In 1981, illegal processing of rapeseed oil by a Spanish oil refinery resulted in the mass foodborne illness epidemic known as Toxic Oil Syndrome (TOS). The toxic oil associated with this epidemic was sold in neighborhood markets and by itinerant salesmen as inexpensive olive oil. Ingestion of the toxic oil resulted in more than 20,000 illnesses and over 1,500 deaths in Spain. The etiologic agent of TOS remains unknown. In addition, animal studies have provided little insight into the mechanisms of toxicity because no animal model exhibits the symptoms of TOS. Researchers of Eosinophilia- Myalgia Syndrome (EMS) are in a similar quandary. EMS occurred in the United States in 1989, and the symptoms of this illness parallel TOS quite closely. The MRL/lpr mouse model has been suggested as a possible model for immunotoxicity caused by environmental exposure. Since the symptoms of most chronic phase patients appeared to be immunologically mediated, the MRL/lpr mouse was chosen as the animal model for the present experiment. Sixty two mice were used. Groups often mice were gavaged with three different dose levels of 2% aniline denatured low-erucic acid rapeseed oil (Canola oil) and mercuric chloride as a positive control. Ten mice were untreated as a naive control. Two mice were sacrificed upon arrival as a negative control. All mice treated with toxic oil displayed a decreased rate of weight gain relative to the naive control. Serum antinuclear antibodies (ANA) were detected using indirect immunofluorescence, and anti-type IV collagen antibodies (ACA) were detected using an ELISA technique. The mice receiving toxic oil displayed increased serum ANA titers relative to the naive control. However, there did not appear to be a relationship between toxic oil dose and ANA titer. All animals receiving oil displayed decreased serum ACA titers relative to the naive control. In this case, a direct relationship existed between ACA [p.2 of abstract missing]. / Graduation date: 1999

Digitized by Kansas Correctional Industries

The potential of fenthion to act as a secondary poisoning hazard to birds of prey was investigated using American kestrels (Falco sparverius) and house sparrows (Passer domesticus) as a representative model of a naturally occurring predator-prey interaction. Kestrels were presented with live sparrows previously exposed to perches containing Rid-A-Bird 1100$ sp circler$ solution (Rid-A-Bird, Inc., Muscatine, IA), 11% fenthion active ingredient, under simulated field conditions. All 14 kestrels tested died following ingestion of fenthion-exposed sparrows. Decreased brain cholinesterase activity and residue analyses of kestrel gastro-intestinal samples confirmed secondary fenthion poisoning. / Prey selection trials were conducted in the laboratory to determine the response of kestrels to a mixed flock of contaminated and uncontaminated sparrows. Kestrels captured fenthion-exposed prey significantly more often (12 out of 15 trials) than normal, unexposed prey. / These results suggest that avian predators and scavengers in the wild are at risk from contact with fenthion-exposed prey in areas where Rid-A-Bird perches are in use.

No description available.

The Quotient Method (QM), a laboratory-based risk assessment methodology used by the Environmental Protection Agency to evaluate pesticides for registration and use, has not been thoroughly field-tested and its performance has not always been reliable. My objective was to determine if variation in vegetation structure or diet of exposed animals could result in adverse ecological effects that were not predicted by the QM. In April and early May 1993, I established populations of herbivorous gray-tailed voles (Microtus canicaudus) and omnivorous deer mice (Peromyscus maniculatus) in 24 0.2-ha enclosures planted with alfalfa (Medicago sativa). Alfalfa in 12 enclosures was mowed on 22 June to reduce vegetation height. Small mammal populations were monitored by live trapping from May through August 1993. On 14 July, an organophosphorus insecticide, azinphos-methyl, was applied at 0, 0.88, and 3.61 kg/ha. Insecticide residues were measured on canopy-level spray cards, soil samples, and alfalfa. I compared the observed residue concentrations with predictions based on the nomogram used to estimate exposure for QM risk assessments. I also compared QM predictions of risk with observed effects on population size and growth, survival, reproductive activity, recruitment, body growth, movements, and diet of the small mammals. Much of the insecticide reached ground level in mowed enclosures, but dense alfalfa intercepted most of the spray in unmowed enclosures. The mean half-life of azinphos-methyl on alfalfa was 3.4 days and was not affected by mowing. Mean residue concentrations on mowed alfalfa and the top 15 cm of unmowed alfalfa were underestimated by the QM exposure nomogram. Therefore, pesticides may pose greater risk to organisms inhabiting sparse vegetation or the tops of plants than predicted by the QM. Treatment with azinphos-methyl at 3.61 kg/ha caused severe effects in both mowed and unmowed enclosures on population size and growth, survival, recruitment, and body growth of voles. Effects of azinphos-methyl on vole recruitment and body growth and on survival of female voles were greater in mowed than in unmowed enclosures. However, I did not find that population-level responses of voles to the chemical differed between mowing treatments. Most effects on voles were of short duration (<27 days) but vole densities in 3.61 kg/ha enclosures remained depressed >6 weeks after spraying. The 3.61 kg/ha application rate resulted in a 42% decrease in deer mouse densities in mowed enclosures during the week of spraying, but the insecticide had no adverse effects on deer mice in unmowed enclosures. In addition, the insecticide may have reduced recruitment of deer mice in mowed enclosures. Analysis of deer mouse feces indicated that consumption of arthropods increased in insecticide-treated enclosures just after spraying occurred. Survival, reproductive activity, body growth, and movements of deer mice were highly variable and not significantly affected by azinphos-methyl. Mowing resulted in greater residue concentrations than predicted and, consequently, the insecticide adversely affected voles and deer mice in mowed enclosures at application rates characterized as low risk by the QM. However, food aversion or selective feeding on alfalfa tops may have resulted in similar exposure of voles to the 3.61 kg/ha treatment in mowed and unmowed enclosures. I did not find that insectivorous feeding behavior of deer mice made them more susceptible than predicted. Although residue concentrations on alfalfa did not follow predictions, the gross pattern of effects on small mammals was consistent with QM risk characterization. However, the QM may underestimate exposure and risk when pesticides are sprayed on sparse vegetation. / Graduation date: 1995

A declining population of ring-necked pheasants (Phasianus colchicus) was studied at Tule Lake National Wildlife Refuge (TLNWR) from the summer of 1990 through the spring of 1993. Pheasant densities/50 ha at TLNWR in 1989, 1991, and 1992 were considerably lower (16.86, 8.49, and 6.81) than the >62 density seen in the mid-1950s. Mean body weight of hen pheasants at TLNWR was significantly lower than hens at nearby Lower Klamath National Wildlife Refuge (LKNWR) which was not intensively farmed. Mean tarsal lengths of hens at TLNWR were also significantly shorter than hens at LKNWR, suggesting reduced skeletal growth and potential nutritional problems. The lack of adequate cover was responsible for poor early nest success at TLNWR. Later in the season, spring planted crops provided adequate cover to conceal nesting hens; however, only 0.21 young in 1991 and 0.02 young in 1992 were produced per radio-equipped hen. These rates are extremely low compared to rates required to maintain a stable population. Most adult mortality occurred during the spring and early summer months at TLNWR before crops provided adequate cover, and long before pesticide applications. The main predator of the pheasants was the golden eagle (Aquila chrvsaetos). Of special concern at TLNWR was pheasant and other wildlife exposure to anticholinesterase (antiChE) insecticides used on agricultural croplands at the refuge. Direct toxicity of antiChE compounds (in this case methamidophos) killed 2 young pheasants, but no adult radio-equipped hens died as a direct result of insecticide intoxication. This finding was of particular interest because 15% of the adult pheasants collected in and around potato fields had 55% brain ChE inhibition. The extent of the effects of insecticide exposure on the survivorship of pheasant young was uncertain as they were not radio-equipped. The overriding factor impacting the pheasant population at TLNWR and to a lesser extent LKNWR was poor habitat, especially in the spring when most mortality occurred. The poor habitat also resulted in extremely low recruitment (up to 1 September). Nearly all adult mortality and most of the low recruitment occurred before the insecticide spray season. The population was nearly extirpated during the severe winter of 1992-93. / Graduation date: 1995

Pesticides are among the most pervasive environmental contaminants and they are an important potential risk for human health. Agricultural workers are constantly exposed to pesticide spray, drift and residues in the soil and foliage. Many agricultural pesticides are readily absorbed by the body, through contact with the skin, the respiratory track, the eyes, and the gastrointestinal system. Multiple studies have reported a strong association between pesticide exposure and various health outcomes including cancer. Oxidative stress and DNA damage have been proposed as mechanisms linking pesticide exposure to health effects and neurological diseases. The focus of the present translational study is to examine the relationship between human exposure to the organophosphate pesticide azinphos methyl (AZM) and oxidative stress by measuring biomarkers of oxidative stress in biological fluids (i.e., urine, serum) and peripheral blood lymphocytes (PBLs) of agricultural workers. The findings from these field studies will be validated in vitro by examining cultures of human lymphocytes treated with AZM for similar biomarkers of oxidative stress. Since the collection of PBLs from study participants is highly invasive and not suitable for studies involving younger subjects, we also examined buccal cells for biomarkers of oxidative stress (i.e., DNA damage) as a more universal source of human tissue to assess oxidative stress in pesticide exposed individuals. We demonstrated in this study that AZM induces oxidative stress and causes DNA damage in human tissues. Agricultural workers who had been exposed to AZM showed elevated serum levels of lipid peroxides, increased urinary levels of 8-OH-dG, and lymphocytes from these individuals showed increased DNA damage and associated changes in oxidative DNA repair enzymes. Biomarkers of oxidative stress were also elevated in human lymphocytes treated with physiologically relevant concentrations of AZM. In cultures of human lymphocytes, AZM caused a concentration-dependent loss of viability and associated increases in ROS and a reduction in intracellular GSH. We also demonstrated that viable leukocytes from the oral cavity can be readily obtained from humans and these buccal cells can be used to assess DNA damage following exposure to occupational and environmental genotoxicants. We also noted that oral leukocytes are especially sensitive to cryopreservation with DMSO and thus, these cells must be cryoprotected with 5% DMSO to preserve the viability of these cells for subsequent biochemical studies. In summary, these in vivo and in vitro studies demonstrated that AZM induces oxidative stress in a dose-dependent matter and that oral lymphocytes are a good source of human tissue for assessing DNA damage and possibly other biochemical changes. The possible health implications of the variations in these biomarkers of oxidative stress and DNA damage are undetermined. Yet the findings from these studies have provided a strong foundation for determining the mechanism by which pesticide induce oxidative stress, to explore the putative relationship between pesticide-induced oxidative stress and disease (e.g. cancer, neurodegenerative disorders) and determine whether tissue damage in humans is brought about by direct or by indirect action of organophosphate pesticides. / Graduation date: 2010