Phosphorus is used as a paste and is generally applied to turf spits on the ground. It is only available to licensed operators.
3.1.1 Physical and chemical properties
Phosphorus is a yellow solid with a waxy lustre that has a melting point of 44.1ºC. Phosphorus is mixed with water, bentonite, and magnesium oxide to produce an emulsion that is incorporated into a fruit paste for the control of rabbits and possums.
Raw phosphorus is a corrosive dangerous product. Pastes have somewhat different properties.
3.1.2 Historical development and use
Phosphorus was first used in rabbit control in New Zealand and Australia in the early 1920s. The initial use of this toxicant was in pollard pellets by dissolving the phosphorus sticks in carbon bi-sulphide or mixing phosphorus in boiled water and then adding pollard to make the pellets. It was also used on oats and wheat.
In the 1950s phosphorus was incorporated into paste for rabbit control. In the 1960s phosphorus pellets were withdrawn from the market because the phosphorus broke down (oxidised) quickly in the bait, and was ineffective. Phosphorus paste is still used by regional councils and is publicly available. Under the Pesticides (Vertebrate Pest Control) Regulations 1977, the operator must either hold a licensed operators certificate or be working under the supervision of a certificate holder to use phosphorus for pest control.
3.1.3 Fate in the environment
Phosphorus is unlikely to be persistent in the environment. Phosphorus is usually added to paste bait for possum control. On exposure to air the phosphorus oxidises to phosphates, which are not poisonous. Accordingly, phosphorus is more stable in paste, which tends to ‘cake’ and protect the phosphorus from oxidation.
In the veterinary literature, phosphorus poisoning is usually categorised in three phases: (1) An acute initial phase occurring within hours of ingestion characterised by gastrointestinal, abdominal, and circulatory signs. Initial signs generally involve vomiting and diarrhoea. If the dosage is sufficiently large, shock, cyanosis, incoordination and coma may develop, with death occurring before the second and third phases appear; (2) An interim or latent phase with apparent recovery occurs at lower doses approximately 48 hours to several days after initial clinical signs; (3) The third stage is characterised by recurrence of marked clinical signs involving the gastrointestinal tract. Liver failure then occurs. These literature reports suggest that death may occur in 1–2 days, or there may be improvement for 1–2 days before vomiting, diarrhoea, and other signs return. Death is usually due to liver necrosis and heart failure. There may be a delay of up to 3 weeks after ingestion before convulsions, coma, and death. Recent trials at Landcare Research have shown that possums eating phosphorus-paste baits die within 18 hours and do not experience the prolonged toxicosis commonly attributed to phosphorus in the scientific and veterinary literature (Eason et al. 1997, 1998b; O’Connor et al. 1998).
There is no antidote to phosphorus, but with early diagnosis the poison may be removed by vomiting or gastric lavage, then treated with 0.1% potassium permanganate or 2% hydrogen peroxide (to oxidise the toxicant to harmless phosphates) and mineral oil (which prevents absorption). However, if there is bleeding or ulceration treatment is more difficult.
Mode of action
The mode of action is unknown. It has not been possible to associate the main clinical or pathological features of intoxication with inhibition of any particular enzyme or class of enzymes. Phosphorus is sometimes referred to as a protoplasmic poison, but it is difficult to distinguish its possible direct effects on the liver, kidney, brain, and heart from the effects of anoxia on those organs. The peripheral vascular dilatation, which is the first and most pervasive systemic effect of phosphorus, contributes to all the disorders that may be seen in various organs. However, the mechanism of this dilatation is not clear.
Phosphorus not only leads to structural damage of vital organs, but also produces serious disruption of their metabolic function, as evidenced by hypoglycemia, azotemia, inhibition of glycogen formation in the liver, and many other disorders.
Pathological changes include gross evidence of fatty degeneration and swollen livers, as well as gastrointestinal irritation, necrosis, and haemorrhage. If death is sufficiently prompt, there is no pathology except irritation of the oesophagus and stomach. Perforation may occur. Following survival for several days, fatty degeneration is striking in the liver, heart, and kidney but may be found in all organs, including the brain. We were unable to locate any material relating to genotoxicity or teratogenicity, or data from other regulatory toxicology studies on phosphorus.
Fate in animals
Phosphorus is readily absorbed but its persistence in lethally and sub-lethally poisoned possums has not been elucidated.
Species variation in response to phosphorus
There is little species variation in response to phosphorus and most species are at risk if they eat bait (Table 23).
Unknown. It is unlikely that significant amounts of phosphorus baits used for possum control will enter watercourses.
3.1.5 Current use
This poison has been in use since the 1920s and is one of the few poisons that is still available to the public as an acute poison for rabbit and possum control. It is also still used in some instances to poison pigs. It is not currently used by the Department of Conservation, but is used around houses and public areas by regional councils where there is a risk to dogs from 1080. However, use of phosphorus is also associated with secondary poisoning of dogs.
Effective (kills of >90% achieved)
Less public opposition than with 1080†
Has some animal welfare concerns‡)
Secondary poisoning risk to dogs and birds
Risk of fire
Antidotes of limited value
† When farmers or the community oppose the use of 1080 they will often accept phosphorus as a replacement.
‡ Studies show that the symptoms of phosphorus poisoning in possums differ from those reported in the veterinary literature for other animals