Avian mortality events in the United States caused by anticholinesterase pesticides: a retrospective summary of National Wildlife Health Center records from 1980 to 2000.

We reviewed the U.S. Geological Survey National Wildlife Health Center (NWHC) mortality database from 1980 to 2000 to identify cases of poisoning caused by organophosphorus and carbamate pesticides. From the 35,022 cases from which one or more avian carcasses were submitted to the NWHC for necropsy, we identified 335 mortality events attributed to anticholinesterase poisoning, 119 of which have been included in earlier reports. Poisoning events were classified as confirmed (n = 205) when supported by findings of > or =50% inhibition of cholinesterase (ChE) activity in brain tissue and the detection of a specific pesticide in the gastrointestinal contents of one or more carcasses. Suspected poisonings (n = 130) were defined as cases where brain ChE activity was > or =50% inhibited or a specific pesticide was identified in gastrointestinal contents. The 335 avian mortality events occurred in 42 states. Washington, Virginia, and Ohio had the highest frequency of events, with 24 (7.2%), 21 (6.3%), and 20 (6.0%) events, respectively. A total of 8877 carcasses of 103 avian species in 12 orders was recovered. Because carcass counts underestimate total mortality, this represents the minimum actual mortality. Of 24 different pesticides identified, the most frequent were famphur (n = 59: 18%), carbofuran (n = 52; 15%), diazinon (n = 40; 12%), and fenthion (n = 17; 5.1%). Falconiformes were reported killed most frequently (49% of all die-offs) but Anseriformes were found dead in the greatest numbers (64% of 8877 found dead). The majority of birds reported killed by famphur were Passeriformes and Falconiformes, with the latter found dead in 90% of famphur-related poisoning events. Carbofuran and famphur were involved in mortality of the greatest variety of species (45 and 33, respectively). Most of the mortality events caused by diazinon involved waterfowl.

Inactivation of p53 and retinoblastoma family pathways in canine osteosarcoma cell lines.

Canine osteosarcoma (OS) has been used as a model system for the study of cancer biology and treatment despite the lack of information regarding its pathogenesis. Expression of tumor suppressor genes known to participate in malignant transformation were studied in five different OS cell lines. Each of the cell lines exhibited properties of transformed cells, and those that were tested grew in soft agarose and formed osteoid-containing tumors when injected subcutaneously into nude mice. p53 function was determined to be defective in each cell line as indicated by the lack of induction of p53-responsive genes, p21 and mdm2, following treatment with 5-fluorouracil. p53 mRNA and protein levels were elevated in three cell lines and were extremely low in two cell lines. p53 protein overexpression correlated with the presence of mutations within the DNA binding domain. Four cell lines appeared to contain normal retinoblastoma (Rb) mRNA and Rb protein and no detectable p16 mRNA or protein. In contrast, the remaining cell line contained high levels of p16 mRNA and protein and significantly reduced levels of Rb, p107, and p130 proteins. These results underscore the importance of inactivating p53 and Rb family pathways in canine OS and suggest that unlike human OS, cells derived from canine OS contain mutations that simultaneously inactivate all three Rb family members.