Ehrlich found that larger amounts of toxin (approximately milligram quantities) applied to mouse eyes caused panophthalmitis and loss of the eye (Hunt et al treatment xanthelasma buy generic mesalamine 800mg. Ricin also may be absorbed systemically after ocular instillation and cause damage to internal organs (Strocchi et al medications covered by blue cross blue shield cheap mesalamine american express. Few controlled animal studies are available for several of these toxins medicine prices discount 400mg mesalamine with amex, and comparisons among laboratories are limited by differences in toxin preparations medications with pseudoephedrine cheap mesalamine uk, animal strains, and methodologies employed. The postexposure observation period is a particularly important variable; for example, the literature values for the acute toxicity of abrin vary by 80-fold depending on whether intoxicated animals are observed for 24 or 48 h after exposure (Dickers et al. There are likely differences among species in susceptibility to related plant toxins but, as with ricin, these are often obscured by interlaboratory variability. Stirpe and colleagues compared the postmortem pathology of laboratory rats exposed to supralethal amounts of ricin, abrin, volkensin, modeccin, or viscumin, and found subtle but consistent differences (Stirpe and Battelli, 1990). Each of the five toxins has a delayed effect and causes ascites and early damage to the lymph nodes, the spleen, and the Kupfer sinusoidal cells of the liver. The liver is the primary site of necrosis for ricin, volkensin, or modeccin, whereas the primary lesion detected in parenchymal organs following abrin exposure is necrosis of the pancreatic acinar cells (Stirpe and Battelli, 1990). Differences in pathology may reflect the relative uptake of target cell populations or differences in toxin biodistribution caused by variations in the carbohydrate specificity of the toxin B-chains. For example, volkensin and modeccin lead to greater interneuron toxicity and destruction of neurons in the ipsilateral substantia nigra and intralaminar thalamus of the rat than do ricin or abrin (Wiley and Stirpe, 1987, 1988). The postmortem pathology observed after modeccin injection is similar but not identical to that observed following ricin or abrin poisoning (Flexner, 1897; Green and Andrews, 1923b; Waller et al. Moreover, continued laboratory observations, pathology, and biochemical studies for 4 months after exposure found that acute or chronic exposure to sublethal amounts of ricin or abrin does not cause delayed damage in dogs (Fodstad et al. The efficiency and yield of the in vitro production method vary greatly, but it can produce toxic heterodimers. Only limited reports are available describing the toxicity of ricin or any of the related plant toxins in humans, and most of this literature describes the consequences of relatively benign oral ingestion of unknown amounts of toxin (Balint, 1974; Knight, 1979; Crompton and Gall, 1980; Kinamore et al. Stillmark and Beauvisage reviewed 150 cases of human ricin poisoning before 1894 and identified 9 fatalities (Hunt et al. A review of castor seed poisoning reports from the early 1900s until 1984 revealed only three deaths, two verified by autopsy, for a mortality rate of approximately 1. Ingestion of castor seeds results in a relatively nonspecific syndrome, resembling infectious, food-borne, or chemical gastroenteritis that typically manifests within a few hours after exposure (Rauber and Heard, 1985). Although humans may be particularly susceptible to ricin poisoning, there is little basis for an informed estimate because of the great variation in the amount of toxin contained in castor seeds, as well as variations in the circumstances of poisoning (Hunt et al. For rare cases when castor seed ingestion is fatal, death typically occurs later than the third day after exposure from multiorgan failure; autopsy findings include ulceration of the mucosa of the stomach and small intestine, nephritis, and necrosis of the liver and mesenteric lymph nodes (Rauber and Heard, 1985). One must recognize, therefore, that the highly successful clinical outcome of treating accidental or intentional cases of oral poisoning with castor seeds may not accurately predict the human morbidity or mortality associated with consumption of pure or stabilized ricin. Patients with castor seed allergic syndrome typically present with acute onset conjunctivitis, rhinitis, sneezing, urticaria, and wheezing, and they generally improve by reducing exposure to castor seed products and conventional allergy treatments (e. In one study, up to 96% of individuals with allergy to castor seed dust possessed IgE specific for 2S albumin (Bashir et al. Additional low molecular weight allergens are also likely present in the castor seeds; for example, contact dermatitis has been attributed to zinc ricinoleate oil found in some cosmetic products (Magerl et al. Due to the technical challenges of generating highly toxic and persistent protein aerosols, we expect the risk of lethality to be less than the risk of operational disruption, prolonged incapacitation from ocular or respiratory tract inflammation, and increased burden on medical and logistical assets. Death occurred by 72 h after exposure, and autopsy revealed pulmonary edema and hemorrhagic necrosis of the small bowel, and hemorrhages in lymph nodes near the injection site, myocardium, testicles, and pancreas (Crompton and Gall, 1980). The victim entered the hospital about 36 h after injecting the toxin with symptoms of nausea, dizziness, weakness, chest and abdominal pain, and myalgia with paraesthesia of the extremities. Hepatorenal and cardiorespiratory failure preceded death from an asystolic arrest approximately 54 h after injection. Ricin is cleared from circulation within 24 h after a bolus injection, with apparently first-order kinetics and 99% clearance by 18 h (Fodstad et al.
The longer the latency period exists before recurrence of symptoms symptoms ruptured ovarian cyst order generic mesalamine line, the milder the ensuring signs and symptoms will be treatment xanthoma generic mesalamine 800mg mastercard. Once a patient is exposed to a lung-damaging agent medications herpes order mesalamine with a visa, observe them at bed rest for a period of many hours afterward; the more the better treatment ulcer mesalamine 400mg with amex. This patient must remain totally asymptomatic and have a normal physical exam (including blood gases, chest auscultation, and chest x-ray) after at least 12 h of bed rest before consideration of patient release can be made. Any signs or symptoms of respiratory insufficiency require at least 48 h of close observation (United States Army Medical Research Institute of Chemical Defense, Chemical Casualty Care Division, 2000). Statistically, bed rest immediately after exposure to lung-damaging agents dramatically improves the outcome. This would require an ensuing need for ventilatory support; consequently, treatment should be aimed at preventing the necessity for artificial ventilatory support. In a mass casualty situation, not enough mechanical ventilators would be available. Exercise increases both the heart rate and blood pressure of the patient; this in turn increases both the pressure and the length of duration of increased pressure on blood vessel and alveolar walls at precisely the time when chemical reactions are simultaneously weakening their cellular structure and decreasing surfactant production. This is the mechanism that leads to the development of pulmonary edema when exercise or physical exertion occurs after exposure to lung-damaging agents. Although the irritant gas toxidrome interferes with oxygen use by affecting the flow of air in the airways, the asphyxiant toxidrome works by displacing oxygen, or at the cellular level by interfering with the transportation or use of oxygen. Examples here include high levels of methane, as in a septic system, carbon dioxide, as would occur when trapped in a small closed environment, or home fuel gases, such as natural or propane gases. Two substances interfere with the ability of hemoglobin in red blood cells to transport the oxygen to the cells. All emergency practitioners should be well versed in this gas and its health effects as it is, unfortunately, all too common an exposure. It binds directly to Emergency Medical Response to a Chemical Terrorist Attack 689 hemoglobin in place of oxygen and also makes it more difficult for the hemoglobin to release the oxygen molecules at the other hemoglobin binding sites. Rather, it is produced in the bloodstream by the chemical effects of several other substances. Although turning cherry red is a late, premorbid finding, what will occur is a lack of blue from cyanosis. When directly visualized, as in phlebotomy blood vials, the carboxyhemoglobin blood will appear redder, and the MetHb will appear chocolate brown. Because this is the ``fuel cell' for the body, energy production ceases within the cell, with cell death following close behind. The key substance implicated here is cyanide, which is usually found only in a chemical laboratory setting, but can also be a side effect of smoke inhalation. As previously mentioned, hydrogen sulfide and carbon monoxide also have some effect at this site. The azides, along with the nitro-ate-ites, are also vasodilators and can cause headaches and hypotension. The first part is the pharmacologically-induced development of MetHb by sodium nitrite. This is to lure the cyanide molecule away from the P-450 cytochrome of the mitochondria and to reversibly bind it to MetHb. The difficulty with this treatment is that for every bit of MetHb produced, that much less hemoglobin A1 is available to supply oxygen transport to cells. MetHb (which does not transport oxygen) levels should always be kept below 40%, and depending on the situation, levels of far less than 30% may be far more appropriate. Patients with ischemic cardiomyopathies, low cardiac ejection fractions, arrhythmias that decrease cardiac output (atrial fibrillation, etc. Patients who have also been exposed to carbon monoxide (as in a fire) have already increased the percentage of carboxyhemoglobin (which carries carbon monoxide tightly bound to hemoglobin) in their total hemoglobin content of whole blood, with a subsequent decrease in the percentage of oxyhemoglobin (which carries oxygen) in their total hemoglobin.
Impact of the chemical protective ensemble on the performance of basic medical tasks medications 10325 mesalamine 400mg visa. Effects of chemical protective clothing on military performance: a review of the issues medicine 72 discount 400mg mesalamine mastercard. Trauma and the Vietnam War generation: Report of Findings from the National Vietnam Veterans Readjustment Study treatment jalapeno skin burn buy mesalamine 400 mg visa. Psycho-anatomy of a disaster: a long term study of post-traumatic neuroses in survivors of a marine explosion medicines 604 billion memory miracle purchase 400mg mesalamine visa. Assessment of a severe-weather warning system and disaster preparedness, Calhoun County, Alabama, 1994. Social stress effects on territorial marking and ultrasonic vocalizations in mice. Repeated prolonged social stress with food and water deprivation induces spatial memory impairment in mice. Persistent avoidance of olfactory cues associated with a prior social stress experience. Chemical Warfare, Chemical Terrorism, and Traumatic Stress Responses 649 Lumley, L. Spatial memory impairment and central muscarinic receptor loss following prolonged treatment with organophosphates. Neuropharmacological mechanisms of nerve agent-induced seizure and neuropathology. Protection against nerve agentinduced neuropathology, but not cardiac pathology, is associated with the anticonvulsant action of drug treatment. Protection and damage from acute and chronic stress: allostasis and allostatic overload and relevance to the pathophysiology of psychiatric disorders. Involvement of hormonal and neuromodulatory systems in the regulation of memory storage. The contribution of pharmacology to research on the mechanisms of memory formation. Maternal care, gene expression, and the transmission of individual differences in stress reactivity across generations. Chronic social stress in mice is associated with increased dendritic spine density in the amygdala. Biological alterations in posttraumatic stress disorder: implications for research and the U. Soman-induced convulsions in rats terminated with pharmacological agents after 45 min: neuropathology and cognitive performance. Coping, functioning, and adjustment of rescue workers after the Oklahoma City bombing. Managing severe gas mask anxiety with a cognitive-behavioral approach: an illustrated case study and treatment protocol. Trauma, proximity, and developmental psychopathology: the effects of war and terrorism on children. Twenty-four hour urinary cortisol and catecholamine excretion in combatrelated posttraumatic stress disorder. Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Analysis of hippocampal subregional changes in neurotrophin gene expression following acute social defeat stress using laser-capture microdissection and microarrays. Chronic, low-level exposure to diisopropylfluorophosphate causes protracted impairment of spatial navigation learning. Effects of chronic, low-level organophosphate exposure on delayed recall, discrimination, and spatial learning in monkeys and rats. Chemical Warfare, Chemical Terrorism, and Traumatic Stress Responses 651 Romano, J.
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However symptoms hiv purchase genuine mesalamine on-line, these single occurrence jobs are excluded from the low range estimate of the analysis (see Section 7 symptoms thyroid problems purchase mesalamine 400 mg online. For each dredging job included in the analysis medicine expiration dates order cheapest mesalamine and mesalamine, the Agency identified: the number of occurrences of this dredging job the time elapsed between occurrences of dredging medicine 81 cheap 400mg mesalamine otc. For the 721 jobs that only occurred once from 1995 to 2008, the number of future dredging jobs is set to one, except in the low estimate, where it is set to zero (see Section 7. November 2009 7-4 Environmental Impact and Benefits Assessment for the C&D Category 7. In addition, for occurrences of the same job that were within 30, 90, or 180 8 days of one another, the occurrences were consolidated into one occurrence and total amount of sediment dredged was summed. The total quantity of sediment dredged for each job (single location) over the past 14 years was divided by the number of occurrences of that job to calculate an average quantity of sediment dredged for an occurrence of that job. November 2009 7-5 Environmental Impact and Benefits Assessment for the C&D Category 7. The quantity of sediment for each dredging job (calculated as described in Section 7. For the post-compliance scenarios, total amount of sediment dredged was determined as described in Section 7. Because costs will occur whenever the waterbody is dredged rather than on an annual basis, each reach will have a unique stream of costs derived from its individual dredging frequency, cost, dredging volume, and reduction in sediment. For example, if the Mississippi River is scheduled to be dredged every 2 years between 2010 and 2023, there will be no dredging costs for year 1, but the dredging costs in year 2 will be equal to the cost per cubic yard multiplied by the amount of sediment dredged, then discounted by 2 years. Dredging costs will then be incurred in year 4 as in year 2, but discounted by 4 years, and so on. The sum of the discounted costs of these six dredging occurrences is the total present value of the dredging cost of the Mississippi River for the next 14 years. Repeating this process for every dredging job in this analysis yields an estimate of national dredging costs over the next 14 years. Alternately, the frequency can be interpreted as occurring at the beginning of each interval rather than at the end, so that in the example above, the Mississippi River would be dredged in year 1, then in year 3, etc. November 2009 7-7 Environmental Impact and Benefits Assessment for the C&D Category Assigning 10th percentile cost and cubic yards dredged estimates for jobs lacking these data Excluding jobs with only one occurrence over the 14 years from 1995 to 2008. Midpoint estimate: Assuming a minimum recurrence interval of 90 days to include jobs with more closely spaced recurrences Using 50th percentile (median) cost and cubic yards dredged estimates for jobs lacking these data Including jobs with only one occurrence over the 14 years from 1995 to 2008 under the assumption that these jobs or similar jobs will occur once over the next 14 years. High estimate: Assuming a minimum recurrence interval of 30 days Using 90th percentile cost and cubic yards dredged estimates for jobs lacking these data Including jobs with only one occurrence between 1995 and 2008 under the assumption that these jobs or similar jobs will occur once over the next 14 years. This analysis also presents costs for all estimates using both 3 and 7 percent discount rates. This annualized cost was calculated using the same interest rates used to discount future dredging costs. Table 7-5 presents estimated total annualized dredging (cubic yards removed) and the estimated costs for navigable waterway dredging for the baseline scenario, including low, midpoint, and high estimates. Under the baseline scenario, midpoint dredging costs projected over the period of 2010 to 2023 are expected to range between $468 and 620 million per year (annualized using a 7 and a 3 percent discount rate, respectively). The high and low estimates produce an overall range between $360 million and $655 million. Regions 4 and 6 are expected to incur the highest costs, as they have the largest percentage of dredging activity and amounts of sediment dredged. Regions 1 and 7 also have considerably lower dredging costs than other regions, due to the small number of recorded dredging jobs in these areas. Each of these estimates was calculated using both 3 and 7 percent rates to discount and annualize costs. Because the discount rate does not make a significant difference in the overall avoided costs, all values discussed are those calculated assuming a 3 percent discount rate. This is due to a large amount of dredging activity in these regions, and a large percentage reduction in sediment runoff expected as a result of the regulation. Due to the lack of significant dredging activity in Region 8, no noticeable benefits are expected in this region. The requirements of Option 4 produce larger reductions in dredged sediment than those of Option 2, as turbidity treatment is required on more sites.
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