University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln USGS Staff -- ubP lished Research US Geological Survey 2012 Wildlife Toxicology: Environmental Contaminants and Their aN tional and International Regulation K. Christiana Grim Center for Species Survival, Smithsonian Conservation Biology Institute Anne Fairbrother EcoSciences Barnett A. Rattner U.S. Geological Survey, [email protected] Follow this and additional works at: http://digitalcommons.unl.edu/usgsstaffpub Part of the Geology Commons, Oceanography and Atmospheric Sciences and Meteorology Commons, Other Earth Sciences Commons, and the Other Environmental Sciences Commons Grim, K. Christiana; Fairbrother, Anne; and Rattner, Barnett A., "Wildlife Toxicology: Environmental Contaminants and Their National and International Regulation" (2012). USGS Staff -- Published Research. 969. http://digitalcommons.unl.edu/usgsstaffpub/969 This Article is brought to you for free and open access by the US Geological Survey at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in USGS Staff -- ubP lished Research by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. Published in New Directions in Conservation Medicine: Applied Cases in Ecological Health, edited by A. Alonso Aguirre, Richard S. Ostfield, and Peter Daszak (New York: Oxford University Press, 2012). Authors K. Christiana Grim, D.V.M. Research Associate Center for Species Survival Smithsonian Conservation Biology Institute Front Royal, Vrrginia Anne Fairbrother, D.V.M., M.S., Ph.D. Senior Managing Scientist EcoSciences Exponent Seattle, Washington Barnett A. Rattner, Ph.D. Ecotoxicologist U.S. Geological Survey Patuxent Wildlife Research Center Beltsville Laboratory Beltsville, Maryland WILDLIFE TOXICOLOGY Environmental Contaminants and Their National and International Regulation K. Christiana Grim, Anne Fairbrother, and Barnett A. Rattner Wildlife toxicology is the study of potentially harmful wildlife mortality events were documented following effects of toxic agents in wild animals, focusing on pesticide application in agricultural and forest habi­ amphibians, reptiles, birds, and mammals. Fish and tats. Field and laboratory studies described effects on aquatic invertebrates are not usually included as part reproduction, survival, tissue reSidues, and tOxicity of wildlife tOXicology since they fall within the field of thresholds in birds. The widespread hazards of spent aquatic toxicology, but collectively both disciplines lead shot, and mercurials from fungicides and indus­ often provide inSight into one another and both are trial activities became apparent. integral parts of ecotoxicology (Hoffman et al. 2003). Scientific observations and the publication of It entails monitoring, hypothesis testing, forensics, Silent Spring (Carson 1962) led to contaminant moni­ and risk assessment; encompasses molecular through toringprograms in the United States, United Kingdom, ecosystem responses and various research venues and Canada during the 1970S. Research highlights (laboratory, mesocosm, field); and has been shaped of this era included bioaccumulation of organochlo­ by chemical use and misuse, ecological mishaps, and rines in food chains, exposure of diverse species (e.g., biomedical research. While human toxicology can be bats, marine mammals), and avian mortality due to traced to ancient Egypt, wildlife toxicology dates back accumulation of lethal pesticide residues. Eggshell to the late 19th century, when unintentional poison­ thinning and population declines in raptorial and ing of birds from ingestion oflead shot and predator fish-eating birds were attributed to DDT (and its control agents, alkali poisoning, and die-offs from oil metabolite DDE), and polychlorinated biphenyls spills appeared in the popular and scientific literature (PCB) were detected and linked to reproductive prob­ (Rattner 2009). lems in mink. Screening programs were launched to By the 1930S, about 30 pesticides were com­ examine chemical toxicity and repellency to birds and monly available (Sheail 1985), and crop-dusting air­ mammals. craft facilitated their use. With the discovery of By the 1980s, heavy metal pollution from mining dichlorodiphenyltrichloroethane (DDT) in 1939, and and smelting activities, agrichemical practices and related compounds shortly thereafter, use of pesti­ non-target effects, selenium toxicosis, PCB pollution, cides increased exponentially. Between 1945 and 1960, die-offs related to anticholinesterase pesticides, 359 :3()O Ecotoxicology and Const'rvation ,\lpdicinc and environmental disasters (e.g., Chernobyl, Exxon use of nontoxic manufacturing processes with mini­ Valdez) were at the forefront of ecotoxicology. mal emissions, and recyclable materials that have few Molecular biomarkers, endocrine disruption, popula­ harmful effects on the environment. Characteristics of tion modeling, and studies with amphibians and newer replacement compounds include short envi­ reptiles dominated the 1990S. With the turn of the ronmental half-lives, limited potential for bioaccumu_ century, interests shifted toward pharmaceuticals, lation, and mechanisms of action that do not evoke flame retardants, and surfactants; toxicogenomics; toxic effects in non-target animals. inter-specific extrapolation of toxicity data; and inter­ connections between wildlife toxicology, ecological integrity, and human health (Rattner 2009). ,\lAJOR ENV1HOl\MENTAL CO'JTAMI~ANT CLASSES Mechanisms of Aetion and Changes OverTime The most widely recognized classes of contaminants that have demonstrated effects or pose risk to wildlife Chemicals pose risks to organisms due to a combina­ and human populations include pesticides, industrial tion of factors that are intrinsic to the compound, par­ chemicals, fossil and mineral fuels, pharmaceuticals ticular species, and/ or from interaction with extrinsic (human and veterinary) and personal care products, factors (e.g., habitat, ambient temperature), and other metals, and fertilizers (Table 25.1). chemicals. The myriad physiological, behavioral, and life history characteristics of different organisms result Pesticides in unique exposure pathways and unusual suscepti­ bilities. For example, physical and chemical properties The vast majority of synthetic chemical substances are of some contaminants may cause them to preferen­ industrial in nature (80,000 to 100,000 registered). tially accumulate in water, sediment, or soil, habitats, Even though there are only about 1,200 active pesti­ or ecosystems, or may cause particular toxicity to cer­ cide compounds, their volume of use is significant tain species. Species and individuals can be affected by Annually, more than 5 billion pounds of pesticides are contaminants directly and indirectly (see Chapter 24 used worldwide, with the United States accounting in this volume). Also, individuals and populations are for 20% to 30% of global usage (USEPA 2001). As of rarely exposed to single contaminants, and the effects 2007, pesticides were detectable in most surface water of exposure to mixtures may differ from the effects of samples, major aquifers, and fish species in tlle United a single chemical through additive, synergistic, antag­ States; they sometimes exceeded water-quality bench­ onistic, or delayed effects. marks for aquatic or fish-eating wildlife (Gilliom Over the past century, discoveries concerning 2007 ). how chemicals move through the environment and Use of cyclodiene insecticides (e.g., DDT, aldrin, the effects they can have on wildlife and people have dieldrin, lindane, and chlorodecone) became wide­ changed the types and properties of synthetic chemi­ spread after World War II. The half-lives of these cals. Within the past decade, chemical-induced cli­ chemicals are on the order of 30 years. They are very mate change and discoveries of pesticides and hydrophobic and accumulate in lipids within animals industrial chemicals in pristine locations have resulted and humans. Consequently, these compounds bio­ in international regulation to restrict chemical manu­ magnify in the food chain, resulting in very high facture and use to those with the least risk to human exposure to top predators and insectivorous birds. health and the environment. As early as the 1990S, Cyclodienes cause toxicity by inhibiting ATPases, the U.S. Environmental Protection Agency (USEPA) antagonizing neurotransmitters, and depolarizing initiated a "Design for the Environment Program" that nerves by interfering with calcium fluxes botll along sought to develop cleaner product processes and the axon and at the neuronal junctions. The neuro­ reduce pollution. One goal ofthe program is to "mini­ logical effects are universal across all animal species, mize environmental damage and maximize efficiency resulting in very nonspecific insecticides. Toxic effects during the life of the product" (www.epa.gov / dfe/ can occur in non-neural tissues; for example, inhibi­ pubs/ comp-dic/factsheet/). The program promotes tion of calcium ATPase in the shell gland of birds \\ildlifc Toxicology Table 25.1 Common Chemical Classes Affecting Wildlife and Human Health Chemical Class Most Common Sub-Classes or Types Unifying characteristic Found in the Environment Pesticides Herbicides/ fungicides/ algaecides Designed to kill, repel, or alter Insecticides/ nematicides/ molluscicides physiological mechanisms in target Avicides/ rodenticides organisms Growth regulators (plant and insect) Industrial Volatiles (e.g., household