Correction to: Anticoagulant Rodenticides and Raptors: Recent Findings from New York, 1998-2001.

In the original version of this article, there is a typographical error in the third sentence of the Results and Discussion section. The number of cases in which anticoagulant-facilitated hemorrhage was considered the cause of death was 19 (not 9). This has been corrected with this erratum.

Poisoning of wildlife with anticoagulant rodenticides in New York.

From 1971 through 1997, we documented 51 cases (55 individual animals) of poisoning of non-target wildlife in New York (plus two cases in adjoining states) (USA) with anticoagulant rodenticides--all but two of these cases occurred in the last 8 yrs. Brodifacoum was implicated in 80% of the incidents. Diphacinone was identified in four cases, bromadiolone in three cases (once in combination with brodifacoum), and chlorophacinone and coumatetralyl were detected once each in the company of brodifacoum. Warfarin accounted for the three cases documented prior to 1989, and one case involving a bald eagle (Haliaeetus leucocephalus) in 1995. Secondary intoxication of raptors, principally great horned owls (Bubo virginianus) and red-tailed hawks (Buteo jamaicensis), comprised one-half of the cases. Gray squirrels (Sciurus carolinensis), raccoons (Procyon lotor) and white-tailed deer (Odocoileus virginianus) were the most frequently poisoned mammals. All of the deer originated from a rather unique situation on a barrier island off southern Long Island (New York). Restrictions on the use of brodifacoum appear warranted.

2,4-D toxicosis.II: A pilot study of clinical pathologic and electroencephalographic effects and residues of 2,4-D in orally dosed dogs.

English pointer dogs dosed po with encapsulated 2,4-dichlorophenoxyacetic acid (2,4-D) at 1.3, 8.8, 43.7, 175 or 220 mg/kg body weight failed to exhibit abnormalities in hematologic, serum biochemical, urinalysis, or electrocardiographic parameters. At the 3 lowest doses, no changes were noted in electro-encephalograms (EEGs). In the dog given 175 mg/kg, at 24 h postdosing mild sedation was accompanied by excessive slowing in the EEG with loss of low voltage fast activity. In the dog given 220 mg/kg, nonspecific alterations in the EEG suggestive of irritation and mild seizure activity was detected 7 h, but the EEG returned to normal by 24 h. A maximum 2,4-D concentration in serum of 1075 ppm was detected 5 h after a po dose of 220 mg/kg. A maximum 2,4-D, concentration in urine of 1792 ppm was detected 2 h after a po dose of 175 mg/kg, while 25 h after that dose kidney issue contained 271 ppm.

2,4-D toxicosis.III: An attempt to produce 2,4-D toxicosis in dogs on treated grass plots.

Eighteen English pointer dogs were randomly assigned to 3 outdoor grass-plot enclosures (6/enclosure) uniformly sprayed once with either the 2,4-dichlorophenoxyacetic acid (2,4-D) dimethylamine formulation (DMA-4) at the maximum recommended application rate, DMA-4 at 4 times the maximum recommended application rate, or the DMA-4 vehicle alone at 4 times the maximum recommended application rate. A heavy rain shower occurred 24 h after application. The dogs were observed for clinical signs and evaluated using an electroencephalograph, electrocardiograph (lead I), and electromyograph prior to exposure, and either 1 or 7 d after continuous exposure. Clinical examination, hematologic and serum biochemical data were obtained, and serum, urine and kidney 2,4-D were quantified. Half of the dogs from each group were killed after 1 d of continuous exposure, while the other half were killed after 7 d. Gross postmortem and histologic examinations were conducted on each dog. No obvious 2,4-D effects were detected in any of the dogs.