Saimiri Sciureus) David Lee Hopper Iowa State University
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Iowa State University Capstones, Theses and Retrospective Theses and Dissertations Dissertations 1976 Delayed matching to sample performance and parathion toxicity in the squirrel monkey (Saimiri sciureus) David Lee Hopper Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/rtd Part of the Experimental Analysis of Behavior Commons, and the Psychiatry and Psychology Commons Recommended Citation Hopper, David Lee, "Delayed matching to sample performance and parathion toxicity in the squirrel monkey (Saimiri sciureus) " (1976). Retrospective Theses and Dissertations. 5746. https://lib.dr.iastate.edu/rtd/5746 This Dissertation is brought to you for free and open access by the Iowa State University Capstones, Theses and Dissertations at Iowa State University Digital Repository. It has been accepted for inclusion in Retrospective Theses and Dissertations by an authorized administrator of Iowa State University Digital Repository. 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Silver prints of "photographs" may be ordered at additional charge by writing the Order Department, giving the catalog number, title, author and specific pages you wish reproduced. 5. PLEASE NOTE: Some pages may have indistinct print. Filmed as received. University Microfilms International 300 North Zeeb Road Ann Arbor, Michigan 48106 USA St. John's Road, Tyler's Green High Wycombe, Bucks, England HP10 8HR 77-10,318 HOPPER, David Lee, 1944- DELAYED MATCHING TO SAMPLE PERFORMANCE AND PARATHION TOXICITY IN THE SQUIRREL MONKEY (SAIMIRI SCIUREUS). Iowa State University, Ph.D., 1976 Psychology, experimental Xerox University Microfilms, Ann Arbor, Michigan48106 Delayed matching to sample performance and parathion toxicity in the squirrel monkey (Saimiri sciureus) by David Lee Hopper A Dissertation Submitted to the Graduate Faculty in Partial Fulfillment of The Requirements for the Degree of DOCTOR OP PHILOSOPHY Major: Psychology Approved; Signature was redacted for privacy. In Charge of Major Work Signature was redacted for privacy. For the Major Department Signature was redacted for privacy. For the Graduate College Iowa State University Ames, Iowa 1976 ii TABLE OF CONTENTS Page Introduction 1 Toxicology of Parathion 3 Mechanism of Action 5 Cholinesterase Alterations 12 Behavioral Effects of the Organophosphorous Compounds 22 in Humans Behavioral Effects of the Organophosphorous Con^unds 26 in Animals Acute e3Ç>osures 26 Chronic e:q>osures 34 Anticholinesterase Agents: Issues Concerning Behavioral 40 Effects Tolerance 40 Central or peripheral effects 42 Cholinesterase depression and behavioral change 43 Selection of the Behavioral Task 44 Purpose 46 Methods 47 Subjects 47 Caging 47 Colony Rooms 52 Test Environment 52 Computer Instrumentation 57 Computer Programming 58 Behavioral Testing Paradigm 61 Behavioral Training Procedures 65 Data Acquisition 70 iii Parathion Exposure Cholinesterase Determinations Subject Attrition Results Treatment Bias Data Analysis Color Matching Form Matching Color Matching Retest Regression Variance Delay Duration Stimulus Discriminability Body Weight Data Cholinesterase Data Discussion Summary References Acknowledgments Appendix A; DMTS Computer Program Appendix B; Monkey Weekly Body Weights 1 Introduction With an ever expanding world population mam's requirements for the basic necessities of life are rapidly increasing, and often exceed his ability to produce such commodities as food, building materials and fuels. This increase in demand fosters the need for continuously more efficient means of production in a world with fixed resources. In the effort to feed the hungry world the industrialized countries have increasingly employed modem pesticides to improve crop production. It has been estimated that 70% of the agricultural crops produced in the United States cannot be successfully grown without the use of insect control measures (Walker, 1970). The estimated total pesticide purchases for farming in the United States increased from 134 million dollars in 1955 to one billion dollars in 1968. Furthermore, in the mid-1960's there was a shift in the type of pesticides used, from the organochlorine to the less stable organophosphorous and carbamate classes (Secretary's Commission on Pesticides, 1969). The increased usage of the organophosphorous pesticides is reflected in production figures from 1951 to 1966; during this period production rose from 3,200 tons in 1951, to 54,000 tons in 1966 (Fest & Schmidt, 1973). The production of parathion-methyl and parathion in the United States in 1965 was approximately 20,700 tons and in 1966, 25,100 tons, or nearly one half of the total organophosphorous pesticide production for the year (Frear, 1968). With a continually increasing quantity of pesticides in the environ ment, particularly the organophosphorous confounds, the balance between the benefits that may be expected versus the possible risk to human health and the potential degradation of environmental quality becomes an important 2 consideration. Because of the extreme neurotoxicity of the organophosphor ous compounds (Wills, 1972), and their lack of highly selective pesticidal action (Murphy, 1975), the use of these compounds must be predicated on selecting quantities and methods of exposure that will minimize the hazard to nontarget organisms. Parathion residues have been present in American food and water at increasing levels for some time (Corneliussen, 1970; Duggan & Weatherwax, 1967; Johnson & Hanske, 1976; Memske & Johnson, 1975; Schulze, Manigold, & Andrews, 1973), these residues do persist to some extent and are mobile in the environment (Deubert & Gray, 1976), and esçosure of agricultural workers and residents in areas where parathion is used has been of growing interest and concern (Li, Fleck, & Kilgore, 1972; Spencer, Cliath, Davis, Spear & Popendorf, 1975; Sumerford, Hayes, Johnston, Walker & Spilleme, 1953). The pesticide hazard to man is real, the mortality rate attributed to poisoning by pesticides has been estimated at 0.65 per one million population in the United States; however, it has also been estimated that there are 100 nonfatal poisonings for each fatal one (Hayes, 1969). Although much attention has been given to overt incidences of pesticide toxicoses, several investigators (Bignami, 1976; O'Brien, 1967; Ruffin, 1963; Van Gelder, Smith & Buck, 1972) have expressed concern for the potential biologic effects of chronic, low-level ei^osure to these agents. The increased utilization, high neurotoxicity, and broad spectrum of toxic action of the organophosphorous compounds, particularly parathion, requires that the effects of long-term, low-level exposure of this pesticide to nontarget organisms be determined. Of specific interest are subtle alterations which might be evidenced in the behavior of em organism which 3 has no apparent clinical signs of toxicosis. Toxicology of Parathion Parathion, 0,0'diethyl 0-p-nitrophenyl thiophosphate, is one of the most widely used organophosphorous compounds, and is manufactured under several trade names.^ Parathion was initially synthesized by Schrader in 1944, and is manufactured by the condensation of diethyl phosphoro- chloridothionate with sodium p-nitrophenate. Pure parathion is a pale yellow liquid with a boiling point of 113°C, and is highly soluble in most organic solvents except alkanes. Its half-life is approximately 203,000 hours at pH 8 and falls to 203 hours at pH 11, with faster hydrolysis in amino acid, chlorine, or copper rich environments (O'Brien, 1967). %e course of the toxicosis following e^osure to an organophosphorous compound has been describe by Namba, Nolte, Jackrel and Grob (1971). the clinical signs and symptoms of organophosphorous toxicosis (see Table 1) are attributable primarily to the accumulation of acetylcholine at the cholinergic synapses and may be divided into