Is sodium fluoroacetate (1080) a humane poison

Abstract

Sodium fluoroacetate (1080) is widely used for the control of vertebrate pests in Australia. While the ecological impact of 1080 baiting on non-target species has been the subject of ongoing research, the animal welfare implications of this practice have received little attention. Literature relevant to the humaneness of 1080 as a vertebrate pest control agent is reviewed in this paper. Previous authors have largely concentrated on the perception of pain during 1080 toxicosis, giving limited attention to other forms of distress in their assessments. Authors who suggest that 1080 is a humane poison largely base their conclusions on the argument that convulsive seizures seen in the final stages of 1080 toxicosis indicate that affected animals are in an unconscious state and unable to perceive pain. Other authors describe awareness during seizures or periodic lucidity that suggests central nervous system (CNS) disruption cannot be assumed to produce a constant pain-free state. Some literature report that 1080 poisoning in humans is painless and free of distress, but this is contradicted by other clinical studies. Using available data an attempt is made to reassess the humane-ness of 1080 using the following criteria: speed and mode of action, appearance and behaviour of affected animals, experiences of human victims, long-term effect on survivors, and welfare risk to non-target animals. It is concluded that sodium fluoroacetate should not be considered a humane poison, and there is an urgent need for research into improving the humaneness of vertebrate control methods in Australia.

Full text

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© 2007 Universities Federation for Animal Welfare
The Old School, Brewhouse Hill, Wheathampstead,
Hertfordshire AL4 8AN, UK
Animal Welfare 2007, 16: 449-458
ISSN 0962-7286
Is sodium fluoroacetate (1080) a humane poison?
M Sherley
RSPCA Australia, PO Box 265, Deakin West, Canberra 2600, Australia; Email: msherley@rspca.org.au
Abstract
Sodium fluoroacetate (1080) is widely used for the control of vertebrate pests in Australia. While the ecological impact of
1080 baiting on non-target species has been the subject of ongoing research, the animal welfare implications of this practice have
received little attention. Literature relevant to the humaneness of 1080 as a vertebrate pest control agent is reviewed in this paper.
Previous authors have largely concentrated on the perception of pain during 1080 toxicosis, giving limited attention to other forms of
distress in their assessments. Authors who suggest that 1080 is a humane poison largely base their conclusions on the argument that
convulsive seizures seen in the final stages of 1080 toxicosis indicate that affected animals are in an unconscious state and unable
to perceive pain. Other authors describe awareness during seizures or periodic lucidity that suggests central nervous system (CNS)
disruption cannot be assumed to produce a constant pain-free state. Some literature report that 1080 poisoning in humans is painless
and free of distress, but this is contradicted by other clinical studies. Using available data an attempt is made to reassess the humane-
ness of 1080 using the following criteria: speed and mode of action, appearance and behaviour of affected animals, experiences of
human victims, long-term effect on survivors, and welfare risk to non-target animals. It is concluded that sodium fluoroacetate should
not be considered a humane poison, and there is an urgent need for research into improving the humaneness of vertebrate control
methods in Australia.
Keywords:1080, animal welfare, bait, poison, sodium fluoroacetate, vertebrate pest
Introduction
Compound 1080 is a proprietary name for the chemical
compound sodium fluoroacetate (Peters 1952). Following
ingestion, 1080 is metabolised to fluorocitrate which
inhibits cellular energy production by inhibiting enzymes
responsible for the conversion of citrate and succinate in the
tricarboxylic acid cycle (Peters 1952; Fanshier et al 1964).
A range of other cellular enzymes are also affected by 1080,
but the relevance of these to toxicosis is not well understood
(Mehlman 1967; Godoy & del Carmen Villarruel 1974;
Taylor et al 1977; Kirsten et al 1978).
In Australia 1080 is widely used in baiting programmes for
the control of vertebrate pest species (Table 1) and as such
has both agricultural and wildlife-management applications
(Biodiversity Group Environment Australia 1999;
Government of Western Australia 2002; Williamson &
Bloomfield 2003). The popularity of 1080 as a vertebrate
pest control agent is based on a range of factors including its
low cost, potency, relative ease of use (particularly in pre-
prepared baits), low risk of persistence in the food chain,
and low risk of wider environmental contamination
(McIlroy 1996). It is widely regarded by users as efficient,
target specific and humane (Government of Western
Australia 2002; Williamson & Bloomfeld 2003).
Nevertheless, the use of 1080 baits is the subject of vigorous
debate in Australia, with concerns over the impact on non-
target animals including rare or endangered native
Australian species, domestic animals (livestock and
working dogs) and companion animals. More recently,
public concerns regarding the humaneness of 1080 baiting
have also been raised. While non-target impacts have been
the ongoing subject of research (McIlroy et al 1986; King
1989; McIlroy & Gifford 1991; Dexter & Meek 1998;
Fairbridge et al 2000, 2003; Glen & Dickman 2003 a,b;
Kortner et al 2003), the animal welfare impacts of
1080 baiting are largely unknown. Only a few publications
have previously considered the humaneness of 1080 and the
welfare of target or non-target animals as a wildlife manage-
ment issue (Bell 1972; Morgan 1990; Saunders et al 1995;
Gregory 1996; McIlroy 1996; Williams 1996; Marks et al
2000; Potter et al 2006).
Publications that have briefly addressed 1080
humaneness
In his review of brushtail possum (Trichosurus vulpecula)
control in New Zealand, Bell (1972) contrasts 1080 with
other poisons, stating that arsenic trioxide and strychnine
alkaloid “appear to bring about exceedingly painful physio-
logical reactions in the animal, more so than does sodium
cyanide or sodium fluoroacetate”. No details are given
regarding the signs of poisoning during the toxicosis
resulting from these compounds and pain was the only
aspect of welfare considered.
Universities Federation for Animal Welfare Science in the Service of Animal Welfare

450 Sherley
Morgan (1990) argues that 1080 is a relatively humane
method of control for possums, based on the finding that
possums were found dead in the morning at the location
where they were observed the previous night. However,
this provides little insight into the progression and nature
of toxicosis in this species, and the author provides no
explanation of how this observation contributes to a
robust assessment of humaneness. A range of signs poten-
tially indicative of pain or distress, including behavioural
changes, deteriorating co-ordination, retching, vomiting,
rapid breathing, lack of response to disturbances and
shivering, were all described in this study. As observa-
tions were limited largely to the first few hours after the
bait was eaten, later signs of poisoning may also have
been overlooked.
Saunders et al (1995) suggest that the evidence regarding
the humaneness of 1080 in the red fox (Vulpes vulpes) is
ambiguous given that anaesthetised dogs (Canis lupus
familiaris) poisoned with 1080 show evidence of extreme
CNS stimulation (Chenoweth & Gilman 1946). It is implied
that the behaviour of unanaesthetised dogs poisoned with
1080 does not, therefore, necessarily indicate pain or
suffering. Assuming that the comparison between fluoroac-
etate poisoning in dogs and foxes is valid (and there is some
support for this [Marks et al 2000]) there are still some
problems with this line of reasoning. Chenoweth and
Gilman (1946) do not clearly define the nature of the CNS
stimulation they observed, nor do they make any attempt to
correlate the signs observed in anaesthetised dogs (pento-
barbital, 35 mg kg–1) with behavioural patterns in unanaes-
thetised dogs during 1080 toxicosis. The relevance of
findings in anaesthetised animals is unclear given that
pentobarbital anaesthesia substantially alters both the signs
of fluoroacetate poisoning and the mechanism of death in
cats (Felis catus; Chenoweth & Gilman 1946) and the EEG
formations recorded in dogs (Chenoweth & St John 1947a).
In the absence of a study where the effects and interactions
of pentobarbital in 1080 toxicosis are controlled, it is not
possible to draw conclusions about the behaviour of
unanaesthetised dogs from findings in anaesthetised ones.
McIlroy (1996) attempts to assess the humaneness of
1080 relative to other lethal agents used in vertebrate pest
control. He states that death from cyanide poisoning is
painless, that death from phosphorus is not, but that the
evidence regarding 1080 is equivocal. He considers aspects
relevant to welfare assessment other than pain, including the
speed of action, the presence or absence of cumulative
effects and the risk to non-target species (in terms of relative
toxicity, the availability of antidotes, degradation in corpses
and degradation in the external environment). Unfortunately,
there is a lack of detail on how these categories are defined
and the categorisation is largely subjective.
Marks et al (2000) differ from earlier authors in that their
research is based on the premise that the humaneness of
1080 baits can be improved. They propose that because
CNS disturbances confuse the objective assessment of the
perception of pain in foxes poisoned with fluoroacetate,
baits should be supplemented with anxiolytic and/or
analgesic compounds in order to minimise the potential for
pain and distress. They note that the early stages of
1080 toxicosis may be associated with suffering, even if
pain and distress are absent in the late stages of toxicosis
once severe CNS dysfunction has developed. Signs of
poisoning that were commonly observed in Marks et al’s
(2000) study of foxes that could be associated with pain or
distress include retching, manic running, tail twitching,
clonospasm, tetanic spasms, and collapse and paddling of
all four limbs. Overall, the period during which there were
overt signs of poisoning in foxes dosed with 1080 typically
lasted from one to two hours. The supplementation of
1080 with diazepam (10 mg kg–1) significantly extended the
duration of this period, but also markedly reduced the
intensity of the signs of poisoning. Marks et al (2000) also
cite the experiments of Chenoweth and Gilman (1946) as
evidence that dogs are unlikely to be conscious during the
convulsions that occur in the latter stages of 1080 toxicosis.
As discussed above, it is not possible to draw such a conclu-
sion from these experiments.
Recently, Potter et al (2006) identify the humaneness of
vertebrate pesticides as an area of current concern. They
describe three discrete stages of 1080 poisoning in stoats
(Mustela erminea); a latent phase lasting on average 1 h,
1 min (range 29 min–2 h 7 min) during which behaviour
appears normal, a period characterised by ataxia and hyper-
activity lasting on average 26 min (range 2 min–1 h
40 min), and a period of recumbency with muscular spasms
and non-responsiveness to stimuli lasting on average 58 min
(range 16 min–2 h). Of these, the ataxic/hyperactive stage is
identified as most likely to be associated with pain or
distress, while it is argued that the latent period is likely to
be associated with minimal pain or distress given the lack of
© 2007 Universities Federation for Animal Welfare
Table 1 The use of 1080 for vertebrate pest control in
Australian states and territories.
* Bennett’s and rufous wallabies. ** Also used experimentally for
the control of pigs, cats, goats, agile wallabies and sulphur-crested
cockatoos.
Data collected from the Report to the Vertebrate Pests
Committee on 1080 Policies, Practices and Procedures in
Australia and New Zealand from the 1080 Working Group of the
Vertebrate Pests Committee, August 2001.
State or territory Target animals
Australian Capital Territory Foxes, rabbits
New South Wales Foxes, rabbits, pigs, dogs, dingoes
Northern Territory Foxes, dingoes
Queensland Foxes, rabbits, pigs, dogs, dingoes,
rats
South Australia Foxes, rabbits, dogs, dingoes
Tasmania Rabbits, wallabies*, brushtail
possums, cats
Victoria Foxes, rabbits, pigs, dogs, dingoes
Western Australia** Foxes, rabbits, dogs, dingoes

Is sodium fluoroacetate (1080) a humane poison? 451
behavioural indicators at this time (although it is noted that
pain and anxiety have been described in humans at the
equivalent stage of fluoroacetate poisoning [Chi et al 1996,
cited in Potter et al 2006]). Potter et al report that para-
aminopropiophenone (PAPP) kills stoats within 1 h (Fischer
et al 2005, cited in Potter et al 2006) but they provide no
further detail or comparison with 1080 toxicosis.
Previous reviews of 1080 humaneness
Two publications focus primarily on a consideration of the
humaneness of 1080 as a vertebrate control agent
(Gregory 1996; Williams 1996) and both were published
as part of the proceedings of a meeting on humaneness and
vertebrate pest control.
Williams (1996) considers the effects of 1080 on European
rabbits (Oryctolagus cuniculus), providing a detailed
description of the signs of poisoning and the proposed
mechanism of toxicity in this species on the basis of earlier
literature. A “lethargic” but conscious state lasting from
2–12 h (depending on dose) is described, during which
poisoned rabbits stop feeding, develop obvious weakness
and lie with the head to one side. Similar findings were
reported by Chenoweth and Gilman (1946), Foss (1948) and
Meldrum (1957). Williams (1996) concludes that this
period is not associated with pain as indicators of pain in
rabbits described by other authors (hypermotility of the gut
and teeth grinding) are absent. However, given the
extensive motor disturbance described, and the possibility
of other neurological involvement, the relevance of these
behavioural indicators to 1080 toxicosis is unclear. There is
no discussion of potential distress or other welfare concerns
associated with the prolonged period of weakness and
immobility described (eg issues relating to increased risk of
predation, decreased access to food and water, or reduced
ability to thermoregulate).
Williams (1996) also describes a convulsive period
occurring later during toxicosis and concludes that convul-
sions are not associated with pain, as laboratory data
suggests that these occur during a state of unconsciousness,
and reflect rapid cerebral anoxia following immediately
after ventricular fibrillation. Periods of consciousness
following convulsions are described, where some rabbits
were observed to re-commence feeding, and this was argued
by Williams (1996) to be evidence that significant suffering
was not experienced at this time. The observation that
rabbits that survived a sub-lethal dose of 1080 were
anorexic for up to 24 h post exposure (Hutchens et al 1949,
cited in Williams 1996) suggests that the possible existence
of adverse animal welfare impacts should not be discounted.
Gregory (1996) discusses the humaneness of
1080 poisoning in a range of species on the basis of reports
in earlier literature. He has been widely cited in government
publications in Australia (eg Biodiversity Group
Environment Australia 1999; Government of Western
Australia 2002; Williamson & Bloomfield 2003). Gregory
(1996) breaks down his discussion according to animal
groups, first discussing the effects of fluoroacetate on herbi-
vores, then carnivores. This division is based on a broad
generalisation that herbivorous animals die of ventricular
fibrillation while carnivores show extensive involvement of
the central nervous system, dying as a result of respiratory
depression, and omnivores exhibit a combination of signs
(Egekeze & Oehme 1979a). This argument grew out of
early research indicating that animals can be placed into
four categories on the basis of the signs they display during
fluoroacetate poisoning (Chenoweth & Gilman 1946).
However, a more recent review demonstrates that there are
substantial similarities in the signs of fluoroacetate poisoning
across a wide range of vertebrate species (Sherley 2004).
Herbivores
Gregory (1996) describes the main signs of 1080 toxicosis
in herbivores as lethargy and ataxia (inco-ordination), with
some developing generalised convulsive seizures. He
implies that these seizures reflect cerebral anoxia resulting
from the loss of blood supply to the brain during ventric-
ular fibrillation, and this is supported by Chenoweth and
Gilman (1946). However, little attention is given to what
may be prolonged periods of signs and symptoms before
the onset of ventricular fibrillation. Neither does he
consider the possible long-term consequences of a period
of cerebral anoxia for animals that recover from a sub-
lethal toxicosis (Pridmore 1978). Gregory (1996) briefly
considers the issue of distress, describing anecdotal
evidence that convulsing rabbits “did not unduly disturb
nearby rabbits” and that these “did not seem to associate
(convulsions) with fear or pain”, however, this appears
speculative and subjective. Potentially painful or
distressing signs of fluoroacetate poisoning in herbivores
have been described in other literature, including; tremor,
hypersensitivity to nervous stimuli, muscular spasms,
myotonic convulsions, muscular weakness, partial
paralysis and respiratory distress (Chenoweth & Gilman
1946; Quin & Clark 1947; Foss 1948; Robison 1970;
McIlroy 1982a; Schultz et al 1982).
Carnivores
Gregory (1996) describes dogs poisoned with 1080 as
hyperexcitable, with abrupt bouts of barking preceding
repeated convulsions interspersed with periods of
normality. In contrast, he argues that all dogs experiencing
pain will appear quiet and less alert, possibly lying still and
adopting an abnormal posture. It is purely speculative to
suggest that the signs of 1080 toxicosis rule out the possi-
bility of pain. Other authors (Marks et al 2000) argue that
disruption of the CNS resulting from 1080 poisoning is
likely to alter behavioural patterns normally used in
assessing pain, therefore making such observations
difficult to interpret.
Dogs affected by fluoroacetate have been described by other
authors as running uncontrollably (sometimes into rigid
objects), retching and vomiting, and experiencing a range of
nervous disruptions including twitching of the legs, tail,
eyelids, and eyes, and prolonged involuntary contractions of
their muscles (Chenoweth & Gilman 1946; Chenoweth & St
Animal Welfare 2007, 16: 449-458

452 Sherley
John 1947b; Foss 1948; Harris 1975). People who have
ingested 1080 frequently report abdominal pain at the same
time as experiencing signs of poisoning commonly attrib-
uted to poisoned dogs including verbosity (unusual vocali-
sation), agitation, and vomiting (Chi et al 1996) and have
also reported pain in association with muscular spasms. In
addition to any pain resulting directly from 1080 toxicosis,
any injuries sustained by running into rigid objects, or
during fits, have the potential to cause pain either at the time
or during the lucid intervals between fits that are often
described (Chenoweth & Gilman 1946; Chenoweth & St
John 1947b; Foss 1948; Gajdusek & Luther 1950; Reigart
1975; McIlroy 1982a; Schultz et al 1982; Chung 1984;
Robinson et al 2002).
Gregory (1996) argues that the early signs of 1080 poisoning
in dogs (barking and hyperactivity) are associated with a
lack of awareness of their predicament or surroundings, and
are not, therefore, distressing. This interpretation is subjec-
tive and does not agree with signs and symptoms reported in
human cases (Chi et al 1996). Moreover, the EEG data that
Gregory uses to support a potential lack of awareness during
this period (Chenoweth & St John 1947b) was obtained from
dogs that had been paralysed with curare before being
poisoned, and could not therefore be directly correlated with
physical signs. Petit mal seizures that Gregory (1996) cites
as indicative of loss of contact with the environment were a
rare outcome of Chenoweth and St John’s (1947b) work and
followed direct injection of fluoroacetate into the lateral
ventricles of the brain. Ward (1947) obtained occasional petit
mal-like EEG recordings following intravenous administra-
tion of fluoroacetate, but again this was an uncommon
finding. Chenoweth and St John’s (1947b) finding that EEG
disturbances similar to grand mal convulsions of epilepsy
were common in poisoned dogs could be interpreted as
supportive for periods of unconsciousness occurring during
fitting, yet another author indicates that in his experiments a
dog poisoned with fluoroacetate was conscious during a
period of clonic-tonic convulsions (Foss 1948). In quoting
Kun’s (1982) statement that convulsive seizures are always
associated with unconsciousness, Gregory (1996) ignores
the fact that focal convulsions (those affecting only part of
the brain and body) are not typically associated with uncon-
sciousness. Even generalised convulsions are not always
associated with loss of consciousness; patients remain fully
conscious during the generalised tonic spasms associated
with strychnine poisoning (Aggarwal & Prakash Wali 1997).
Both localised muscle spasms and tonic convulsions are
frequently described in 1080 toxicosis prior to the onset of
clonic-tonic convulsions (reviewed in Sherley 2004). It is
therefore inappropriate to suggest that all convulsive
episodes observed in dogs poisoned with 1080 are gener-
alised seizures, and that they are reliably associated with
unconsciousness and a pain and distress free state.
Gregory (1996) argues that 1080 toxicosis may also be
likened to hyperinsulinism because in each case there is a
depletion of cellular energy. Conditions affecting aspects of
cellular energy metabolism do not necessarily have the
same symptoms. Cyanide inhibits cellular energy metabo-
lism by blocking the electron transport chain, and arsenite
(like fluoroacetate) inhibits energy metabolism by blocking
the citric acid cycle (at multiple sites), yet the human
symptoms of arsenite poisoning (violent gastroenteritis,
burning oesophageal pain, vomiting, and watery or bloody
diarrhoea containing shreds of mucus) differ substantially
from those of cyanide (dizziness, rapid respiration,
vomiting, flushing, headache, drowsiness, circulatory
collapse, and unconsciousness) or 1080 poisoning
(vomiting, excitability, tonic-clonic convulsions, irregu-
larity of the heartbeat and respiration, exhaustion, coma,
and respiratory depression) (Dreisbach 1983). The cause of
fluoroacetate’s toxic effect is probably a combination of the
depletion of energy at a cellular level, an accumulation of
citrate in the affected tissues (Foss 1948), and other
resulting electrolyte disturbances including hypocalcaemia
and hypokalaemia (Chi et al 1996).
How should humaneness be defined?
A major problem with previous considerations of the
humaneness of 1080 poisoning, has been the absence of
agreed criteria for assessing humaneness. Previous authors
have primarily focused on the perception of pain, particu-
larly during the late stages of poisoning, with limited
consideration of other aspects of welfare such as distress.
Mason and Littin (2003) assessed humaneness of rodent
control by: 1) speed of action; 2) mode of action; 3) the
appearance and behaviour of affected animals; 4) the expe-
riences of human victims; 5) the long-term effect on
survivors, and, 6) the welfare risk to non-target animals.
Using available data, these categories are applied in an
attempt to investigate the humaneness of 1080 toxicosis.
Speed of action
There is a lag-time between the ingestion of 1080 and the
onset of obvious signs of toxicosis. The duration of this lag
period, and the time from exposure until death, vary signif-
icantly between vertebrate species (McIlroy 1986; Table 2),
with some animals dying within minutes and others
surviving for several days. Data regarding the time from
exposure until signs of toxicosis or death has typically been
published as part of studies designed to determine the
median lethal dose of 1080. If the duration of the toxicosis
is dependent upon the dose rate of 1080, the lower doses
used in many of these studies may not accurately reflect the
outcome that can be expected from baits that deliver lethal
doses. Evidence regarding the relationship between dose
and effect in 1080 toxicosis is variable. Human poisoning
cases appear to vary in the length of time elapsed before the
onset of neurological or cardiac involvement, and in the
severity of signs and symptoms, depending on dosage
(Gajdusek & Luther 1950; Brockman 1955; Reigart 1975;
Peters et al 1981; Chung 1984; Robinson et al 2002).
Chenoweth and St John (1947b) also reported a strong
effect of dose size on the signs of poisoning in dogs.
Another study on the effects of 1080 on herbivores demon-
strated that the time from exposure until death is positively
© 2007 Universities Federation for Animal Welfare

Is sodium fluoroacetate (1080) a humane poison? 453
related to dose for some species but not for others (McIlroy
1982a). There may be considerable variation between indi-
viduals of the same species given equal doses of poison, in
the time from exposure to first signs of toxicosis, the time
from exposure until death, and in the signs of toxicosis
(Schultz et al 1982).
Despite efforts to ensure that baits contain a lethal dose, in
the field there is limited control over the intake of poison.
The initial concentration of poison in baits can be
controlled, but environmental conditions affect the rate of
degradation and loss of 1080 over time (McIlroy et al 1988;
King et al 1994; Bowen et al 1995). The number of baits, or
Animal Welfare 2007, 16: 449-458
Table 2 The median lethal dose and progression of fluoroacetate toxicosis in a range of vertebrate species.
Only a few of the species for which toxicology data are available have been included (McIlroy 1981; 1982a, b; 1983; 1984; 1985; Meldrum
1957; Marks et al 2000; Robison 1970). The median lethal dose is expressed as milligrams of fluoroacetate per kilogram bodyweight (mg
kg-1). Time until signs of poisoning and time from exposure until death are given in hours. * Australian target species. 1Data for V. vulpes
were obtained using a known lethal dose (0.5 mg kg-1) of fluoroacetate. All other values were obtained during toxicology studies, hence
a range of doses were used.
Animal LD50 (mg kg–1) Time until signs (h) Time until death (h)
Mammals
Marsupuial herbivores
Brushtail possum (Trichosurus vulpecula)* 0.47–0.79 1.0–19.8 5.0–97.0
Bennett’s wallaby (Macropus rufogriseus)* > 0.21 < 16.9–23.2 8.9–38.9
Southern hairy-nosed wombat (Lasiorhinus latifrons) 0.21 5.1–39.4 16.2–59.3
Eastern grey kangaroo (Macropus giganteus)∼0.1–0.35 < 13.2–23.9 20.9–62.1
Eutherian herbivores
Horse (Equus caballus) 1.0 ∼1.5–2.0 6.0–10.5
Sheep (Ovis aries) 0.5 6.2–37.6 9.6–61.6
Rabbit (Oryctolagus cuniculus)* 0.34–0.50 1.1–10.1 3.0–44.3
Cattle (Bos taurus) 0.39 1.5–29.0 1.5–29.3
Marsupial omnivores/carnivores
Northern quoll (Dasyurus hallucatus) 5.66 3.0–361.9 10.0–450.7
Tasmanian devil (Sarcophilus harrisii) 4.24 0.3–1.6 2.6–22.3
Eastern quoll (Dasyurus viverrinus) 3.73 0.2–2.4 < 2.0–63.2
Stripe-faced dunnart (Sminthopsis macroura) 0.95 1.7–4.0 3.4–13.1
Eutherian omnivores/carnivores
Feral pig (Sus scrofa)* 1.0 1.9–47.3 2.8–80
Cat (Felis catus)* 0.40 1.0–5.6 20.7–21.0
Dingo (Canis lupus dingo)* 0.11 4.8–14.6 5.3–10.8
Red fox (Vulpes vulpes)* 0.12 4.115.51
Rodents
House mouse (Mus musculus) 8.33 1.3–2.8 2.2–68.3
Grassland melomys (Melomys burtoni) 2.65 0.6–1.9 14.1–205.8
Bush rat (Rattus fuscipes) 1.13 0.6–5.1 0.7–24.8
Black rat (Rattus rattus)* 0.76 0.8–27.8 2.4–36.5
Reptiles and Amphibians
Blotched blue-tongued lizard (Tiliqua nigrolutea) 336.4 13.3–160.9 14.4–522.5
Bearded dragon (Pogona vitticeps) < 110 15.2 14.9–24.2
Spotted grass frog (Limnodynastes tasmaniensis)∼60 12.9–77.5 36.8–98.3
Gould’s monitor (Varanus gouldii) 43.6 24.2–141.2 66.5–292.5
Birds
Emu (Dromaius novaehollandae)∼278 1.5–5.8 124
Sulphur-crested cockatoo (Cacatus galerita) 3.46 9.9–17.7 9.0–73.7
Australian magpie (Gymnorhina tibicen) 9.93 3.6–10.7 5.7–59.5
Wedge-tailed eagle (Aquila audax) 9.49 1.0–60.0 8.0–158.5

454 Sherley
amount of bait material, taken by individuals cannot be
completely controlled, hence the speed of onset and time to
death may be variable. Some baits may be taken by non-
target animals for which the median lethal dose differs from
that of the target or with substantially different body-
weights. In the primary target species in Australia, the time
from 1080 exposure until death ranges from 2.4–80 h, given
a range of doses (Table 2) and may indicate that time to
death may be highly variable in the field, given the
constraints on delivering accurate, lethal doses with
predictable lethal outcomes. In a highly susceptible species
(eg the red fox) animals given a known lethal dose showed
no overt signs of poisoning for approximately 4.05 (± 0.86)
h; P< 0.05 with 1.57 (± 0.46) h; P< 0.05) from first visible
signs until death (Marks et al 2000).
Mode of action
In addition to energy depletion (Peters 1952; Fanshier et al
1964) and resulting cellular damage, 1080, by blocking the
conversion of citrate in the tricarboxylic acid cycle, also
results in the build-up of citric acid in the tissues and blood,
which leads to a metabolic acidosis (Peters 1952). This
build-up of citrate, along with associated electrolyte distur-
bances (Chi et al 1996), is the likely cause of some of the
signs and symptoms of 1080 toxicosis (DuBose 2005;
Singer & Brenner 2005). It may be possible to adapt baits in
order to ameliorate some of the signs and symptoms
resulting from 1080 poisoning, without affecting lethality,
but to date there has been little published research in this
area (Marks et al 2000).
Appearance and behaviour of affected animals
Poisoned animals are sometimes divided into the four cate-
gories proposed by Chenoweth and Gilman (1946): class I,
where the main effects are on the heart; class II, where both
the heart and central nervous system are involved; class III,
where the main effect is on the nervous system; and class
IV, where there is an atypical response typified by slow,
shallow breathing and a slow heart-rate. As noted above,
this system of categorisation belies substantial similarities
in the signs of fluoroacetate poisoning across a wide-range
of vertebrate species (Sherley 2004). It also fails to take into
account the sometimes substantial variation observed in
individuals of a single species (eg Schultz et al 1982). In
general, animals that have been poisoned with fluoroacetate
initially display a range of signs including lethargy, retching
and vomiting, trembling, faecal and urinary incontinence,
unusual vocalisations, hyperactivity, excessive salivation,
muscular weakness, unco-ordination, hypersensitivity to
nervous stimuli, and respiratory distress. Localised nervous
signs including tail twitching, twitching or jerking of limbs,
twitching of facial muscles, nystagmus, and tetanic
seizures, are common, and may progress to generalised
convusions. These begin typically as tetanic convulsions
before taking on a clonic-tonic form (reviewed in Sherley
2004). Generalised seizures typically occur cyclically, with
periods of lucidity in-between (Chenoweth & St John
1947b; Foss 1948; Gajdusek & Luther 1950; McIlroy
1982a; Schultz et al 1982). Death may occur either during
convulsions or during these lucid periods (Foss 1948).
Several of the signs of toxicosis listed above are potentially
painful and/or distressing.
Experiences of human victims
Several cases of 1080 poisoning in humans have been
reported, although few address patient perceptions, most
focusing on the overt signs of poisoning. This partly reflects
a rapid deterioration in the condition of most patients by the
time they have obtained medical assistance. Anxiety, irri-
tability, verbosity, agitation, confusion, nausea, vomiting,
faecal incontinence, tetanic spasms, cardiac irregularity,
gradual loss of alertness culminating in coma, epileptiform
convulsions with periods of lucidity between convulsions,
and partial paralysis are all commonly described in human
fluoroacetate-poisoning cases (reviewed in Sherley 2004).
Gregory (1996) argues that people do not experience pain,
referring to three case studies (Williams 1948; Gadjusek &
Luther 1950; Reigart 1975). Of these, Gadjusek and Luther
(1950) report on a toddler who was brought to hospital
already in a comatose state and hence unable to communi-
cate any pain he may previously have experienced. Reigart
(1975) describes an unusually mild case of poisoning in an
eight month old girl who, given her age, was similarly
unable to verbally report pain (she was described by the
author as anxious, agitated and irritable, but not distressed).
Williams (1946) reported that after accidentally inhaling
1080 powder he experienced immediate sensations of
tingling and numbness at the site of exposure but did not
notice any pain during the period of onset. He experienced
what he described as a “sour stomach”, and suffered from
headache for a period of five days following exposure.
Other human case studies have reported pain, including
epigastric pain, headache, and localised pain associated
with muscular spasms (Brockman et al 1955; Peters et al
1981; Chung 1984). A more recent survey by Chi et al
(1996) found that 26% of patients reported abdominal pain
while 74% experienced nausea and vomiting, 29% experi-
enced diarrhoea, 29% reported feelings of agitation and
21% reported respiratory distress.
Long-term effect on survivors
Sub-lethal amounts of fluoroacetate are rapidly metabolised
and excreted by affected animals and there is little evidence
of harm resulting from long-term, low-level exposure to
fluoroacetate (Eason & Turck 2002). Complete recovery in
survivors of sub-lethal 1080 toxicosis may take from a few
hours to several days (Chenoweth & Gilman 1946; McIlroy
1981, 1982a, 1983). Neurological complications including
weakness, convulsions and partial paralysis (especially of
the hind limbs) are common and may persist for prolonged
periods (Gajdusek & Luther 1950; Chenoweth & Gilman
1964; McTaggart 1970; McIlroy 1981, 1982a, 1983;
Schultz 1982). For example, both feral pigs (Sus scrofa) and
frogs have been described as remaining partially paralysed
24 hours after exposure to fluoroacetate (Chenoweth &
Gilman 1964; McIlroy 1983). Animals may have an
extruded tongue and/or penis during generalised convul-
sions, and have been described as moving significant
© 2007 Universities Federation for Animal Welfare

Is sodium fluoroacetate (1080) a humane poison? 455
distances while convulsing (McIlroy 1981; Marks et al
2000; Potter et al 2006), thus there may be an opportunity
for serious injuries to occur during fitting. Convulsions
may occasionally be severe enough to cause physical
injury themselves. For example, in a study of fluoroacteate
poisoning in rats (Rattus rattus; Egekeze & Oehme
1979b), one rat convulsed so severely that blood began to
drip from its eyes.
One of the most detailed descriptions of recovery from
1080 poisoning is McTaggart’s (1970) report of a child
who ingested rabbit bait: Ten days after ingesting 1080,
the boy began to recover during hospitalisation. He was
able to keep his eyes open, and to appreciate some
movement, but had marked hypertonicity of all limbs with
frequent spasms of his arms and legs. At this time he was
incapable of spontaneous movement, and remained unable
to feed himself for a full two weeks after regaining
consciousness. Twenty-four days after he ingested 1080,
the boy had regained some range of movement in his arms
and was able to recognise familiar people and objects. Ten
years later there was evidence of mental retardation with a
verbal IQ of 65, he was still unable to walk without
crutches, and suffered from tetraplegia, hypertonicity of
all limbs, cogwheel rigidity of the wrists, moderate to
severe cortical blindness, divergent squint, and epilepsy. It
is likely that the mental retardation was the result of brain
damage caused by anoxia during periods of fitting
(Pridmore 1978), although there is evidence of brain
damage resulting directly from fluoroacetate poisoning
(Trabes et al 1983). Other patients have experienced a
similar prolonged recovery period (5–6 days) (Gajdusek &
Luther 1950; Robinson et al 2002) with complete eventual
recovery. Pneumonia is a frequent complication of human
1080 poisoning cases (Williams 1948; Brockman et al
1955; Pridmore 1978; Ramirez 1986). While these infec-
tions may reflect hospital intervention, it is also possible
that infection is promoted because of the increased respi-
ratory secretions typical of 1080 exposure (Chenoweth &
Gilman 1946; Quin & Clark 1947; Brockman et al 1955;
McIlroy 1981, 1982a, 1983, 1984, 1985).
Welfare risk to non-target animals
A wide range of vertebrate species are susceptible to fluo-
roacetate poisoning, including eutherian and marsupial
mammals, birds, reptiles and amphibians (reviewed in
Sherley 2004) however, the median lethal dose varies
substantially between species, with canids generally the
most sensitive, followed by other carnivores, then herbi-
vores, birds, and finally reptiles and amphibians (McIlroy
1986; Table 2). In some areas of northern and western
Australia fluoroacetate is produced naturally by native
vegetation and some local populations of native animals
have co-evolved a tolerance to this poison that sometimes
greatly exceeds that found in conspecifics in eastern
Australia (McIlroy 1982a; Twigg 1994).
Given that all vertebrate species are potentially susceptible
to 1080 poisoning in a dose-dependent manner, the risk to
non-target species during 1080 baiting is determined by risk
of exposure to 1080 during baiting and the hazard that
1080 poses after exposure. These factors are influenced by
the target specificity of the method used to deliver the
poison, the dose of 1080 used in the bait and the amount
consumed, the comparative median lethal dose for the target
species compared to likely non-target species and the
relative bodyweight of the non-target species.
In Australia a wide range of strategies are used to limit the
exposure of non-target species of this poison applied to baits
including (from Sharp and Saunders undated; Biodiversity
Group Environment Australia 1999; Government of
Western Australia 2002; Williamson & Bloomfield 2003):
• Consideration of the size, colour, material and placement
of baits so that non-target species are less prone to discover
them.
• The use of tough, dried meat baits for canids.
• The use of large baits containing a precisely determined,
known lethal dose for canids.
• Wide dispersal of baits to minimise caching by canids.
• The burying of baits intended for canids.
• Timing of baiting campaigns to avoid periods when food
sources for most non-target species are scarce.
• Pre-feeding to maximise bait uptake in the target species.
• The use of dyes to reduce attractiveness of baits to birds.
• The use of bait refuges that allow bait consumption by
rabbits but exclude many non-target species.
• The regular removal of uneaten baits, and removal of the
carcasses of dead rabbits during rabbit baiting campaigns.
Saunders et al (1995) argues that the relative sensitivity of
foxes to 1080 is an important advantage of 1080 as it
improves the target-specificity of lethal baiting. Yet many
other vertebrate pests against which 1080 baits are used in
Australia have similar sensitivities to 1080 as other non-
target species (Table 2). Furthermore, as foxes are rela-
tively large in comparison with some non-target species,
those species for which the median lethal dose is compar-
atively high may still be at risk if they have a substantially
lower bodyweight (McIlroy et al 1986). Although the risk
of death may be lower for species with a high tolerance to
1080 and/or a large bodyweight, a sub-lethal dose can
have impacts upon the welfare of animals that survive, as
previously discussed.
Buried predator baits can be excavated and consumed by
native rats, southern brown bandicoots (Isoodon obesulus;
Fairbridge et al 2000), brush-tailed phascogales
(Phascogale tapoatafa; Fairbridge et al 2003) and quolls
(Dasyurus spp) (Glen & Dickman 2003a,b). A reduction in
the abundance of Antechinus spp (small, carnivorous,
mouse-like mammals native to Australia) after 1080 trail-
baiting for wild dogs has been reported (McIlroy 1982c).
The use of poison meat baits in urban and semi-urban areas
is inappropriate because of the risk associated with bait
movement and accidental poisoning of domestic animals
(Meenken & Booth 1997; Van Polanen Petal et al 2001). A
study of 1080 baiting for wild dogs in south-eastern
Animal Welfare 2007, 16: 449-458

456 Sherley
Australia found that approximately 45% of uncoloured,
unburied, fresh-meat baits, and 20% of green baits, was
taken by birds. Less than 10% of either bait type was taken
by the target species over an 18-day period (McIlroy et al
1986). The M-44 ejector is an alternative means to deliver
toxicants to foxes and dogs as only larger species capable
of pulling a lure with enough force to trigger the ejection
of toxicant will be exposed (Marks et al 2004). The device
is estimated to exclude 26/31 mammals that may
otherwise be exposed to conventional meat baits that have
toxicants directly injected into them (Marks & Wilson
2005). Given the large concentrations of 1080 required to
achieve a lethal outcome in feral pigs, McIlroy (1983)
estimated that of 40 non-target species likely to consume
pig baits, all but one could consume enough bait to be
poisoned. In south-eastern Australia 35 endemic mammals
are considered to be capable of consuming meat baits used
for fox and wild dog control and being exposed to the
toxicants they contain (Marks 2001).
Regardless of all possible care taken with bait preparation
and deployment, there is a potential risk to a range of non-
target species of using 1080 baits. It is appropriate that the
welfare risks of baiting practices for non-target species are
considered as a part of a general assessment of the
humaneness of 1080 baiting.
Conclusions
Previous assessments of the humaneness of 1080 have
failed to adequately address welfare issues such as distress.
They focus on the difficulties surrounding the interpretation
of pain states in the late stages of poisoning, with little
regard for earlier stages of toxicosis. The extensive CNS
disruption in the late stages of 1080 poisoning poses a
dilemma as abnormal electrical activity in the brain makes
judgements regarding consciousness and perception
difficult to make, and CNS involvement in the toxicosis
may alter behavioural indicators of pain and distress. As the
involvement of the CNS is progressive, an assessment of
humaneness thus becomes more difficult to make as
poisoning progresses.
In the initial stages of 1080 poisoning, animals display a
range of signs that potentially cause them distress, or are
indicative of distress. Conscious human patients who have
ingested 1080 frequently report pain and anxiety at this
time. A majority of species develop nervous involvement
including inco-ordination, partial paralysis, and tetanic
convulsions (rigid contractions of the muscles). The
potential for suffering is probably greatest during this
period of toxicosis. In some species neurological involve-
ment may further progress to generalised convulsions that
are typically cyclic with periods of awareness between fits.
The degree of awareness during fits is difficult to assess but
at least one author indicates that some animals remain
conscious during fitting (Foss 1948). Overall, the period
from ingestion of 1080 to death can range from less than an
hour to several days, with a similarly wide-ranging sympto-
matic period. Survivors may suffer from partial paralysis or
other nervous conditions for a period of several days before
they fully recover and permanent neurological damage is a
possible outcome. The extent of sub-lethal debilitation that
results from 1080 baiting programmes is unknown. Apart
from the possibility of pain and distress occurring in the
initial stages of poisoning, or convulsive episodes, there are
important welfare concerns associated with prolonged
periods of repeated convulsions. Animals may experience
confusion and distress during the onset of generalised
convulsions before the entire cortex has become involved
(Chenoweth & St John 1947b; Ward 1947) and in periods of
lucidity between convulsions. Given the severity of convul-
sions and potential for movement during convulsions that has
been observed (Egekeze & Oehme 1979a,b; McIlroy 1981;
Marks et al 2000; Potter et al 2006), there is a potential for
injury to occur during fitting, and affected animals experi-
encing periods of conscious awareness between convulsions
or eventually recovering from a sub-lethal dose of 1080 may
be capable of suffering as a result of any injuries sustained. A
poison that caused death more rapidly, or with less opportu-
nity for injury, would clearly be more desirable from a
welfare perspective. Para-aminopropiophenone (PAPP) has
been shown to produce a much more rapid death in red foxes
that is not associated with many of the signs that may be
indicative of distress during 1080 toxicosis (Marks et al
2004). There is some scope for reducing the severity of signs
and symptoms associated with 1080 toxicosis by combina-
tion with other pharmacologic agents that could be co-admin-
istered in a bait and mitigate distress experienced by poisoned
animals (Marks et al 2000).
Mason and Littin (2003) argue that the most desirable
poisons have a minimum number of symptoms before
rapid loss of consciousness and death, with no lasting ill-
effects on the survivors. Sodium fluoroacetate does not
clearly meet these criteria and it is inappropriate to claim
that 1080 is a humane poison based upon prior reviews
that fail to consider wider welfare impacts and do not use
a consistent framework for assessing humaneness. Given
the widespread use of this poison in countries such as
Australia and New Zealand, research into alternative
control methods and/or improving the humaneness of
1080 baits should be made a priority.
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