 H14 N2 CL2)
Molecular weight 257.16
The term Paraquat applies also to
1,1'-DIMETHYL-4',4'-BIPYRIDILIUM DIMETHYLSULPHATE
Formula (C12 H14 N2 CH3 SO4)2)
3.3 Physical properties
3.3.1 Colour
yellowish-white
3.3.2 State/form
Solid, but usually available as concentrated
(20-24%) solution
3.3.3 Description
Melting point = decomposes at about 300°C
Vapour pressure = < 0.1 kPa
Flammability = Non flammable and not explosive
Solubility = Very soluble in water (700 g/l at 20°C).
Practically insoluble in most other organic solvents.
Stability = Stable in acid or neutral solutions but
decomposes in the presence of UV light, unstable in
alkaline solutions, inactivated by inert clays and
ionic surfactants.
pH = 6.5 - 7.5 (liquid formulation)
3.4 Hazardous Characteristics
Pure paraquat salts are white and the technical products
yellow. They are crystalline, odorless, hydroscopic,
nonvolatile powders. They are corrosive to metals and
incompatible with alkyl aryl sulphonate wetting agents.
Normal potential at 30°C = -0.44 volts.
4. USES
4.1.1 Uses
Herbicide
4.1.2 Description
Paraquat is a non-selective foliage applied
contact herbicide which is inactivated on contact with
soil, so that replanting can be performed almost
immediately after spraying. Usage is worldwide.
Household formulations are also available for clearing
paths and flower or vegetable beds.
4.2 High risk circumstances of poisoning
Risk is greatest to those who have access to paraquat
where inadequate precautions are taken during transport,
storage and use.
4.3 Occupationally exposed populations
Farmers, especially in tropical countries, where the
climate is not conducive to wearing full protective
clothing.
5. ROUTES OF ENTRY
5.1 Oral
Ingestion with suicidal intent is by far the commonest
route of entry. Oral ingestion may also occur accidentally
or from swallowing spray droplets deposited in the pharynx,
usually without systemic poisoning.
5.2 Inhalation
There have been no substantiated cases of systemic
poisoning by inhalation of microscopic paraquat droplets,
although animal experiments suggest high toxicity of aerosols
with a particle size of <5 µm.
Inhalation of sprayed mist does occur, but the systems used
deliver only large droplets, which are deposited in the upper
respiratory tract where they cause irritation .
5.3 Dermal
Intact, normal skin provides a good barrier against
absorption and systemic toxicity. However, if there is
prolonged contact and extensive skin damage , systemic
poisoning can occur and may result in severe toxicity or even
death. Prolonged skin contact and trauma exacerbate skin
damage. This is, however rare.
5.4 Eye
Concentrated paraquat splashes may cause severe eye
irritation, which if not properly treated, may result in
extensive loss of superficial areas of the corneal and
conjunctival epithelium. The inflammation develops over 24
hrs and ulcerated areas are at risk from secondary infection.
If adequate medical attention is given, healing although
slow, is usually complete.
5.5 Parenteral
Systemic toxicity has followed rare cases of deliberate
subcutaneous, intraperitoneal, and intravenous injection of
paraquat.
5.6 Others
No data available.
6. KINETICS
6.1 Absorption by route of exposure
Rat and dog studies (Smith et al., 1974; Bennet et al.,
1976) revealed that rapid but incomplete absorption of
paraquat occurred from the gastrointestinal tract somewhere
beyond the stomach. Probably less than 5% is absorbed.
Information on paraquat absorption in man is sparse but is
assumed to be the same, however there is limited evidence to
support this (Smith, 1987).
Information on absorption from other routes is even more
scanty. However it is known that absorption does occur from
damaged skin, but is very limited from intact skin (0.3% of
an applied dose, Wester et al., 1984).
6.2 Distribution by route of exposure
The absorbed paraquat is distributed via the
bloodstream to practically all organs and tissues of the
body, but no prolonged storage takes place in any tissue.
The distribution of paraquat is best described by a
three-compartment open model with input to and elimination
from the central compartment (Hawksworth et al., 1981). The
lung then selectively accumulates paraquat from the plasma,
by an energy dependent process.
6.3 Biological half-life by route of exposure
Houze et al. (1990) found that the concentration-time
curve in 15 adult patients (not haemodialysed) was best
described by a bi-exponential curve, with the elimination
half lives of the early and late phase being 5 and 84 hours,
respectively.
6.4 Metabolism
Paraquat is not metabolized but is reduced to an
unstable free radical which is then re-oxidized to reform the
cation and produce a superoxide anion.
6.5 Elimination and excretion
Animal studies have shown paraquat to be excreted
rapidly by the kidneys. 80 to 90% is excreted within 6 hours
and almost 100% within 24 hours, in the absence of paraquat
induced renal disease. However paraquat may cause renal
tubular necrosis which can prolong excretion up to 10 to 20
days. Excretion in humans is though to be similar and to
involve active renal secretion as well as glomerular
filtration (Hawksworth et al., 1981).
7. TOXICOLOGY
7.1 Mode of Action
It is now well established that "Redox Cycling" is the
primary reaction responsible for the toxicity of paraquat.
In anaerobic conditions the paraquat cation can be reduced by
NADPH-dependant microsomal flavoprotein reductase to form the
reduced radical. This then reacts with molecular oxygen to
reform the paraquat cation and the superoxide ion. Paraquat
will then continue to cycle from its oxidized to reduced form
with the electrons and oxygen. Paraquat is thought to cause
cell death by lipid peroxidation or NADPH depletion, as in
the lung where there is selective accumulation (Smith,
1987).
7.2 Toxicology
7.2.1 Human data
7.2.1.1 Adults
The minimum single oral toxic dose
for man is estimated to be 20mg per
Kg.
7.2.1.2 Children
Based on human poisoning cases
children are considered to show a similar
susceptibility and clinical picture of
paraquat poisoning compared to
adults.
7.2.2 Relevant animal data
The oral LD50 of paraquat dichloride in rats
is about 150 mg/kg. Mice are less sensitive to orally
administered paraquat than rats, while guinea pigs,
cats, monkeys and rabbits are more susceptible.
Dermal toxicity in the rabbit was found dependent on
application technique, whether the site was occluded
and whether the animals were prevented from grooming.
Under conditions where this was prevented the LD50
was found to be >480 mg/kg paraquat ion (McElligott,
1972)
7.2.3 Relevant in vitro data
No data available
7.2.4 Workplace standards
UK HSE: 0.08mg/mg3 (8hr TWA) respirable dust
ACGIH: 0.5 mg/m3 (TLV-TWA) total dust (as cation)
0.1 mg/m3 (TLV-TWA) respirable fraction
7.2.5 Acceptable daily intake (ADI)
JMPR 1986: 0.004 mg/kg/day as paraquat ion
7.3 Carcinogenicity
The potential carcinogenicity of paraquat has been
investigated in long term studies in the rat and in the
mouse. In both species, it was concluded that paraquat was
not a carcinogen (FAO/WHO, 1986).
The US EPA classifies paraquat as a "Group E" chemical which
evidences that it is not a human carcinogen (US Environmental
Protection Agency, 1997.
7.4 Teratogenicity
Paraquat has no effect on fertility, is not teratogenic
and only produces fetotoxicity at doses that are maternally
toxic. The main finding in multigeneration studies was lung
damage (IPCS, 1984).
7.5 Mutagenicity
Paraquat has minimal to no genotoxic activity when
evaluated in a variety of in vitro and in vivo systems (IPCS,
1984).
7.6 Interactions
Oxygen is contraindicated in the treatment of paraquat
poisoning as it may worsen lung damage, except to relieve
pain and distress in terminal care.
8. TOXICOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS
8.1 Material sampling plan
8.1.1 Sampling and specimen collection
8.1.1.1 Toxicological analyses
8.1.1.2 Biomedical analyses
8.1.1.3 Arterial blood gas analysis
8.1.1.4 Haematological analyses
8.1.1.5 Other (unspecified) analyses
8.1.2 Storage of laboratory samples and specimens
8.1.2.1 Toxicological analyses
8.1.2.2 Biomedical analyses
8.1.2.3 Arterial blood gas analysis
8.1.2.4 Haematological analyses
8.1.2.5 Other (unspecified) analyses
8.1.3 Transport of laboratory samples and specimens
8.1.3.1 Toxicological analyses
8.1.3.2 Biomedical analyses
8.1.3.3 Arterial blood gas analysis
8.1.3.4 Haematological analyses
8.1.3.5 Other (unspecified) analyses
8.2 Toxicological Analyses and Their Interpretation
8.2.1 Tests on toxic ingredient(s) of material
8.2.1.1 Simple Qualitative Test(s)
8.2.1.2 Advanced Qualitative Confirmation Test(s)
8.2.1.3 Simple Quantitative Method(s)
8.2.1.4 Advanced Quantitative Method(s)
8.2.2 Tests for biological specimens
8.2.2.1 Simple Qualitative Test(s)
There is a simple "spot" test for
paraquat in the urine and gastric aspirate
which should be available on an emergency
basis for a quick confirmation of paraquat
poisoning. It is based on the reduction of
paraquat cation to a stable blue radical ion
in the presence of alkali and sodium
dithionate. This test is only reliable up to
12 hours after ingestion and can detect
concentrations of paraquat in urine down to 1
mg/L. Depending on the result of this test
and/or clinical observation, a quantitative
test should be initiated.
8.2.2.2 Advanced Qualitative Confirmation Test(s)
8.2.2.3 Simple Quantitative Method(s)
8.2.2.4 Advanced Quantitative Method(s)
There are a variety of
spectrophotometric, liquid chromatographic
and radioimmunoassay techniques available for
measurement of paraquat in biological fluids.
A few of the more reliable and rapid
techniques are outlined here. A more
detailed review has been published by
Braithewaite (1986).
Radioimmunoassay
A specific radioimmunoassay procedure for the
determination of paraquat at low
concentrations in plasma and urine has been
developed by Levitt (1977 & 1979). The
procedure is based on antibodies, raised
against a paraquat derivative of monoquat, in
rabbits and used 3H-labelled paraquat as the
tracer and a dextran/charcoal separation
technique. Liquid scintillation counting is
used to determine the radioactivity of
separated unbound paraquat. The sensitivity
of the assay is 6 ng paraquat ion per ml of
plasma.
High Performance Liquid Chromatography
(HPLC): Gill et al. (1983) have described an
HPLC method based on the initial extraction
of paraquat and diquat using a sep-pak C18
cartridge, with ethyl viologen
(1,1 dimethyl-4.4'-bipyridium salt as an
internal standard. Chromatography is carried
out using an ods - silica column and ion pair
separation with methanol and sodium heptane -
paraquat in urine is 1 mg/L.
Spectrophotometry following solid-phase
extraction and reduction with sodium
dithionite has been described by Smith et al.
(1993) for quantification of paraquat in
biological fluids.
8.2.2.5 Other Dedicated Method(s)
8.2.3 Interpretation of toxicological analyses
8.3 Biomedical investigations and their interpretation
8.3.1 Biochemical analysis
8.3.1.1 Blood, plasma or serum
8.3.1.2 Urine
8.3.1.3 Other fluids
8.3.2 Arterial blood gas analyses
8.3.3 Haematological analyses
8.3.4 Interpretation of biomedical investigations
8.4 Other biomedical (diagnostic) investigations and their
interpretation
8.5 Overall interpretation of all toxicological analyses and
toxicological investigations
Accurate and rapid qualitative and quantitative analysis
of paraquat in blood and urine is important for the diagnosis
and prognosis of a patient poisoned with paraquat.
Toxic lethal concentrations
Time is a considerable factor in determining what is a lethal
concentration. For example a concentration of 100 g/l at
4 hrs indicates a 70% chance of survival but at 20 hrs
indicates less than a 10% chance of survival.
8.6 References
9. CLINICAL EFFECTS
9.1 Acute poisoning
9.1.1 Ingestion
Ingestion, particularly of the concentrates,
causes a burning sensation in the mouth, nausea,
vomiting, abdominal pain and diarrhoea occasionally
bloody. After some hours, inflammation and ulceration
of the mouth, throat and gastrointestinal tract may
occur. The initial gastrointestinal symptoms settle
after two to three days if the patient survives.
Other effects are dose dependant.
Low dose (<20 mg paraquat ion per Kg body weight =
<10 mL 20 to 24% concentrate):
Patients are often asymptomatic or may develop
vomiting or diarrhoea. Complete recovery occurs but
there may be a transient impairment of lung function
tests.
Moderate dose (20 to 40 mg paraquat ion per Kg body
weight = 10 to 20 mL of 20 to 24% concentrate):
After 2 to 3 days urea and creatinine may rise and the
liver function tests may become abnormal. For the
next 3 to 4 days renal function tends to continue to
deteriorate and the patient may become acidotic and
anuric. Mucosal damage may become apparent with
sloughing of the mucous membranes in the mouth.
Dyspnoea may develop at this stage in the more severe
cases. By 10 days crepitations and radiological signs
of lung damage have usually developed although this
may rarely be delayed to 14 days. Renal function may
return to normal at this stage.
Massive pulmonary fibrosis manifested by progressive
severe dyspnoea may cause death from 2 to 4 weeks from
ingestion. Death may also occur earlier from renal
failure. If the patient survive the lungs usually
recover completely, although some abnormalities of
lung function have been observed months after an
episode of acute poisoning.
High dose (>40 mg paraquat ion per kg body weight =
> 20 mL of 20 to 24% concentrate):
Toxicity is much more severe and death occurs early
(24-48 hrs) from multiple organ failure. The initial
gastrointestinal symptoms are similar but very severe
with considerable fluid loss. Renal failure, cardiac
arrythmias, acute cardiac failure, coma, convulsions,
oesophageal perforation and death soon
follows.
9.1.2 Inhalation
There have been no substantiated cases of
systemic poisoning by inhalation of microscopic
paraquat droplets although animal experiments suggest
pulmonary uptake is significant. Inhalation of
sprayed mist does occur but the systems used deliver
only large droplets which are deposited in the upper
respiratory tract where they cause irritation only.
The patient may present with a sore nose and throat as
well as possible nose bleeds (Bismuth, 1995).
9.1.3 Skin exposure
Paraquat, especially in concentrated forms, is
irritating to skin and if left in contact for several
hours skin damage may occur. Necrosis with skin loss
and weeping areas are seen. Intact, normal skin
provides a good barrier against absorption and
systemic toxicity. However, if extensive skin damage
occurs in the presence of sufficient paraquat,
systemic poisoning can occur and may result in severe
toxicity or even death. Prolonged skin contact and
trauma exacerbate skin damage and hence absorption and
systemic toxicity is then more likely. Nail contact
may result in white spotting or in severe cases
transverse cracking with loss of nail. Damage may be
delayed from the time of exposure, since the effect is
on the nail bed and it takes some weeks for damage to
grow with the nail. Regrowth of the nail is
uncomplicated. Chronic occupational exposure may
produce a cracking dermatitis and nail atrophy
(Bismuth, 1995).
9.1.4 Eye contact
Concentrated paraquat may cause severe eye
irritation, which if untreated, may result in
extensive loss of superficial areas of the corneal and
conjunctival epithelium. Corneal oedema may persist
for up to 3 to 4 weeks with temporary blurring of
vision. The inflammation develops over 14hrs and
ulcerated areas are at risk from secondary infection.
If adequate medical attention is given, healing
although slow is usually complete (Bismuth,
1995).
9.1.5 Parenteral exposure
Systemic toxicity has followed subcutaneous,
intraperitoneal, and intravenous injection of paraquat
(Chandrasiri, 1999).
9.1.6 Other
No data available
9.2 Chronic poisoning
9.2.1 Ingestion
No data available
9.2.2 Inhalation
There are very few problems from chronic
exposure. However contact of the nasal mucosa with
fingers contaminated with the concentrate may also
cause nosebleeds as well as direct skin and nail
toxicity.
Comprehensive medical surveys in paraquat-exposed
spray operators in Malaysia (Howard et al., 1981) and
Sri Lanka (Senanayake et al., 1993), including
detailed clinical examinations, lung function
measurements (CO diffusion capacity), haematological
and biochemical investigations, concluded that the
long term spraying of paraquat was not associated with
any measurable adverse health effects.
9.2.3 Skin exposure
Chronic occupational exposure may produce a
cracking dermatitis and nail atrophy.
9.2.4 Eye contact
No data available
9.2.5 Parenteral exposure
No data available
9.2.6 Other
There are very few problems reported on chronic
exposure, however contact of the nasal mucosa with
fingers contaminated with the concentrate may also
cause nosebleeds as well as direct skin and nail
toxicity described above
9.3 Course, prognosis, cause of death
Symptoms are largely dependent on the route of exposure,
concentration of paraquat in the product and the amount
involved. Some products contain an emetic causing
vomiting.
After massive ingestion the symptoms and signs are: vomiting,
abdominal pain, diarhoea, renal failure as well as hepatic
and cardiac failure develop within the first 24 hours,
sometimes ending with death due to acute cardiac failure.
Ingestion of moderate amounts of paraquat causes the sequence
of 3 stages of morbid course:
Stage I: lasting 1 to 5 days. Local corrosive action
Haemoptysis, ulcerations of mucous membranes, nausea,
diarrhea, oliguria
Stage II: lasting 2 to 8 days. Signs of liver, kidney,
cardiac damage
Jaundice, fever, tachycardia, myocarditis, respiratory
distress, cyanosis, elevated BUN, creatinine, serum alkaline
phosphatase, serum bilirubin, serum transaminases, low
prothrombin.
Stage III: lasting 3 14 days. Pulmonary fibrosis
Coughe, dyspnea, tachypnea, edema, pleural effusions,
atelectasis, low arterial oxygen tension, inceasrd alveolar
oxygen tension gradient, respiratory failure
Ingestion of small amounts may cause minor symptoms followed
by full recovery.
Overall mortality rate of accidental poisoning is estimated
to be 33 - 50% (ref. Haddad, L.M. and Winchester J.F.:
Poisoning and Drug Overdose, eds. Second edition, 1990,
Saunders)
9.4 Systematic description of clinical effects:
9.4.1 Cardiovascular
Patients develop tachycardia and sometimes
arrhythmia. Circulatory failure may cause death within
24 hours
9.4.2 Respiratory
Victims of paraquat poisoning, who survive the
first two weeks usually make a full recovery within a
few weeks. Even patients who survive severe pulmonary
complications, when followed up, have little residual
evidence of lung damage. Smokers are an exception and
have been shown to have mild to moderate disturbances
of lung function, but it is not known whether these
would have been present prior to paraquat
ingestion.
Unless the patient is considered to be terminal,
oxygen therapy is contraindicated as it may potentiate
pulmonary damage. Occasionally pneumothorax, pleural
effusion, or iatrogenic pulmonary oedema, may
precipitate dyspnoea and should be treated as
usual.
In severely poisoned patients, cough, respiratory
failure with progressive dyspnoea and cyanosis develop
within 5 to 14 days. This is usually due to pulmonary
edema, atelectases and sometimes pleural effusions.
Arterial blood gases indicate hypoxaemia. If the
patient survives pulmonary fibrosis ensues with signs
of severe respiratory failure, which is usually fatal.
Some patients have survived, eventually returning to
near normal lung function.
9.4.3 Neurologic
9.4.3.1 CNS
Coma and convulsions may be due to
multiorgan damage.
9.4.3.2 Peripheral nervous system
No data available
9.4.3.3 Autonomic nervous system
No data available
9.4.3.4 Skeletal and smooth muscle
Paraquat induced myopathy, where
remarkable degeneration of type 1 muscle
fibers, was observed in prolonged paraquat
poisoning (Tabata et al., 1999).
9.4.3 Gastrointestinal
Burning sensation in the mouth and throat,
nausea, vomiting, diarrhoea with haematemesis and
abdominal pain are the early gastrointestinal features
The abdomen is tender and rigid. Withina few days
painful sloughing mouth ulcers develop. The tongue is
swollen and there is dysphagia. Ulcerations and
perforation of the oropharynx and oesophagus causes
subcutaneous emphysema.
9.4.4 Hepatic
Within 2 to 3 days of ingestion, hepatotoxicity
is manifested by jaundice, and a tender enlarged
liver. The liver function tests are abnormal. If the
patient survives up to the second week, liver function
may improve.
9.4.6 Urinary
9.4.6.1 Renal
Within 2 to 3 days of ingestion,
renal toxicity is manifested by oliguria,
proteinuria, and rising creatinine and urea
levels. Acute renal failure usually improve
in the second week.
9.4.6.2 Others
9.4.7 Endrocrine and reproductive systems
No other information available.
9.4.8 Dermatological
Paraquat, especially in concentrated forms, is
irritating to skin and if left in contact for several
hours skin damage may occur. Necrosis with skin loss
and weeping areas are seen. Intact, normal skin
provides a good barrier against absorption and
systemic toxicity. However, if extensive skin damage
occurs due to extensive exposure to paraquat,
systemic poisoning can follow and may result in
severe toxicity or even death. Prolonged skin contact
and trauma exacerbate skin damage and hence absorption
and systemic toxicity is then more likely. Nail
contact may result in white spotting or in severe
cases transverse cracking with loss of nail. Damage
maybe delayed from the time of exposure, since the
effect is on the nail bed and it takes some weeks for
damage to grow with the nail. Regrowth of the nail is
uncomplicated. Chronic occupational exposure may
produce a cracking dermatitis and nail atrophy
9.4.9 Eye, ear, nose, throat: local effects
Eye
Concentrated paraquat may cause severe eye irritation,
which if untreated, may result in extensive loss of
superficial areas of the corneal and conjunctival
epithelium. Corneal oedema may persist for up to 3-4
weeks with temporary blurring of vision. The
inflammation develops over 14hrs and ulcerated areas
are at risk from secondary infection. If adequate
medical attention is given, healing although slow is
usually complete (Bismuth, 1995).
9.4.10 Hematological
No data available
9.4.11 Immunological
No data available
9.4.12 Metabolic
9.4.12.1 Acid base disturbances
Metabolic acidosis mainly due to
renal failure.
9.4.12.2 Fluid and electrolyte disturbances
Vomiting and diarhoea may cause
hypovolaemia. Hyperkalaemia may develop due
to renal failure. Hypokalaemia of uncertain
origin was also observed (Sato, S: Human
Paraquat Toxicology, in Bismuth, Ch, Hall,
Paraquat Poisoning, Marcel Dekker, Inc. New
York,1995).
9.4.12.3 Others
No data available
9.4.13 Allergic reactions
There has been one case report of immune
complex glomerulonephritis following exposure to
paraquat (Stratta, 1988). Exposure to paraquat was
followed 1 week later by mild respiratory distress in
a previously healthy farmer who developed a mixed
nephrotic/nephritic syndrome 3 moths later.
9.4.14 Other clinical effects
No data available
9.4.15 Special risks
There are very few problems from chronic
exposure, however contact of the nasal mucosa with
fingers contaminated with the concentrate may also
cause nosebleeds as well as direct skin and nail
toxicity described above.
9.5 Others
There is no evidence of carcinogenicity.
Animal studies have shown no evidence of teratogenicity, or
effects on reproduction. There is also no evidence of such
effects in man.
9.6 Summary
10. MANAGEMENT
10.1 General principles
Ingestion
The immediate priority is to prevent any further absorption
of paraquat. In the first aid situation if the patient is
not vomiting give activated charcoal (100 g for adults or
2 g/kg body weight for children or Fuller's Earth (15%
slurry, 1 litre for adults or 15 mL/kg body weight for
children). Do not give oxygen as this may potentiate
harmfull superoxide formation. Superoxides are thought to be
involved in the pathogenesis of pulmonary damage. The
patient should immediately be transferred to the nearest
hospital.
On arrival in hospital vomiting should be controlled with
phenothiazine or ondansetron. An adsorbent should be given
orally or via a nasogastric tube. Previous guidelines have
considered Fullers Earth to be the absorbent of choice but
activated charcoal appears to be equally effective and is
usually more readily available. A purgative such as mannitol
or sorbitol (200 mL of a 20% aqueous solution or magnesium
sulphate should also be given. The dose of absorbent and
purgative should be repeated until the absorbent can be seen
in the stools. In patients with acute renal failure large
amounts of Magnesium salts may be hazardous and Mannitol
would therefore be preferable. Different preparations of
activated charcoal are known to produce diarrhoea (U.K.
Medicoal) or constipation (U.K. Carbomix). This should also
be taken into consideration when deciding on type and amount
or purgative. Some other charcoal preparations are poor
binders for paraquat and local poisons unit should be
consulted.
Gastric lavage must be considered within the first hour after
ingestion.
Patients may have considerable fluid loss from diarrhoea and
vomiting and an intravenous fluid infusion should be
commenced on admission. Having instituted measures to
prevent further absorption and fluid replacement the
diagnosis should be confirmed by the "spot" test for paraquat
and the prognosis assessed by the measurement of plasma
paraquat. The paraquat level should be interpreted together
with the time of ingestion on the graph attached. If the
levels are very high and the prognosis hopeless good pain
relief and terminal care are more important than heroic
attempts to save the patient. Oxygen supplements are in
general contraindicated but are appropriate in the dying
patient with severe dyspnoea. Diarrhoea from purgatives
given to clear the gut may produce further fluid loss and
supplement should be given to replace such losses. Mouth
ulceration may produce severe pain which may be helped by
mouth washes, ice-cold fluids (e.g. milk, ice-cream, lemon
mucilage), and local anaesthetic preparations. If there is
any possibility of oesophageal perforation the patient should
not be allowed to take anything by mouth until perforation
has been excluded. Secondary infection of mouth ulcers
should treated with antibiotics. Profound acidosis may occur
in the early stages due to poor tissue perfusion and should
be corrected with intravenous sodium bicarbonate.
Renal Damage
Acute renal failure may require treatment with haemodialysis
or peritoneal dialysis and if the patient survives complete
recovery of renal function occurs. The indications for
commencing dialysis are as in any another form of acute renal
failure. Although these methods are to some extent
effective at removing paraquat from the body they do not
influence the pulmonary complications.
Skin exposure
Any contaminated clothing should be removed and the skin
washed with soap and copious amount of water, taking care to
avoid abrasions.
Eye exposure
The eyes should be irrigated with running water for at least
15 minutes. An ophthalmic examination should be carried out
24 hours after exposure when the irritation is beginning to
subside and secondary infection should be prevented with a
topical antibiotic. Steroid creams will aid resolution of
granulation tissue. Blurring of vision may persist up to
three weeks due to corneal oedema.
10.2 Life supportive procedures and symptomatic treatment
Make a proper assessment of airway, breathing,
circulation and neurological status of the patient.
Maintain a clear airway.
Open and maintain at least one iv route
Administer iv fluids
Monitor vital signs
Correct hypotension as required
Monitor fluid and electrolyte balance
Monitor acid/base balance
Relieve pain as required.
An ophthalmic examination should be carried out 24 hours
after exposure when the irritation is beginning to subside
and secondary infection should be prevented with a topical
antibiotic. Steroid creams will aid resolution of
granulation tissue. Blurring of vision may persist up to
three weeks due to corneal oedema.
10.3 Decontamination
The immediate priority is to prevent any further
absorption of paraquat. Any contaminated clothing should be
removed immediately and once removed, should be washed before
re-use or burnt. The skin should be thoroughly washed in
running water and soap on two occasions. The eyes should be
irrigated with running water for at least 15 minutes.
In the first aid situation if the patient is not vomiting
give activated charcoal (100 g for adults or 2 g/kg body
weight for children or Fuller's Earth (15% slurry, 1 litre
for adults or 15 mL/kg body weight for children). Do not
give oxygen as this may potentiate harmfull superoxide
formation. Superoxides are thought to be involved in the
pathogenesis of pulmonary damage. The patient should
immediately be transferred to the nearest hospital.
10.4 Enhanced elimination
Unfortunately dialysis, forced diuresis, and charcoal
haemoperfusion are largely ineffective in that they make no
difference to outcome. The only possible exception is
prolonged haemoperfusion in a small group of patients who are
moderately poisoned with paraquat, and who develop early
renal failure. The procedure also needs to be started within
6 to 18 hrs after ingestion. As there is no conclusive
evidence of benefit we would consider haemoperfusion to be a
research tool and all cases should be carefully documented
with the cooperation of a poisons information centre.
10.5 Antidote treatment
10.5.1 Adults
There is no antidote as such available
10.5.2 Children
There is no antidote as such available
10.6 Management discussion
The management outlined above is not controversial,
however many approaches at treatment have been tried without
much success. These include superoxide dismutase,
propranolol, Vitamin E, ascorbic acid, selenium, clofibrate,
acetylcysteine, nitric oxide, magnesium sulphate and
pulmonary irradiation. Lung transplantation has also been
tried but has been successful only in one patient (Licker et
al., 1998). At present, the use of cyclophosphamide and
dexamethasone seems the most promising, in moderately
poisoned patients who are at risk of developing pulmonary
fibrosis.The effectiveness of this regime has not as yet been
proven and it should only be used in a specialist centre
Jones et al. (1999) has worked out an equation to predict the
probability of survival for any specified time (up to at
least 200 hours) and concentration.
Paraquat adsorbents
In order of preference
Type Dose
1. Activated charcoal 100 gm
(child 2 g/Kg)
2. Fullers Earth 1 liter 15% aqueous
suspension & purgative
3. Bentonite 1 liter 7% aqueous
suspension & purgative
11. ILLUSTRATIVE CASES
11.1 Case reports from the literature
Death following subcutaneous injection
NPIS 88/010456 A 24 year old woman injected paraquat liquid
concentrated subcutaneously into her left arm. Next morning
she injected herself again then went to hospital. On
admission she had a tachycardia of 130 beats/min and blood
pressure 120/80. There was a green papule at the injection
site. Chest X ray showed the lungs were clear and white blood
cell count was raised at 14.7 × 106 per litre. The
paracetamol and salicylate screens were negative, and the
serum paraquat concentration was 1300 milligrams per litre
(concentrations greater than 1000 milligrams per litre are
usually fatal). The papule at the injection site was
excised. Within 12 hours of admission kidney function began
to deteriorate, over the next 23 days there was progressive
deterioration in liver, kidney and respiratory function. She
developed widespread muscle pain, oedema, jaundice, hypoxia
and myocarditis with widespread T wave inversion. Treatment
was supportive with buprenorphine then diamorphine to control
pain. She became comatose 6 days after admission and died 2
days later.
Death following subcutaneous injection:
A case of homicidal paraquat poisoning by intramuscular
injection has been reported (Chandrasisi, 1999)
Skin exposure
NPIS 89/011455. While decanting paraquat liquid concentrate
from a large to a small container, a 46 year old man spilt it
onto his trousers soaking the scrotal region. He did not
wash the skin until 48 hours afterwards. He became
progressively dyspnoeic over the next week and went to
hospital 9 days afterwards. On admission he was cyanosed,
tachypnoeic, and auscultation showed diffuse fine bilateral
crepitations in the mid and lower lung zones. Pulse rate was
130 per minute and blood pressure 160/90 mmhg. The perineal
skin was raw, macerated and oozing pus. Arterial blood gas
analysis on air showed a pH of 7.352, PaO2 2.8 kPa, PaCO2
2.7 kPs and base excess of 3.2. On 100% oxygen arterial
blood gas analysis showed a pH of 7.443, PaO2 6.9 kPa, Pa CO2
5.0 kPa and base excess + 1.5. Serum potassium was 2.8
mmol/l, urea 25 mmol/l and creatinine 311 micromol/l. Serum
haemoglobin was 14.5 g/dl, and the white cell count was 25 ×
10/l with neutrophilia. ECG was normal and chest X ray
showed diffuse bliateral alveolar infiltrates in mid and
lower zones. Urine screen showed paraquat was present. He
was given intermittent positive pressure ventilation,
intravenous fluids and antibiotics. Renal failure on
developed on day 10 and was treated with dopamine and
haemodialysis for 24 hours until renal function. Lung
function deteriorated and he died 15 days after the accident.
Post mortem examination showed acute pleurisy with bilateral
panlobular pneumonitis.
Ingestion
NPIS 86/06961. A 45 year old man drank 2 sachets of solid
paraquat (3.00g paraquat ion) mixed with soda water and
alcohol. He was admitted to hospital 2 hours later. He
vomited within 2 hours before treatment was given, thus it
was suspected that he had taken a formulation of paraquat
containing an emetic. Some irritation of the fauces was
noticed 24 hours after ingestion. He was given a gastric
lavage and fuller's earth with a purgative 2hr 15 minutes
after ingestion and vomited a second time. Blood ethanol
concentration after 2 hours was 3162 mg/l/, and plasma
paraquat concentration at 5hrs 30mins was 1.1 mg/l.
Haemoperfusion was started 8hr 30 minutes after ingestion.
Magnesium sulphate enemas were given after 30 hours to induce
diarrhoea. Cyclophosphamide 5mg/kg/day and dexamethasone 8
mg three times daily were given for 2 weeks, with high fluid
intake and diuretics. There was transient hepatic damage
shown by raised AST, alkaline phosphatase and bilirubin, but
no evidence of renal damage. Formal lung function tests
showed a marked fall in lung volumes and gas transferance 6
weeks after the overdose. After 4 months the patient was
asymptomatic and the formal tests showed improvements in lung
function.
12. ADDITIONAL INFORMATION
12.1 Specific preventive measures
12.2 Other
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14. AUTHOR(S), REVIEWER(S) DATA (INCLUDING EACH UP-DATE), COMPLETE
ADDRESSES
Author: Dr C. Ashton and Mr N. Leahy
Poisons Unit
New Cross Hospital
Avonley Road
London SE14 5ER
United Kingdom
Date: April 1989
Reviewer: Dr N. Besbelli
Ankara
Turkey
Peer review: London, United Kingdom, September 1992
(group members: Dr N. Besbelli, Dr C.
Dell'Acqua, Dr B. Fahim, Dr T. Matainaho, Dr
B. Sener, Dr W. Temple, Dr A.N.P. van
Heijst)
Review: Prof. Ravindra Fernando
National poisons information Centre
National Hospital of Sri Lanka
Colombo 8
Sri Lanka
October 2000
Peer review: INTOX 12 Meeting, 7 - 11 November 2000
Drs J. Szajewski, C.Alonzo, R. Fernando.