ES&T FEATURE Wildlife toxicology Integrated field and laboratory studies using selected model species might lead to ways of quantifying adverse effects of chemical contaminants
Ronald J. Kendall Huxley College of Environmental Studies Western Washington University Bellingham, Wash. 98225 Human health is believed to be threatened by exposure to such chemical contaminants as agricultural pesticides and industrial wastes. Does it not stand to reason, therefore, that the health of wildlife could be affected similarly by toxic chemical pollutants? There is ample evidence to suggest that this is indeed the case. For instance, millions of waterfowl have died of lead poisoning after ingesting spent lead shot (/). Also, scientists now believe that brown pelican (Pelecanus occidental) populations declined as residual levels of DDE (1,1-dichloro2,2-bis [p-chlorophenyl] ethylene) in their eggs increased (2). However, it is difficult to quantify the impacts of chemical contaminants on wildlife populations. For instance, how does one determine the numbers or percentages of a wildlife species that are killed outright, that are made more susceptible to diseases or prédation, or that are suffering reproductive impairment after exposure to toxic chemicals? To attempt to carry out such quantifications, scientists are turning to wildlife toxicology, which develops and uses ecological and related acute and chronic toxicological information concerning the organism(s) being studied. Wildlife toxicology may be defined as the study of the effects of environmental contaminants on wildlife species, as related to their wellbeing, general health, and reproduction. 448A
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A state of well-being implies, for instance, that there is no significant increase in the probability of being preyed upon, or that there is no aberration in migratory behavior. A state of good general health means that the organism(s) can maintain homeostasis (relatively stable physiological conditions) and, therefore, can survive in a variety of environmental situations. Since the reproductive process is often very sensitive to the influence of chemical contaminants in the environment, it should be accorded a high research priority. The term "wildlife" usually pertains to vertebrate animals living in a natural, undomesticated state, although there are no clear taxonomic guidelines for defining the word. Here, emphasis will be on those species of wildlife, particularly birds and mammals, from which economic benefits, in terms of hunting and fishing, sources of food, nature photography, or aesthetic pleasures, may be derived. This emphasis is in line with the concept that the most often mentioned species of wildlife are those that provide benefits (or detriments) to human society (J). This is not meant to say, however, that other species are not equally important components of the ecosystem. Controlled experiments needed Environmental contaminants affecting wildlife include pesticides, other organic compounds such as polychlorinated biphenyls (PGBs), and heavy metals (e.g., cadmium, lead, and mercury). A fundamental consideration in wildlife toxicological research is determining which of these or other harmful substances wildlife species are exposed to in their habitats, in what amounts, and for how long.
One might ask these questions with regard to osprey {Pandion haliaëtus), for instance. This species has suffered population declines in the eastern U.S., as have other raptors (birds of prey). These losses are attributed partly to deleterious effects of pesticides on their reproduction (4). Osprey exposure to DDT ( 1,1,1-trichloro-2,2-i>/5·[p-chlorophenyl]ethane) is primarily through fish, their major food source. Fish concentrate DDT in their tissues, so osprey, being principal predators in the aquatic ecological food chain, receive elevated exposures to the compound (5). DDT and a metabolite, DDE, appear to impair calcium metabolism in many avian (bird) systems; therefore, eggs break easily because of fragile, calcium-deficient shells, thereby adversely affecting reproduction (6", 7). Mink (Mustela vison) have been shown to be susceptible to reproductive impairment after exposure to PCBs, such as Aroclor 1254, at concentrations in their diet as low as 2 ppm. Mink that died after consuming Lake Michigan coho salmon (Oncorhynchus) containing PCBs showed similar clinical signs and lesions (for example, anorexia, bloody stools, fatty liver, kidney degeneration, and gastric ulcers) as mink that died when given diets containing administered PCBs In teratological studies involving avian wildlife, mallard (Anas platyrhynchos) eggs treated with paraquat (1,1 '-dimethyl-4,4'-bipyridylium dichloride) suffered impaired embryo development; slight teratogenic signs were apparent at .exposure levels that would be equivalent to one-half of the field level of application (9). Such results might lead one to suspect that
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Osprey: was their reproduction impaired by DDT?
Bird eggs: calcium deficiency may make shells fragile
paraquat could affect developing embryos of other wild avian species in a similar manner. Data gathered from these studies show why it is necessary to estimate dose levels of toxicants that might be received by wildlife, in order that effects might be predicted. Predictive capability of contaminant impacts would allow at least some opportunity to reduce or eliminate the hazards of given toxicant exposures to wildlife. Wildlife toxicology can provide a new aid to wildlife management with respect to the determination of adverse effects of contaminants on wildlife species. Until now, impairment of health, disturbance of reproductive processes, or increased susceptibility to prédation have been difficult to measure. To try to overcome this situation, scientific approaches involve both field and laboratory experimentation to investigate contaminant impacts on wildlife populations (10,11). Laboratory experiments can be controlled to a point at which effects of contaminants on wildlife can be measured in a situation wherein other variables such as rain, snow, and changing temperature are removed. This allows more precise observations of the effects of contaminants on wildlife systems without confounding Environ. Sci. Technol., Vol. 16, No. 8, 1982
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stresses from other uncontrolled variables. Laboratory experimental work is necessary and useful for developing data on pathological effects of contaminants in wildlife (for example, establishing dose-response relationships of lead effects on blood delta aminolevulinic acid dehydratase activity concomitant with analyses of tissue lead concentrations in mourning doves), that could have field applications such as obtaining blood samples from wild mourning doves, and predicting body burdens of lead as a function of depression of the enzyme, delta aminolevulinic acid dehydratase. Real-life investigations However, field studies with contaminants are also necessary, for it is here that "real-life situations" involving contaminant exposure in a wildlife population can be investigated. In field experiments, the response of wildlife populations to chemical exposure can be studied to document deleterious effects of toxicants on such populations. Although these studies are often difficult to carry out, if a toxicant has demonstrable negative impacts on a wildlife population (such as DDE impacts on brown pelicans), this information would be extremely useful in trying to find ways to mitigate these impacts. Innovative combinations of field and laboratory experiments will allow one to begin to understand more clearly how contaminants affect wildlife; how to reduce or eliminate pesticide treatments in certain areas if wildlife is being harmed; how to identify wildlife species sensitive to oil pollution, and monitor their population closely in areas that might receive an oil spill; or how to reduce dumping of toxic wastes in vital wildlife habitat areas, for instance. Actually, wildlife has been monitored for environmental contaminant exposure for many years. For example, extensive investigations along these lines have been conducted by scientists at the Patuxent Wildlife Research Center (Laurel, Md.). Considerable information has been developed concerning contaminant residue levels (generally expressed as parts per million, or ppm) of various pesticides, heavy metals, and PCBs in the tissues of wildlife. Although these analytical data are extremely important in assessing exposure of wildlife to toxicants, key questions that are being addressed by wildlife toxicologists at Patuxent and elsewhere include: What does it mean for a wildlife species, such as bobwhite 450A
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Bobwhite quail: assessing pesticide effects quail (Colinus virginianus), to have 2 ppm of pesticides in its breast muscle or 20 ppm in fatty tissue? Could these levels of toxicant be affecting reproduction or even be lethal to this wildlife species? This kind of information is difficult to elucidate, particularly if one works entirely under field conditions. However, the integration of field and laboratory research allows more insight to be gained into the problem, and provides more control over experimentation. When humans must keep out An integrated field and laboratory approach could permit monitoring of wildlife for various toxins and their effects. For instance, might a chemical applied to soybeans be killing bobwhite quail that inhabit the borders of treated fields? This is an important question to ask, since humans are often not allowed to enter organophosphate-treated fields until a sufficient amount of time has passed after spray application. This waiting period varies with the kind of pesticide used, temperature, humidity, rainfall, and other environmental parameters. But because areas bordering these fields are inhabited by many wildlife species, these organisms are exposed to the multitude of chemicals used to control weeds, insects, fungi, and so forth. Exposure effects can sometimes be readily visible, and dramatic. For example, several years ago, a cotton field was sprayed aerially with a pesticide of an unknown type. Small frogs jumping into puddles of water in the sprayed area were seen to go into tetanic contractions almost immediately; the cause was suspected to be pesticide
residues in the water. One wonders how birds using these puddles for drinking water might have been affected. That may be difficult to ascertain. In the case of bobwhite quail, for instance, finding birds whose deaths result from pesticide exposure in the wild is unlikely, since sickened wildlife, such as quail, generally hide themselves, or probably are caught and eaten by predators (12). Therefore collection of quail from a field area before and after pesticide applications would be necessary. Analyses of various tissues or some other index of toxin exposure (such as blood and brain assays of acetylcholinesterase activity in the case of organophosphate-exposed avian and mammalian species) could be used to determine levels of exposure in animals before and after pesticide treatment. These analyses would provide information on what would be normal as compared to elevated tissue pesticide levels. However, if any animals were found dead in the treated area, they could provide extremely valuable information on lethal pesticide levels in the field. In the laboratory, such fieldcollected specimens would be classified according to sex, age, weight, food habits, and date and place of collection. From this data base collected from field specimens, some decisions could be made concerning the approach needed in further laboratory investigations. Organophosphate poisoning Pesticides applied to soybean fields visited by bobwhite quail would probably be sprayed seasonally (spring
through fall), and would most likely include an organophosphate, such as methyl parathion (Ο,Ο-dimethyl Op-nitrophenyl phosphorothioate). Al though organophosphates are a form of insecticide that can often be poi sonous to wildlife (13), their toxicity in the environment generally decreases quickly, and a buildup of residues in food chains (as is the case with DDT in raptors) is not likely to occur. There fore, investigations of the effects of organophosphate pesticide doses given to quail over a short length of time re quire the use of birds raised in captive colonies. Results of preliminary ex periments would determine how much of the pesticide administered orally would result in tissue levels compara ble to those of field-collected ani mals. Bobwhites are often insectivorous during their breeding period (12), and might have a high exposure to the in secticide by eating poisoned insects. Thus, experiments could be conducted with quail that would receive oral doses of pesticides below, at, and above levels detected in field-collected animals. Data collected could include evalua tions of the number of deaths (corre lated with tissue pesticide levels), number of sickened animals, types of toxic symptoms (lethargy, trembling, and so forth), and percentages of ani mals that experience poisoning symp toms at all levels of treatment. With this type of controlled laboratory in formation, one would be in a much better position to evaluate toxic vs. nontoxic levels of the insecticide for that species. Although there are limitations, the capability does exist to determine what happens if bobwhite quail ingest in sects that have just been poisoned during a soybean insecticide applica tion, or are directly exposed to the pesticide spray. If pesticide spraying is determined to be toxic to bobwhites, management plans might entail re duction of insecticide treatments, or using a form of insecticide less toxic to birds. To be sure, other animals subject to toxin exposure must be considered, as well as the necessity to control
crop-damaging insects. Again, an in tegrated approach to the problem comes much closer to providing an swers than do field or laboratory studies conducted in a disjointed fashion. Chlorinated hydrocarbons The evaluation of the impacts of chlorinated hydrocarbon insecti cides (for example, DDT, mirex, and heptachlor) that are stable in the environment, and can enter and become magnified in food chains, entails a different approach. First, field monitoring of the pesticide levels in animal tissues is important. Mirex (dodecachlorooctahydro-1,3,4metheno-2H-cyclobuta [cd] pentalene) for instance, has been sprayed extensively over the Southeast for control of the imported fire ant (solenopsis invicta); mirex residues have been detected in bobwhite quail, probably as a result of this spraying (14). Although some studies showed that quail did not receive lethal shortterm doses of mirex (application rates are generally low), they were exposed to it throughout the year because of the very slow rate of degradation of mirex in the environment (14,15). Further more, since quail are insectivorous during the breeding period, their ex posure potential to the insecticide is increased. Other chlorinated hydro carbons (such as DDT in raptors) have been shown to affect reproduction in avian species adversely (5). That is one reason why, on the basis of field stud ies, mirex came under suspicion of having similar effects on bobwhite quail. To confirm impairments on re production, as well as other long-term effects, laboratory studies would be useful. Investigation of this problem in volved placing breeding pairs of bobwhites in a controlled laboratory sit uation. Mirex was mixed with their food in such a manner as to bring about tissue concentrations at levels below, at, and above those exposure levels detected in field-collected bobwhite quail. On the basis of experi mental results, the pesticide, investi
Methyl parathion—A potent insecticide, but one which does not seem to bioaccumuiate in the food chain
(CHaOfcP
NO2
gated over a generation of bobwhites, was found not to affect reproduction adversely (16). Incidentally, this kind of information would have been diffi cult, if not impossible, to obtain in a field experiment. Although mirex did not seriously affect quail reproduction, there was, nevertheless, a great deal of concern about its persistence in the environment, and its high toxicity to certain estuarine species (17). For these reasons it has been banned by the EPA. It is imperative that the interactive effects of different forms of stress (starvation, cold), nutrition, and age can be considered along with the toxic effects of contaminants. For instance, it is known that birds in general can store high levels of chlorinated hy drocarbon pesticides in their fat de posits; however, during a starvation period, these poisons can be released into their systems because of fat utili zation. Rapid buildup of these toxins in the bloodstream can result in death (18). Lead Heavy metals have also posed haz ards to wildlife. For instance; water fowl mortality from lead shot poison ing has been a well-recognized prob lem for a number of years (18). How ever, little attention has been focused on potential lead shot exposure prob lems in upland game birds or mourning doves (Zenaida macroura). Mourning doves are important game species in most of the Southeast, and are often hunted on wildlife man agement areas where birds are con centrated around corn, millet, and wheat plantings. Extensive shooting around these fields leaves a substantial number of lead shot pellets (19). Wildlife researchers have found lead shot in gizzards of mourning doves that frequent these shot-over fields. Apparently, these birds ingest pel lets, possibly mistaken for grit particles necessary to grind food during the di gestion process, while they feed in and around these managed dove hunting areas. Wildlife investigators have re ported that the proportion of mourning doves found to have at least one lead shot in the gizzard at any given col lection has ranged from 1-6.5% of the birds (19, 20, 21). The relative lack of information on mourning dove expo sure to lead shot, and the potential deleterious effects on mourning dove populations, has led to the initiation of a large-scale lead research project in mourning doves on wildlife manage ment areas in four mid-Atlantic states: Maryland, Virginia, North Carolina, and South Carolina (21). Environ. Sci. Technol., Vol. 16, No. 8, 1982
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A total of 412 mourning doves was collected from six wildlife management areas. Each bird was identified as to date and place of collection and age, and examined for lead shot in the gizzard. Additionally, in the laboratory, chemical analysis of mourning dove tissue (liver as an index of short-term high exposure to lead, and bone as an index of long-term exposure to lead) provided an insight into the toxicological significance of lead shot exposure. It should be realized that although mourning doves ingest lead shot, they are also exposed to other forms of lead, such as environmental lead along roadways. Automobile exhaust results in the deposition of large concentrations of lead along the edges of roadways (22), places often selected by mourning doves to obtain small gravel particles or grit. For that reason, it was necessary not only to examine birds for lead shot in the gizzard, but to analyze their tissues for lead. In that way, not only lead shot exposure, but also exposure to environmental lead could be assessed. Results of the study indicated that 2.4% of the mourning doves were found to have a lead pellet in the gizzard. Only one bird had two lead shots. Chemical analyses of the liver indicated that lead concentrations in approximately 5% of the birds were high enough to suggest recent exposure to a high amount of lead, possibly lead shot. This assessment was based on laboratory determinations that, within 24 hours after ingestion of a lead shot, mourning dove and Japanese quail (Coturnix coturnix japonica) liver lead concentrations are substantially above background concentrations (23, 24). Data on bone lead concentration provided interesting results. Overall, bone lead concentrations in mourning doves were elevated. A total of 10.9% of the doves had in excess of 100 ppm lead in their femur bone. In contrast, mourning doves that have recently fledged the nest and probably have had relatively little exposure to lead have been found to Jiave bone lead often ranging between 1-10 ppm ( / / ) . Bone lead analyses have also been conducted on ruffed grouse (Bonasa umbellus), a bird generally inhabiting remote areas. Ruffed grouse studies indicated that low bone lead concentration varied with the location of specimen collection. Mourning doves collected from wildlife management areas that were associated with higher adjacent human population densities (generally more roads, therefore, more potential environmental lead exposure) 452A
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Ruffed grouse: studied for bone lead concentrations
had higher bone lead concentrations than did those collected from more rural areas. Apparently, these birds reflected increased environmental lead in some areas, as measured in their bone lead. Although lead shot ingestion can increase bone lead concentration through erosion and absorption of lead pellets, bone lead concentration also varies with long-term buildup of lead that could be consumed in the form of lead-contaminated roadside grit, or inhalation of lead aerosols emitted from automobiles. Bone lead studies provided other interesting observations. For instance, adult mourning dove bone lead concentrations were generally significantly higher than those of juvenile birds. This finding would seem reasonable, in that adult birds would have been living longer in the environment, and therefore exposed to a greater amount of environmental lead over a longer period of time. However, some juvenile mourning doves contained very high bone lead concentrations that were not found in adults. It has been determined in laboratory studies that juvenile doves exposed to lead even for relatively short lengths of time can concentrate very high levels of lead in their femur bones (11). So it appears that some juvenile mourning doves are being exposed to lead and are building up high bone lead concentrations that possibly could be associated with their deaths before they reach adult status. These findings are inconclusive, and further studies along these lines are needed.
Biologically, the ingestion of a lead pellet or lead salts can result in elevated tissue lead, which in turn can result in anemia (25), kidney disease (26), testicular and liver lesions (27), and neurological disorders associated with elevated brain lead concentrations (28) in doves. Extensive laboratory studies have been conducted along these lines, and the results indicate that lead shot ingestion can be harmful to the health of doves, and could possibly cause death. However, with sufficient time available after ingestion of lead shot, it appears that some doves can recover from lead poisoning, and appear as healthy as nondosed birds (II). Overall, the results indicated that under some circumstances lead shot ingestion can be highly toxic (for instance, a dove on a corn diet while being exposed to cold stress), whereas at other times it can be relatively less toxic (in the case of a nutritious laboratory diet with doves maintained in room-temperature environments). Further studies are needed to characterize patterns of lead exposure and determine its biological significance. Lead exposure via lead shot ingestion is an important consideration, but environmental lead exposure in mourning doves through ingestion of lead-contaminated roadside grit should also receive a high research priority. Long-term exposure to an element such as lead may not cause outright death, but rather lead to delayed, subtle deleterious effects on the population, possibly by slowing down reproduction, or through losses of in-
dividual birds to diseases such as kid ney necrosis. Behavioral studies Researchers in the Wildlife Toxi cology Laboratory at Western Wash ington University are currently de veloping new techniques to measure the impact of contaminants on be havior of wildlife. In particular, the bobwhite quail is being used as an ex perimental animal model. Measure ments of behavioral toxicity appear to be a sensitive measure of effects of chemicals in this species. Tests are conducted to measure impacts of contaminants on such behavior as muscle coordination and control, dis crimination ability, and learning. Under semicontrolled field condi tions, additional studies are being conducted in order to evaluate impacts of chemicals on predator-prey rela tionships involving bobwhite quail. Many wildlife species may not die outright from toxic Chemical exposure, but even slight modifications of be havior could alter the manner in which they try to escape from predators, to locate and select nutritious food, or to adapt to a changing environment. Such modifications in behavior could lead to "ecological death" of wildlife. Preliminary experimentation suggests that behavioral toxicology could be an extremely useful technique for evalu ating and monitoring impacts of toxic substances on wildlife. Wildlife toxicology is still in its early stages of development, and the future appears to have many research op portunities available. For instance, relatively little is known about the ef fects of multiple contaminant exposure (such as to heavy metals and pesti cides) on wildlife; this certainly occurs in the environment. In addition, much needs to be learned about how various forms of stress, such as starvation, diseases, or exposure to cold, modify the impact of a toxicant on wildlife. Many wildlife toxicological studies have been conducted on healthy wild life species in an optimum environ ment, with adequate food and water available. Although such controlled laboratory studies are needed to characterize dose-response relation ships of toxicant exposure in wildlife, they often simulate natural exposure conditions poorly. For these reasons, semicontrolled field studies (for ex ample, placing penned bobwhite quail in areas sprayed with pesticides) are needed to document population im pacts of toxicants on wildlife. However, even with field studies, it is often difficult to define clearly the relationship between exposure to a
toxicant and a population decline of a species of wildlife. More extensive and accurate quantitative assessments of population trends are needed for those wildlife species that may be affected by a chemical, as well as valid analytical techniques identifying toxicant expo sure patterns. Computer simulation models could be used to integrate toxicological in formation (such as LD50 data) with exposure patterns of wildlife to toxi cants, and possibly predict population fluctuations (29). At this time, pre dictive models of contaminant impacts on wildlife are, in general, relatively unsophisticated. However, if valid predictive models could be evolved, they would be extremely useful man agement tools, particularly for wildlife being exposed to pesticides. In essence, one could forecast wildlife impacts at various levels of pesticide application, and make a decision concerning the amount of pesticide to apply on the basis of the level of pest control needed. At present, wildlife toxicologists cannot assess the impact of toxicants on all species of wildlife, so model species, such as the bobwhite quail, must be identified. Their population ecology must be studied extensively, and their exposure to toxicants must be monitored. It is hoped that, through wildlife toxicological studies inte grating field and laboratory research, contaminant impacts can be better understood and, perhaps, alleviated. Acknowledgment The effort of Crystal Driver of the Huxley College of Environmental Studies, Western Washington University, with re spect to reviewing the manuscript, is ac knowledged. Prior to publication this article was read and commented on for suitability and ap propriateness for inclusion in ES&T by David J. Eaton, Department of Environ mental Health, University of Washington, Seattle, Wash. 98195, and Pat Scanlon, Department of Fisheries and Wildlife Sciences, Virginia Polytechnic Institute and State University, Blacksburg, Va. 24061
References (1) Bellrose, F. C. ///. Nat. Hist. Surv. Bull. 1959,27,235-288. (2) Blus, L. J.; Belisle, Α. Α.; Prouty, R. M. Pest. Monitor. J. 1974, 7, 181-194. (3) Giles, R. H., Jr. "Wildlife Management"; W. H. Freeman and Co.: San Francisco, 1978. (4) Ames, P. L. J. Appl. Ecol. 1966, 3, 8797. (5) Risebrough, R. W.; Davis, J.; Anderson, D. W. In "The Biological Impact of Pesticides in the Environment"; Gillett, J. W., Ed., Envi ron. Health Series 1; Oregon St?te Univ., 1970; pp. 40-53. (6) Ratcliffe, D. A. Nature 1967, 215, 208210.
(7) Bitman, J.; Cecil, H. C ; Harris, S. J.; Fries, G. F. Nature 1969, 224(5214), 44-46. (8) Aulerich, R. J.; Ringer, R. K. Arch. Envi ron. Contam. Toxicol. 1977, 6, 279-292. (9) Hoffman, D. J.; Eastin, W. C , Jr. Arch. Environ. Contam. Toxicol. 1982, / / , 7986. (10) Kendall, R. J., M.Sc. Thesis, Clemson University, S.C. 1976. (11) Kendall, R. J., Ph.D. Dissertation, Virginia Polytechnic Institute and State University, Blacksburg, Va., 1980. (12) Rosene, W. "The Bobwhite Quail, Its Life and Management"; Rutgers University Press: New Brunswick, N.J., 1969. (13) Tucker, R. K.; Crabtree, D. G., "Hand book of Toxicity of Pesticides to Wildlife"; U.S.D.I., Resource Pub. No. 84., 1970. (14) Kendall, R. J.; Noblet, R.; Hair, J. D.; Jackson, H. B. Pest. Monitor. J. 1977,11(2), 64-68. (15) Kaiser, K. L. E. Science 1974, 185, 523-525. (16) Kendall, R. J.; Noblet, R.; Senn, L. H.; Holman, J. R. Poultry Science 1978, 57(6), 1539-1545. (17) Mirex report. "Report of the Mirex Ad visory Committee," E.P.A., Washington, D.C., 1972. ( 18) Van Velzen, A. C ; Stiles, W. B.; Stickel, L. F. J. mid. Manage. 1972, 56(3), 733739. (19) Lewis, J. C ; Legler, E., Jr. J. mid. Manage. 1968, 32(3), 476-482. (20) Locke, L. N.; Bagley, G. E. J. mid. Manage. 1967, 31 (3), 515-518. (21) Kendall, R. J.; Scanlon, P. F. Proc. Ann. Conf. S.E. Assoc. Fish Wild. Agencies 1979, 33, 165-172. (22) Goldsmith, C. D„ Jr.; Scanlon, P. F.; Pirie, W. R. Bull. Environ. Contam. Toxicol. 1976, 16, 66-70. (23) Kendall, R. J.; Scanlon, P. F. Bull. Envi ron. Contam. Toxicol. 1981, 26, 652-655. (24) Kendall, R. J.; Scanlon, P. F. Arch. En viron. Contam. Toxicol. 1982, / / ( 3 ) , 269272. (25) Kendall, R. J.; Scanlon, P. F. Environ. Poll. 1982, 27, 255-262. (26) Kendall, R. J.; Scanlon, P. F. Poultry Sci. 1981,60(9), 2028-2032. (27) Kendall, R. J.; Veit, H. P.; Scanlon, P. F. J. Toxicol. Environ. Health 1981, 8, 649658. (28) Kendall, R. J.; Scanlon, P. F. J. Environ. Pathol. Toxicol. 1982, in press. (29) Tipton, A. R.; Kendall, R. J.; Coyle, J. F.; Scanlon, P. F. Bull. Environ. Contam. Tox icol. 1980, 25, 586-593.
Ron Kendall is an assistant professor of environmental technology at Huxley College of Environmental Studies, West ern Washington University, where he teaches and conducts research in wildlife toxicology. He received his B.S. in biology in 1974 from the University of South Carolina, his M.S. in wildlife biology in 1976 from Clemson University, and his Ph.D. in fisheries and wildlife science from the Virginia Polytechnic Institute and State University. Under an EPA-sponsored traineeship, Kendall received post doctoral training in toxicology at the Massachusetts institute of Technology. Environ. Sci. Technol., Vol. 16, No. 8, 1982
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