Current evaluations of the anticoagulant diphacinone for field control of introduced rodents in New Zealand include risk assessment with respect to non-target mortality, secondary poisoning, and environmental contamination. As non-target wildlife of rodent control operations, feral pigs may be exposed to vertebrate pesticides if they access toxic baits or scavenge the carcasses of poisoned animals. Feral pigs are also a significant resource for recreational hunters who harvest wild pork for food, hence the need to assess the risks of human exposure to diphacinone residues through feral pigs. Pen trials with domestic pigs were used to evaluate the potential for pig mortality through oral exposure to diphacinone and the residual persistence of diphacinone in pig tissues following a sublethal exposure. In the first trial, pigs were offered palatable food containing diphacinone doses of 12.5 mg/kg, 0.25 mg/kg/day for 3 days, or 0.5 mg/kg/day for 5 days. Significant elevations in coagulation time tests were measured 2 days after dosing, but these had returned to baseline values by 7 days. Two of the dosed pigs were euthanased due to lameness, which was accompanied by elevated prothrombin times and severe hemorrhage in a leg joint. In the second trial, pigs were dosed with 12.5 mg/kg diphacinone and then euthanased in groups for tissue sampling at Days 1, 4, and 10. Liver, muscle, and fat samples were analysed for diphacinone residues using an HPLC method. Data fitted to an exponential decay model estimated the hepatic elimination half-life as between 5.43 days (overall) and 14.12 days (terminal phase only). Half-lives of diphacinone in pig muscle and fat were 4.48 and 2.29 days respectively. A conservative withholding period of approximately 160 days is suggested before feral pigs should be taken for human consumption from areas where diphacinone baits have been used. This would minimize the likelihood of detectable diphacinone residues (≥0.02 µg/g) occurring in wild pork.

Prolonged persistence of second-generation anticoagulant rodenticides (SGARs) in animal tissues facilitates trophic transfer of residues, with exposure of predatory and scavenging non-target wildlife now widely reported. In many instances, antico-agulant residue levels measured in wildlife are apparently sublethal, although longer-term effects of such exposures are currently not well understood. Conversely, prolonged metabolic persistence is of practical utility when compounds are used as biological markers to determine food uptake by animals. We required two effective and distinct marker compounds to progress field-based research on optimal baiting strategies to manage introduced brushtail possums in New Zealand. Two SGARs (flocoumafen and bromadiolone) were evaluated, as neither are currently registered for application as rodenticides in areas typically subject to possum management. All captive possums ingesting small, sublethal (2-6 g) quantities of food containing 0.0005% (by weight) of either SGAR were reliably marked by the presence of residual concentrations in liver as measured by HPLC analysis. This marking persisted for at least six weeks, and liver concentrations in marked possums did not decline between three and six weeks after the marker was ingested. Marking was also quantitative for both SGARs with a correlation between liver residue concentration and the amount of marker ingested. Using such marker baits would provide at least a six-week period in which to recover possums in field research. By recording bodyweight and testing liver samples from such possums for both markers, regression equations generated from the work reported here will enable back-estimation, with confidence intervals, of the amounts of marker bait eaten by each possum.

Residues of brodifacoum and other second-generation anticoagulant rodenticides are reported worldwide in a range of non-target wildlife, especially predatory or scavenging birds and mammals. Determination of exposure to brodifacoum in such cases relies on analysis of liver tissue. This limits current monitoring efforts to either destructive sampling of live birds or mammals to obtain liver, but more commonly opportunistic post-mortem liver sampling from carcasses in suitable condition. Also, detection of brodifacoum in liver often cannot be confirmed as a contributor to mortality, and within a potential ‘sublethal’ concentration range the toxicological significance of its presence is uncertain. We sought to determine whether dried blood spot (DBS) sampling could form the basis of a non-lethal, minimally invasive method for determining sublethal exposure to brodifacoum in live birds. Validation of a method for detecting brodifacoum in DBS samples, and preliminary comparison of brodifacoum concentrations in DBS and plasma samples, are described.

Aerial application of brodifacoum bait for eradication of invasive rodents from islands raises concerns about environmental contamination and adverse effects on nontarget wildlife. We summarize results of environmental monitoring for brodifacoum residues after New Zealand eradications in a fenced reserve at Maungatautari and on the offshore islands Little Barrier, Rangitoto, and Motutapu. Brodifacoum was not detected in extensive freshwater monitoring at Maungatautari, or in freshwater samples from Little Barrier Island. Residual concentrations were present in soil samples from underneath degrading bait pellets on Little Barrier, and decreased to near the limit of detection by c. 100 days after application. No brodifacoum was present in marine shellfish sampled from Little Barrier, Rangitoto or Motutapu. A range of birds, including a kiwi from Little Barrier, were considered nontarget mortalities. Nine little blue penguins found dead on beaches outside the Rangitoto/Motutapu area after baiting were considered most likely to have died of starvation, despite the detection of brodifacoum in three birds. This result highlights the critical role of post-application environmental monitoring in rodent eradications, and information gaps regarding the movement, persistence, and effects of brodifacoum in the environment.

Vertebrate pesticides for wild animal control in New Zealand came under scrutiny in the 1980s and 1990s, which engendered considerable research to update the toxicology databases of older compounds, such as 1080 or diphacinone, to meet current international registration standards. In parallel there was a focus on identifying “use patterns” and formulations that are effective at killing pests and less hazardous to other wildlife. Improved bait quality and reduced sowing rates for 1080 bait for possum control in New Zealand, down from 10-15 kg of bait per hectare to 1-3 kg, has been accompanied by increased effectiveness and reduced non-target risk. This has been coupled with an improved understanding of 1080 toxicology and risk communication amongst pest control professionals and with the community. In addition, in vivo metabolism and persistence studies coupled with field surveys have improved understanding of the toxicokinetics and non-target effects of different anticoagulants. This enabled improved choice of tools for island versus mainland use in New Zealand. The risks associated with “one-off” applications of baits containing second-generation anticoagulants for rodent eradication on islands are considered to be very substantially outweighed by the potential benefits to their ecosystems. On the mainland, contamination of wildlife and game species and risk of secondary poisoning have been substantially reduced by switching from second- to first-generation anticoagulants. Finally, these developments were coupled with the identification of improved baits for ground control of possums and rodents, such as encapsulated cyanide and gel baits containing cholecalciferol, which in turn reduced an over-reliance on 1080 and anticoagulants alone. Nevertheless, safer use patterns, improved formulations and target specificity, and new vertebrate pesticides are still required, and this will be a major challenge for the 21st Century.