3 research outputs found

    Limiting Wind-Induced Resuspension of Radioactively Contaminated Particles to Enhance First Responder, Early Phase Worker and Public Safety—Part 1

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    An accidental radiological release or the operation of a radiological dispersal device (RDD) may lead to the contamination of a large area. Such scenarios may lead to health and safety risks associated with the resuspension of contaminated particles due to aeolian (wind-induced) soil erosion and tracking activities. Stabilization technologies limiting resuspension are therefore needed to avoid spreading contamination and to reduce exposures to first responders and decontamination workers. Resuspension testing was performed on soils from two sites of the Negev Desert following treatment with three different stabilization materials: calcium chloride, magnesium chloride, and saltwater from the Dead Sea in Israel. Two and six weeks post-treatment, resuspension was examined by inducing wind-driven resuspension and quantitatively measuring particle emission from the soils using a boundary-layer wind tunnel system. Experiments were conducted under typical wind velocities of this region. Treating the soils reduced resuspension fluxes of particulate matter 10) and saltating (sand-sized) particles to around background levels. Resuspension suppression efficiencies from the treated soils were a minimum of 94% for all three stabilizers, and the Dead Sea salt solution yielded 100% efficiency over all wind velocities tested. The impact of the salt solutions (brine) was directly related to the salt treatment rather than the wetting of the soils. Stabilization was still observed six weeks post-treatment, supporting that this technique can effectively limit resuspension for a prolonged duration, allowing sufficient time for decision making and management of further actions

    Part 2: Stabilization/Containment of Radiological Particle Contamination to Enhance First Responder, Early Phase Worker, and Public Safety

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    The application of stabilization technologies to a radiologically contaminated surface has the potential for reducing the spread of contamination and, as a result, decreasing worker exposure to radiation. Three stabilization technologies, calcium chloride (CaCl2), flame retardant Phos-Chek® MVP-Fx, and Soil2OTM were investigated to evaluate their ability to reduce the resuspension and tracking of radiological contamination during response activities such as vehicle and foot traffic. Concrete pavers, asphalt pavers, and sandy soil walking paths were used as test surfaces, along with simulated fallout material (SFM) tagged with radiostrontium (Sr-85) applied as the contaminant. Radiological activities were measured using gamma spectrometry before and after simulated vehicle operation and foot traffic experiments, conducted with each stabilization technology and without application as a nonstabilized control. These measurements were acquired separately for each combination of surface and vehicle/foot traffic experiment. The resulting data describes the extent of SFM removed from each surface onto the tires or boots, the extent of SFM transferred to adjacent surfaces, and the residual SFM remaining on the tires or boots after each experiment. The type of surface and response worker actions influenced the stabilization results. For instance, when walked over, less than 2% of particles were removed from nonstabilized concrete, 4% from asphalt, and 40% of the particles were removed from the sand surface. By contrast, for vehicle experiments, ~40% of particles were again removed from the sand, but 7% and 15% from concrete and asphalt, respectively. In most cases, the stabilization technologies did provide improved stabilization. The improvement was related to the type of surface, worker actions, and stabilizer; a statistical analysis of these variables is presented. Overall, the results suggest an ability to utilize these technologies during the planning and implementation of response activities involving foot and vehicle traffic. In addition, resuspension of aerosolizable range SFM was monitored during walking path foot traffic experiments, and all stabilizing agents decreased the measured radioactivity, with the Soil2OTM decrease being 3 fold, whereas the CaCl2 and Phos-Chek MVP-Fx surfaces generated no detectable radioactivity. Overall, these results suggest that the stabilization technologies decrease the availability of particles respirable by response workers under these conditions

    Vorapaxar in the secondary prevention of atherothrombotic events

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    Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)
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