History of wildlife toxicology

The field of wildlife toxicology can be traced to the late nineteenth and early twentieth centuries. Initial reports included unintentional poisoning of birds from ingestion of spent lead shot and predator control agents, alkali poisoning of waterbirds, and die-offs from maritime oil spills. With the advent of synthetic pesticides in the 1930s and 1940s, effects of DDT and other pesticides were investigated in free-ranging and captive wildlife. In response to research findings in the US and UK, and the publication of Silent Spring in 1962, public debate on the hazards of pollutants arose and national contaminant monitoring programs were initiated. Shortly thereafter, population-level effects of DDT on raptorial and fish-eating birds were documented, and effects on other species (e.g., bats) were suspected. Realization of the global nature of organochlorine pesticide contamination, and the discovery of PCBs in environmental samples, launched longrange studies in birds and mammals. With the birth of ecotoxicology in 1969 and the establishment of the Society of Environmental Toxicology and Chemistry in 1979, an international infrastructure began to emerge. In the 1980s, heavy metal pollution related to mining and smelting, agrichemical practices and non-target effects, selenium toxicosis, and disasters such as Chernobyl and the Exxon Valdez dominated the field. Biomarker development, endocrine disruption, population modeling, and studies with amphibians and reptiles were major issues of the 1990s. With the turn of the century, there was interest in new and emerging compounds (pharmaceuticals, flame retardants, surfactants), and potential population-level effects of some compounds. Based upon its history, wildlife toxicology is driven by chemical use and misuse, ecological disasters, and pollution-related events affecting humans. Current challenges include the need to more thoroughly estimate and predict exposure and effects of chemical-related anthropogenic activities on wildlife and their supporting habitat

History of wildlife toxicology

The field of wildlife toxicology can be traced to the late nineteenth and early twentieth centuries. Initial reports included unintentional poisoning of birds from ingestion of spent lead shot and predator control agents, alkali poisoning of waterbirds, and die-offs from maritime oil spills. With the advent of synthetic pesticides in the 1930s and 1940s, effects of DDT and other pesticides were investigated in free-ranging and captive wildlife. In response to research findings in the US and UK, and the publication of Silent Spring in 1962, public debate on the hazards of pollutants arose and national contaminant monitoring programs were initiated. Shortly thereafter, population-level effects of DDT on raptorial and fish-eating birds were documented, and effects on other species (e.g., bats) were suspected. Realization of the global nature of organochlorine pesticide contamination, and the discovery of PCBs in environmental samples, launched longrange studies in birds and mammals. With the birth of ecotoxicology in 1969 and the establishment of the Society of Environmental Toxicology and Chemistry in 1979, an international infrastructure began to emerge. In the 1980s, heavy metal pollution related to mining and smelting, agrichemical practices and non-target effects, selenium toxicosis, and disasters such as Chernobyl and the Exxon Valdez dominated the field. Biomarker development, endocrine disruption, population modeling, and studies with amphibians and reptiles were major issues of the 1990s. With the turn of the century, there was interest in new and emerging compounds (pharmaceuticals, flame retardants, surfactants), and potential population-level effects of some compounds. Based upon its history, wildlife toxicology is driven by chemical use and misuse, ecological disasters, and pollution-related events affecting humans. Current challenges include the need to more thoroughly estimate and predict exposure and effects of chemical-related anthropogenic activities on wildlife and their supporting habitat

Critique on the Use of the Standardized Avian Acute Oral Toxicity Test for First Generation Anticoagulant Rodenticides

Avian risk assessments for rodenticides are often driven by the results of standardized acute oral toxicity tests without regards to a toxicant’s mode of action and time course of adverse effects. First generation anticoagulant rodenticides (FGARs) generally require multiple feedings over several days to achieve a threshold concentration in tissue and cause adverse effects. This exposure regimen is much different than that used in the standardized acute oral toxicity test methodology. Median lethal dose values derived from standardized acute oral toxicity tests underestimate the environmental hazard and risk of FGARs. Caution is warranted when FGAR toxicity, physiological effects, and pharmacokinetics derived from standardized acute oral toxicity testing are used for forensic confirmation of the cause of death in avian mortality incidents and when characterizing FGARs’ risks to free-ranging birds

Anticoagulant Rodenticide Toxicity to Non-target Wildlife Under Controlled Exposure Conditions

Our knowledge of the toxicity of anticoagulant rodenticides (ARs) can be traced to investigations of Karl Paul Link and colleagues on “bleeding disease” in cattle, the eventual isolation of dicoumarol from moldy sweet clover, synthesis of this causative agent, and its application as a therapeutic anticoagulant in clinical medicine in 1941 (Link 1959). The notion of a coumarin-based rodenticide as a better “mouse-trap” occurred to Link in 1945 while reviewing laboratory chemical and bioassay data. By 1948, the highly potent compound number 42, warfarin, was promoted as a rodenticide (Link 1959; Last 2002). Through laboratory studies and clinical use of warfarin (Coumadin), a detailed understanding of the mechanism of action and toxicity of warfarin and related ARs (Fig. 3.1) unfolded in the decades that followed

Critique on the Use of the Standardized Avian Acute Oral Toxicity Test for First Generation Anticoagulant Rodenticides

Avian risk assessments for rodenticides are often driven by the results of standardized acute oral toxicity tests without regards to a toxicant’s mode of action and time course of adverse effects. First generation anticoagulant rodenticides (FGARs) generally require multiple feedings over several days to achieve a threshold concentration in tissue and cause adverse effects. This exposure regimen is much different than that used in the standardized acute oral toxicity test methodology. Median lethal dose values derived from standardized acute oral toxicity tests underestimate the environmental hazard and risk of FGARs. Caution is warranted when FGAR toxicity, physiological effects, and pharmacokinetics derived from standardized acute oral toxicity testing are used for forensic confirmation of the cause of death in avian mortality incidents and when characterizing FGARs’ risks to free-ranging birds

The Toll of Toxics: Investigating Environmental Contaminants

Two recent events [the Deepwater Horizon oil spill and the Asarco settlement] bring to the fore the work of wildlife toxicologists. Focusing on amphibians, reptiles, birds, and mammals, wildlife toxicology is a component of ecotoxicology--the study of toxic effects caused by natural or synthetic pollutants on living organisms and other constituents of ecosystems (Truhaut 1977). Now a distinct discipline within the wildlife profession-practiced by members of The Wildlife Society\u27s own Wildlife Toxicology Working Group, among others-wildlife toxicology has become increasingly important as human populations and industry have spread, causing contaminants to multiply. Emerging Environmental Contaminants (EECs) include an array of chemicals and substances that are discharged into the environment. According to the U.S. Geological Survey Toxic Substances Hydrology Program (2006), EECs include veterinary and human antibiotics, human drugs, industrial and household wastewater products, and sex and steroidal hormones. Beyond these four groupings, some experts also include phthalates that are used as plasticizers, chemicals used for disinfection in homes and industries, flame retardants, and extremely small particulates or nanomaterials (GRAC 2008, Sadler et al. 2003). Studies by wildlife toxicologists have only skimmed the surface of how the thousands of chemicals in the environment affect wildlife, and new regulations and novel applications of old laws are constantly changing how toxicologists approach their work. Recent lawsuits brought against the EPA by the Center for Biological Diversity, for example, note that pesticides used on the landscape may be impacting endangered species in violation of the ESA (CBD 2010). That\u27s really driving a lot of EPA attention right now, says Exponent\u27s Anne Fairbrother, and I think that\u27s likely to continue. Wildlife toxicologists will help determine the impacts on at-risk species. With so many questions to answer about the ecological effects of contaminants on wildlife, wildlife toxicologists have more than enough work for many decades of productive scientific research

Wildlife Toxicology: Environmental Contaminants and Their National and International Regulation

Wildlife toxicology is the study of potentially harmful effects of toxic agents in wild animals, focusing on amphibians, reptiles, birds, and mammals. Fish and aquatic invertebrates are not usually included as part of wildlife toxicology since they fall within the field of aquatic toxicology, but collectively both disciplines often provide inSight into one another and both are integral parts of ecotoxicology (Hoffman et al. 2003). It entails monitoring, hypothesis testing, forensics, and risk assessment; encompasses molecular through ecosystem responses and various research venues (laboratory, mesocosm, field); and has been shaped by chemical use and misuse, ecological mishaps, and biomedical research. While human toxicology can be traced to ancient Egypt, wildlife toxicology dates back to the late 19th century, when unintentional poisoning of birds from ingestion oflead shot and predator control agents, alkali poisoning, and die-offs from oil spills appeared in the popular and scientific literature (Rattner 2009)

Wildlife Toxicology: Environmental Contaminants and Their National and International Regulation

Wildlife toxicology is the study of potentially harmful effects of toxic agents in wild animals, focusing on amphibians, reptiles, birds, and mammals. Fish and aquatic invertebrates are not usually included as part of wildlife toxicology since they fall within the field of aquatic toxicology, but collectively both disciplines often provide inSight into one another and both are integral parts of ecotoxicology (Hoffman et al. 2003). It entails monitoring, hypothesis testing, forensics, and risk assessment; encompasses molecular through ecosystem responses and various research venues (laboratory, mesocosm, field); and has been shaped by chemical use and misuse, ecological mishaps, and biomedical research. While human toxicology can be traced to ancient Egypt, wildlife toxicology dates back to the late 19th century, when unintentional poisoning of birds from ingestion oflead shot and predator control agents, alkali poisoning, and die-offs from oil spills appeared in the popular and scientific literature (Rattner 2009)

History of Wildlife Toxicology and the Interpretation of Contaminant Concentrations in Tissues

The detection and interpretation of contaminants in tissues of wildlife belongs to the field of toxicology, a scientific discipline with a long, intriguing, and illustrious history (reviewed by Hayes 1991, Gallo 2001, Gilbert and Hayes 2006, Wax 2006). We review its history briefly, to provide a context for understanding the use of tissue residues in toxicology, and to explain how their use has developed over time. Because so much work has been conducted on mercury, and dioxins and polychlorinated biphenyls (PCBs), separate case histories are included that describe the evolution of the use of tissue concentrations to assess exposure and effects of these two groups of contaminants in wildlife. The roots of toxicology date back to early man, who used plant and animal extracts as poisons for hunting and warfare. The Ebers papyrus (Egypt -1550 BC) contains formulations for hemlock, aconite (arrow poison), opium, and various metals used as poisons. Hippocrates (-400 BC) is sometimes credited with proposing the treatment of poisoning by decreasing absorption and using antidotes (Lane and Borzelleca 2007). Chanakya (350-283 BC), Indian advisor of the Maurya Emperor Chandragupta (340-293 BC), urged the use of food tasters as a precaution against poisoning, and the Roman emperor Claudius may have even been poisoned by his taster Halotus in 54 AD. Moses ben Maimon (1135-1204), author of a treatise on poisoning, noted that dairy products could delay absorption of some poisons. Paracelsus (1493-1541) shaped the field of toxicology with his corollaries that experimentation is essential to examining the response, that therapeutic properties should be distinguished from toxic properties, that chemicals have specific modes of action, and that the dose makes the poison. The art of concocting and using poisons reached its zenith during the Italian Renaissance, eventually culminating in its commercialization by Catherine Deshayes (a.k.a., La Voisine, 1640-1680) in France. One of the first to suggest a chemical method for the detection of a poison in modern times was Herman Boerhaave (1668-1738), a physician and botanist, who, according to Jurgen Thorwald (The Century of the Detective), placed the suspected poison on red-hot coals, and tested for odors. The Spanish physician Orfila (1787-1853) served in the French court, and was the first toxicologist to systematically use autopsy and chemical analysis to prove poisoning. He has been credited with developing and refining techniques to detect arsenic poisoning. Other historic accounts include extraction of alkaloids from postmortem specimens (Jean Servais Stas ~1851) as evidence in a nicotine poisoning case (Levine 2003). The chemical analysis of organs and tissues became the basis for establishing poisoning. Much of the early history of toxicology addressed whether someone had been poisoned and how to treat poisoning

Retrospective: Adjusting Contaminant Concentrations in Bird Eggs to Account for Moisture and Lipid Loss During Their Incubation

By the 1960s, research and monitoring efforts on chlorinated pesticide residues in tissues of wildlife were well underway in North America and Europe. Conservationists and natural resource managers were attempting to resolve whether pesticide exposure and accumulated residues were related to population declines in several species of predatory and scavenging birds (e.g., bald eagle Haliaeetus leucocephalus, peregrine falcon Falco peregrinus, brown pelican Pelecanus occidentalis and osprey Pandion haliaetus). The avian egg was a favored sampling matrix even before the realization that eggshell thinning was linked to population declines (Ratcliffe 1967; Hickey and Anderson 1968) and that the concentration of p,p’-DDE in an egg was associated with the shell thinning phenomenon (e.g., Blus et al. 1972; Wiemeyer et al. 1988). The necessity for making wet-weight concentration adjustments to account for natural moisture loss during incubation of viable eggs was realized. Correction for the more dramatic moisture loss in non-viable decaying eggs was recognized as being paramount. For example, the ∑DDT residues in osprey eggs were reported to vary by as much as eightfold without accounting for moisture loss adjustments (Stickel et al. 1965). In the absence of adjusting concentrations to the fresh wet-weight that was present at the time of egg laying, the uncorrected values exaggerated contaminant concentrations, yielding artifactual results and ultimately incorrect conclusions. The adjustment to fresh wet-weight concentration is equally important for many other persistent contaminants including PCBs, dioxins, furans, and brominated diphenyl ethers