Academic literature on the topic 'Orange county (va.)'

Abstract An experiment was conducted in Orange County, Va., to determine the effectiveness of several commercial and experimental granular insecticides against corn rootworm larvae. The field used in this experiment has been in continuous corn for more than 20 years. The predominant soil type for this field is a Manassas silt loam, with some areas of Penn silt loam and Rapidan silt loam. The experimental design involved a randomized complete block wtih 4 replications. Plots were 30-ft long and consisted of 2 rows spaced 30 inches apart. A John Deere, 2-row Max-Emerge planter was used to plant all plots on 7 Jun at a plant population density of 26,000 plants/acre. Insecticide granules were applied in front of the press wheels either directly in the seed furrow or in a 5-inch T-band over the furrow, depending on the treatment. Prior to application, the regular granular insecticide applicators were removed from each side of the planter in order to accommodate 2 wooden boxes designed to hold inverted pint canning jars (Mason) for dispensing the insecticide granules. Attached to the underside of both wooden boxes was a plastic funnel and tube through which the insecticide granules flowed. A single opening, drilled into the lid of each jar, was laboratory-calibrated to deliver insecticides accurately at a speed of 3 mph. The possibility of mixing one or more insecticides was avoided by using a separate jar and lid for each treatment. At the start of application, 2 jars containing the appropriate insecticide granules were inverted and placed in the box holders. This method helped minimize soil compaction because the tractor made only 2 pass/plot. Stand counts were made on 29 Jun, by determining the number of corn plants in 3 separate, 3.3-row ft sections/ plot. The roots of 5 consecutive corn plants were dug from each plot on 19 Jul and washed of excess soil. Corn rootworm damage ratings were based on the Iowa 1-6 scale (1—no feeding; 6—3 or more root nodes completely destroyed).

Abstract On 14 Aug, 20 oak trees in Virginia Beach, VA, were used to evaluate 4 insecticides for control of orange-striped oakworm. Insecticides were applied using a 1 gal B & G compressed air sprayer at 30 psi. Plants were treated to runoff. Larval counts of the replicated treatments were made 48h after treatment. Temperature at time of treatment was 77°F and 1.95 inches of rainfall fell between application and evaluation.

Abstract On 8 Aug ‘85, 21 oak trees 5-7 ft tall in Virginia Beach, VA were ! reared to runoff using a 1-gal B & G compressed air sprayer at 30 psi. Larval counts of the treatments (3 replicates per treatment) were made 24 !i and 96 h posttreatment. Temperature at time of treatment was 80 F and .11 inches of rainfall fell between application and evaluation.

Abstract Abstract 4575 Background: From 1962–1971, 19 million gallons of Agent Orange (AO) and other herbicides were sprayed in South Vietnam and Cambodia to destroy dense jungle and crops used to conceal and feed enemy troops. In 2004, the Department of Veterans Affairs added chronic lymphocytic leukemia (CLL) to the list of Veterans Diseases Associated with Agent Orange, based upon data from agricultural exposure suggesting a causative association. In our retrospective cohort study, we evaluated if Agent Orange exposure was associated with an altered prognosis, time to treatment, or overall survival in veterans with newly diagnosed CLL. Methods: Clinical data was reviewed from 205 patients (pts) with CLL diagnosed from 2000–2010, identified through the Minneapolis MN VA Tumor Registry. Demographic information and laboratory parameters at diagnosis were collected, and Rai disease stage, marrow cytogenetics and lymphocyte doubling time were determined. Baseline labs, lymphocyte doubling time and time to initial CLL treatment were compared between exposed and unexposed pts using Student's t-test. Kaplan Meier analysis compared overall survival between Agent Orange-exposed and unexposed pts. Results: Of the 199 (97%) pts confirmed to have CLL, 33 pts (16.6%) had Agent Orange exposure. Median follow-up time was 40.7 months (0.1–123 months). Pts with Agent Orange exposure were younger at diagnosis (61 vs. 72 years, p=0.001). WBC, hemoglobin, platelet count, Rai stage, and LDH at diagnosis were similar between the groups. Mean lymphocyte doubling time was comparable in exposed and unexposed pts (27 vs. 23 months (mos), respectively p=0.6). Cytogenetic analysis was limited as 24% of pts underwent a bone marrow biopsy. Poor risk cytogenetics (17p-, 11q-) were found in 1 of 10 (10%) pts with Agent Orange exposure and 3 of 37 (8%) unexposed pts. Time to first CLL treatment was significantly shorter in pts with Agent Orange exposure [9.6 (range 0.1–23.7) vs. 30.2 mos (range 0.1–163.3), respectively; p=0.02]. No significant difference in reason for treatment initiation was found between the groups. First line fludarabine therapy was used more often in exposed than unexposed pts, which may have been due to their younger age at diagnosis (100% AO exposed vs 36% AO unexposed, Fisher's Exact p=0.01). No difference in overall survival was found between exposed and unexposed pts (Wilcoxon p=0.28). In a multivariable Cox regression model adjusted for age, Agent Orange exposure had a hazard ratio of death of 1.8 compared to non-exposure (95% CI: 0.7– 4.5, p = 0.24). Conclusions: CLL pts with Agent Orange exposure were diagnosed at a younger age and had a shorter time to first treatment, as compared to unexposed pts. Agent Orange exposure was not associated with a difference in prognosis in these patients. Although our hazard ratio result was not statistically significant, the high estimate of the mortality hazard combined with the relatively low numbers in the exposure group suggest that further examination of this issue in a larger patient population is warranted. Disclosures: No relevant conflicts of interest to declare.

Abstract BACKGROUND: Agent Orange (AO), a 1:1 mixture of herbicides + TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin), was used during the Vietnam War to destroy dense jungle and enemy crops. In 2002 the Department of Veteran Affairs (VA) determined that chronic lymphocytic leukemia (CLL) was associated with AO exposure. Case-control studies suggest an increased risk of death from CLL in areas where herbicide use was highest. There is also an increased incidence of other cancers (prostate, melanoma) in AO-exposed veterans. Limited data exists as to the specific impact of AO exposure on CLL disease presentation and outcome. METHODS: Patients (pts) diagnosed with CLL from 2009-2013 were identified in the National VAMC Tumor Registry. Baseline demographic and laboratory parameters were obtained, including Rai stage, marrow cytogenetics (when available), and lymphocyte doubling time (LDT). AO exposure was identified according to the medical record. The VA Benefits and Compensation officers determine AO exposure based on whether a person served on land and in the brown waters in Vietnam during the appropriate timeframe. Timing and types of CLL therapies were identified to determine if AO exposure influenced CLL treatment. RESULTS: 2052 CLL pts were identified, of which 418 had AO exposure. AO-exposed pts presented at a younger age (63.2 versus [vs] 70.5 years (yrs), p <0.0001), had a higher hemoglobin (14.3 vs 13.8 g/dl, p<0.001) and lower lactate dehydrogenase (LDH) (203 vs 227 IU/L, p = 0.01) compared to those without AO exposure. There were no differences in white cell, platelet, or absolute lymphocyte counts, Rai stage or LDT among the groups. Cytogenetic data was available for 1167 pts. There was no difference in the incidence of 17p-, 11q-, or 13q- between the two groups. Median overall survival (OS) was significantly better in patients with AO exposure, even when adjusted for age and Rai stage (median not reached vs 91.2 months, p <0.0001. OS benefit was primarily seen in pts age 60-69 yrs (p = 0.002), and those with 11q- (p = 0.001). No OS differences were found in pts with 17p- or 13q-. Among all pts, regardless of AO exposure status, OS decreased with higher Rai stage. There was a trend towards AO-exposed pts to be more likely to receive CLL-directed therapies (37% vs 32%, p = 0.07). AO exposed pts were more likely, than unexposed pts, to receive therapies as follows: fludarabine, chlorambucil, rituximab (FCR) first-line (38% vs 21%) and second-line (11.6 vs 5%); bendamustine + rituximab (BR) first-line (25% vs 18%), second-line (35 vs 26%), and third-line (31 vs 23%). Pts with no AO exposure were more likely to receive single agent chlorambucil or cyclophosphamide as first-line therapy (17 vs 10%). CONCLUSION: Pts with AO exposure, compared to unexposed pts, had an OS benefit independent of age and Rai stage, with this benefit seen primarily in younger pts (age 60-69 yrs) and in those with 11q-. AO-exposed pts were also more likely to receive disease-specific therapy. This unexpected OS finding will require further analyses for confounding variables, but could potentially be related to earlier treatment with regimens as FCR or BR. Disclosures Morrison: Celgene: Speakers Bureau; Genentech: Speakers Bureau; Gilead: Speakers Bureau; Pharmacyclics: Speakers Bureau; Celgene: Other: Data Monitoring Committee; Merck: Other: Adjudication Committee.