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1 Weapons of Mass Destruction The Chemical Agents.

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2 1 Weapons of Mass Destruction The Chemical Agents

3 2 Stevan Cordas DO MPH Consultant Bioterrorism - Chemical WMD - Texas Department of Health Local Emergency Planning Committee - Tarrant county (toxicology) Medical Reserve Corps oversight committee. Clinical Associate Professor TCOM Certified internal medicine, allergy immunology, occupational medicine

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6 5 Nerve Agents Are related to organophosphate pesticides. Are lethal in small amounts. Act as cholinesterase inhibitors at receptor sites. 5 nerve agents are currently recognized – GA or tabun, GB or sarin, GD or soman, GF and VX.

7 6 Organophosphates and Carbamyl Agents Diazinon (Spectracide) Malathion Parathion Chlorfenviphos Dimethoate Ronnel Nerve Gas Agents Pyridostigmine (Mestinon) Physostigmine (Antilirium) Neostigmine (Prostigmine) Cognex and others Sevin Dust, Carbaryl and many others

8 7 History of Nerve Gas First organophosphate –1854 Tabun (GA) - Schroeder – discovered 1936 Sarin (GB) – Schroeder – discovered 1937 Military production of tabun –nazi – 1942 30,000 tons of tabun produced 1942- 45 Soman (GD) – discovered 1944

9 8 History of Nerve Gas GF discovered Schroeder – 1944 VX discovered Port Down, England – 1955 Russians captured tabun factories and start their own production-1946 United states and England start their own production. – Edgewood chemical and biologic center. –1950- 1970

10 9 History of Nerve Gas President Nixon orders all chemical and biologic agents destroyed. – 1969. Chemical stockpiles partially destroyed in the United States. Soviet union continued production – 1946-91 - developed Novilchek agents - current production status uncertain.

11 10 History of Nerve Gas Iraq develops tabun and uses it against Iran – 1982-1985. Iraq also used tabun against Kurdish dissidents. Iraq admits to placing sarin in scuds and artillery 1991- operation desert storm. Large amounts of chemical containers destroyed by U.S. forces 1991 – 98,900 low level exposures. – Gulf war syndrome emerges.

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13 12 History of Nerve Gas 1994 - First attack by Japanese cult using sarin gas – 7 dead and 200 injured. 1995 – Second attack – same cult using sarin in Tokyo subways – 12 dead and 6000 injured. 1998 – Traces of VX found in Iraqi warheads. 2001-London police find sarin plans – thwart attack. 2001- Insecticide bomb found on terrorist in Israel.

14 13 Sarin Also known as GB; phosphonofluoridic acid, methyl, isopropyl ester; Isoproposmethylphosphonyl fluoride Odorless and colorless Heavier than air – hovers near the ground More lethal in higher temperature Degrades faster with rise in humidity 26 times more deadly than cyanide gas

15 14 Basic Mechanism Nerve gases bind to an esterase (ChE) that breaks down acetylcholine after it is released from the nerve end plate. After a period of time this binding undergoes complex changes and cannot not be reversed – this is called aging. This results in an excess acetylcholine (ACh) syndrome which affects the muscarinic and nicotinic receptors.

16 15 The ACh Goes to Muscarinic and Nicotinic Receptor Sites.

17 16 Signs and symptoms of Nerve Gas Miosis, dim vision, pain in eyes Severe rhinorrhea, lacrymation Bronchorrhea Nausea, Vomiting Diaphoresis Memory, fatigue, anxious, impaired judgment

18 17 Signs and symptoms of Nerve Gas Increased airways resistance. Diarrhea and involuntary micturition. Local or generalized muscle fasciculations. Muscle fatigue then flaccid paralysis. Convulsions and Coma. DUMBELS

19 18 Clinical Picture When Exposed to Nerve Gas Vapor In mild cases, miosis, rhinorrhea, slight tightness in chest or bronchospasm,slight dyspnea, increased secretions, ocular pain and frontal headaches. In moderate cases. An exaggeration of the above symptoms with marked dyspnea, nausea and vomiting.

20 19 Clinical Picture In severe cases the same symptoms as for moderate but also confusion, unconsciousness, muscular fasciculations (generalized), involuntary micturition and defecation, apnea, flaccid paralysis, convulsions, arrhythmias.

21 20 Case 1 27 year old male exposed to unknown substance that was lethal to others in the area. Subjective: Anxiety, nausea, rhinorrhea, mild chest tightness. Objective: Miosis, diaphoresis, elevated BP, regular heart rate, short onset time, seems stable. RBC cholinesterase 30% of normal.

22 21 Hazard to Health Professionals Persons whose skin or clothing is contaminated with nerve agent can contaminate rescuers by direct contact or through off-gassing vapor. Persons whose skin is exposed only to nerve agent vapor pose no risk of secondary contamination; however, clothing can trap vapor.

23 22 Protect Yourself Nerve agent vapor is readily absorbed by inhalation and ocular contact and produces rapid local and systemic effects. The liquid is readily absorbed thorough the skin; however, effects may be delayed for several minutes to up to18 hours.

24 23 Respiratory Protection: Pressure-demand, self- contained breathing apparatus (SCBA) is recommended in response situations that involve exposure to any nerve agent vapor or liquid. Skin Protection: Chemical- protective clothing and butyl rubber gloves are recommended when skin contact is possible because nerve agent liquid is rapidly absorbed through the skin and may cause systemic toxicity.

25 24 Chemical casualty triage is based on walking feasibility, respiratory status, age, and additional conventional injuries. The triage officer must know the natural course of a given injury, the medical resources immediately available, the current and likely casualty flow, and the medical evacuation capabilities.

26 25 CategoryEffectsClinical Signs Immediate Moderate to severe effects in two or more systems (e.g., respiratory, GI, muscular, CNS) Seizing or post- ictal, severe respiratory distress or apneic. Recent cardiac arrest. DelayedRecovering from agent exposure or antidote Diminished secretions, improving respiration

27 26 MinimalWalking and talking Miosis, rhinorrhea, mild to moderate dyspnea Expectant Unconscious, Cardiac/respiratory arrest of long duration. Not expected to survive

28 27 Treat ABC Quickly ensure that the victim has a patent airway. Maintain adequate circulation. If trauma is suspected, maintain cervical immobilization manually and apply a decontaminable cervical collar and a backboard when feasible. Apply direct pressure to stop arterial bleeding, if present.

29 28 General Principles of Triage for Chemical Exposure Check triage tag/card for any previous treatment or triage. Survey for evidence of associated traumatic/blast injuries. Observe for sweating, labored breathing, coughing/vomiting, secretions. Severe casualty triaged as immediate if assisted breathing is required.

30 29 General Principles of Triage for Chemical Exposure Blast injuries or other trauma, where there is question whether there is chemical exposure, victims must be tagged as immediate in most cases. Blast victims evidence delayed effects such as ARDS, etc. Mild/moderate casualty: self/buddy aid, triaged as delayed or minimal and release is based on strict follow up and instructions.

31 30 Treatment of Nerve Gas Agents Hold your breath. Get fresh air as soon as possible. If you have a respirator, put it on. In the military there are three kits – use them all. In the civilian sector the same first three rules apply. If the patient only has miosis 5 or 10 minutes after removal from agent, they probably dont need treatment.

32 31 Mark I Kit If the military Mark I kits containing autoinjectors are available, they provide the best way to administer the antidotes. One autoinjector automatically delivers 2 mg atropine and the other automatically delivers 600 mg 2-PAM Cl.

33 32 Decontaminate as a Priority Rapid decontamination is critical to prevent further absorption by the patient and to prevent exposure to others. Decontaminable gurneys and back boards should be used if possible when managing casualties in a contaminated area. Decontaminable gurneys are made of a monofilament polypropylene fabric that allows drainage of liquids, does not absorb chemical agents, and is easily decontaminated.

34 33 If water supplies are limited, and showers are not available, an alternative form of decontamination is to use 0.5% sodium hypochlorite solution, or absorbent powders such as flour, talcum powder, or Fuller's earth If exposure to vapor only is certain, remove outer clothing and wash exposed skin with soap and water or 0.5% sodium hypochlorite. Place contaminated clothes and personal belongings in a sealed double bag.

35 34 Specific Therapy for Nerve Gas Give atropine sulfate 2mg IV and 2 mg IM stat. Manage Airways, breathing and circulation. Early intubation and ventilatory support with oxygenation. Repeat atropine 2mg IM every 5 or 10 minutes and watch for return of copious secretions and increasing dyspnea. For severe sx, 6 mg is given initially. Follow atropine with Pralidoxime (2-PAM) Protopam in I g vials. 15 to 25 mg/kg or given over 15 minutes IV. 15 mg/kg IM for mild to moderate cases

36 35 2 PAM 1. 2-PAM Cl solution needs to be prepared from the ampoule containing 1 gram of desiccated 2- PAM Cl: inject 3 ml of saline, 5% distilled or sterile water into ampoule and shake well. Resulting solution is 3.3 ml of 300 mg/ml. Mild/Moderate symptoms include localized sweating, muscle fasciculations, nausea, vomiting, weakness, dyspnea. 2. Severe symptoms include unconsciousness, convulsions, apnea, flaccid paralysis.

37 36 Effect of Atropine

38 37 Treatment (contd.) Little effect of 2 PAM treatment on Soman (GD) due to rapid aging. Pyridostigmine pretreatment is most helpful here and has some value with GA. Given orally 30mg every 8 hours. If the individual is alive 5 minutes after inhaling the vapor they probably can make it with your help.

39 38 RBC Cholinesterase Levels With minor adverse effects there is no correlation with RBC-ChE levels. With vomiting one can suspect that at least inhibition of 50 to 90% of the baseline ChE has occurred. Often used to verify organophosphate poisonings. Only decreased by pernicious anemia.

40 39 Late effects of Nerve Gas Attacks Generally no serious adverse effects 6 months late. With convulsions and apnea, inability to learn new tasks, memory impairment and retrograde amnesia has occurred. No clear evidence of peripheral neuropathy or intermediate syndrome.

41 40 Resource for more information Agency for Toxic Substances and Disease Registry Division of Toxicology 1600 Clifton Road NE, Mailstop F-32 Atlanta, GA 30333 Phone: 1-888-42-ATSDR (1-888- 422-8737) FAX: (770)-488-4178 Email:

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43 42 Blister Gases HD, H, HN2, HN3, CX, L

44 43 Sulfur Mustard, 2,2, - Di (Chloro-ethyl)- sulfide

45 44 H and HD Pure Mustard Gas is HD, impure is H. Sulfur Mustard is a vesicant and a respiratory irritant. It was the most effective chemical agent in WWI accounting for 85% of the chemical injuries. Besides being a severe respiratory irritant, it affected the skin like a burn with painful blisters,. The eyes, axilla and scrotum were especially sensitive.

46 45 History of Blister Gas 1822- First discovered. 1860- Ability to produce burns and vesicles proven. 1917 – Used by Germans for the first time at Ypres, France. Called Yperite by French. Lost by Germans. Called yellow cross by the allies and later H and HD. H stood for Hun. HD produced 85% of chemical casualties in WWI.

47 46 History of Blister Gas French quickly followed as did English. The US troops used French blister canisters and shells. Captain Lewis team discovers lewisite 1918. US production after WWI begins Pine Bluff and Aberdeen Proving Ground as chemical warfare department under war department forms in latter days of WWI. Especially from 1950 to 1969.

48 47 History of Blister Gases No use in WWII, Korea or Viet Nam of blister gases. Bari incident Dec 2 1943. 1981 Iraq uses HD against Iran. 1984 Iraq uses HD against Kurds. 1991 Iraq deploys HD but doesnt have a chance to use them.

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50 49 WWI Mustard Casualties and % Death Germany200,0004.5 France190,0004.2 Britain189,0004.2 U.S.73,0002 Russia475,00011.8

51 50 Physical Properties Thick oily amber to brown liquid which freezes/melts at 58° F. Heavier than air (vapor) or water (liquid). Persistent. Penetrates skin in 2 minutes. Causes cellular damage in 5 minutes. Delayed onset of clinical effects. 2-48 hours.

52 51 Diagnosis Delayed onset of clinical symptoms. Urinary thiodiglycol levels elevated. Possible chemical pneumonia manifestations on x-ray. Mainly a clinical diagnosis depending on the circumstances. M8, M9 ( paper if liquid Mustard). CAM.

53 52 Although it is a nonspecific finding, leukopenia can indicate vesicant exposure. It usually begins 3 to 5 days after exposure. With a white blood cell count < 500, the prognosis is poor.

54 53 Effects of Mustard Mustard enter the skin rapidly and convert to cyclic agents that are alkylating agents. They are mutagenic, teratogenic, cytotoxic, and ultimately carcinogenic. DNA adducts are formed and cross linkage damage occurs. The incidence of lung cancer is increased slightly in Mustard survivors than controls.

55 54 Clinical Aspects of Mustard Mild cases –the eyes will develop an irritating conjunctivitis that lasts approximately two weeks. Respiratory symptoms do not occur. The skin will turn reddish and itch or burn. There is always a latent period of 4 to 12 hours before clinical symptoms occur with Mustard even though the damage occurs quickly. In slightly more severe cases the skin will look like scarlet fever.

56 55 Clinical Aspects of Mustard High doses will increase mortality, usually from delayed toxic pulmonary edema. CNS effects including convulsions occur. Severe neutropenia and thrombocytopenia can occur. Those who recover are often hospitalized for months even in the more recent poisonings.

57 56 Differential diagnosis Barbiturates Chemotherapeutic agents Carbon monoxide Stevens-Johnson syndrome Staphylococcus scalded skin syndrome Toxic epidermal necrolysis Bullous pemphigoid Pemphigus vulgaris Other chemical burns (such as with strong acids, bases, or corrosives)

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59 58 Treatment of Mustard Gas Casualties Decontaminate the eyes with water, saline or a weak sodium bicarbonate solution. Remove clothes and bag properly. Decontaminate the skin with 0.5% (1 to 10 dilution) Clorox. Wash this off after 4 or 5 minutes with soap and water. Antibacterial eye drops. Systemic narcotics prn.

60 59 Management Eyes – Avoid topical anesthetics or analgesics. Use mydriatics, topical antibiotics. Vaseline on lids (Dont use eye patch. Sunglasses.

61 60 Skin Unroof blisters. Fluid is non-toxic. Debridement of burns. Soothing lotions. Frequent irrigations. Systemic analgesics. Electrolyte and fluid replacement but not like that for burns.

62 61 Airways Steam, Cough suppressants. Oxygen. Bronchodilators, Steroids. Early intubation may be required. Specific antibiotic administration. Avoid prophylactic antibiotics, Assisted ventilation.

63 62 Marrow May need to use: Reverse isolation. Hormonal therapy. Marrow transplants. Cellular replacement i.e. platelet transfusions etc.

64 63 Death Usually pulmonary with higher exposure concentrations. Secondary infection common and can be fatal. Radiomimetic effect of HD depresses immunity.

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66 65 Lewisite Lewisite or L (NATO) an immediate reacting vesicant that closes the eyes with blepharospasm quickly and produces vesicles. And respiratory effects including pulmonary edema circulatory effects and death can result from this agent.

67 66 Treatment of Lewisite Poisoning Decontamination is critical and must be performed rapidly as the number one priority. Remove form the agent, Remove the clothes, Make sure you decontaminate the hair. Give BAL, DMPS or DMSA to act as an antidote to this agent.

68 67 Phosgene Oxime Dichlorformoxime is a colorless powder that is not a vesicant but an urticant. It commonly produces deep necrosis of the skin and muscle as well and is one of the most severe irritants known. It is termed CX by NATO. It will vaporize at room temperatures. Can cause pulmonary edema and death.

69 68 As a review of signs and symptoms as pertain to different vesicants the following slides are offered as a review of systems.

70 69 Respiratory signs and symptoms Clear rhinorrhea Nasal irritation/pain Sore throat Cough Dyspnea (shortness of breath) Chest tightness Tachypnea Hemoptysis

71 70 Dermal signs and symptoms Itching Immediate blanching (phosgene oxime) Erythema (immediate with lewisite and phosgene oxime, may be delayed for 2 to 24 hours with mustards) Blisters (within 1 hour with phosgene oxime, delayed for 2 to 12 hours with lewisite, delayed for 2 to 24 hours with mustards) Necrosis and eschar (over a period of 7 to 10 days)

72 71 Ocular signs and symptoms Conjunctivitis Lacrimation Eye pain/burning Photophobia Blurred vision Eyelid edema Corneal ulceration Blindness

73 72 Cardiovascular signs Hypotension (with high-dose exposure to lewisite) Atrioventricular block and cardiac arrest (with high-dose exposure) Gastrointestinal signs and symptoms (prominent if ingestion is a route of exposure) Abdominal pain Nausea and vomiting Hematemesis Diarrhea (sometimes bloody)

74 73 Central nervous system signs and symptoms (with exposure to high doses) Tremors Convulsions Ataxia Coma

75 74 Because no antidote exists for mustard exposure, the best thing to do is avoid it. If the nitrogen mustard release was indoors, get out of the building. If the release was outdoors, move away from the area of the release, stay upwind if possible, and seek higher ground. Quickly moving to an area where fresh air is available is highly effective in reducing the possibility of death from exposure to nitrogen mustard.

76 75 Remove Clothing If you think you may have been exposed, you should remove your clothing, rapidly wash your entire body with soap and water, and get medical care as quickly as possible. Quickly take off clothing that has nitrogen mustard on it. Any clothing that has to be pulled over the head should be cut off the body instead of pulled over the head.

77 76 Washing yourself: As quickly as possible, wash any nitrogen mustard from your skin with large amounts of soap and water. Washing with soap and water will help protect people from any chemicals on their bodies. If your eyes are burning or your vision is blurred, rinse your eyes with plain water for 10 to 15 minutes. If you wear contacts, remove them and put them with the contaminated clothing. Do not put the contacts back in your eyes (even if they are not disposable contacts). If you wear eyeglasses, wash them with soap and water.

78 77 Dispose Place your clothing inside a plastic bag. Avoid touching contaminated areas of the clothing. If you can't avoid touching contaminated areas, or you aren't sure where the contaminated areas are, wear rubber gloves or put the clothing in the bag using tongs, tool handles, sticks, or similar objects. Anything that touches the contaminated clothing should also be placed in the bag.

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80 79 Cyanogens Cyanogen chloride (CK) and hydrogen cyanide (AC)

81 80 Sources of Cyanide Available without a prescription Rodenticides, Insecticides Silver and metal polishing solutions Fumigating products Photographic development solutions Tanning and electroplating industries Metallurgy - jewelers

82 81 History of Cyanides Used as a potion to kill friends and enemies since ancient Rome. Isolated and identified by Sheele 1784. Continues to be used in the gas chamber as potassium cyanide dropped into dilute sulfuric acid. Still popular in murder and suicide. Used by France 1915-16 as hydrogen cyanide gas. Called AC by military.

83 82 History of Cyanide Cyanogen chloride, also called CK by the military, introduced September 1916. Austrians tried cyanogen bromide about the same time. In WWII millions of civilians and captured soldiers died from hydrocyanic acid adsorbed on a dispersible base (Zyklon B), a rodenticide. Aum Shinrikyo 1995 attempt to kill more in Tokyo.

84 83 History of Cyanide Iraq felt to have used cyanide against Iran, the Kurds and a village in Syria in 1981-85. 7 killed from poisoned Tylenol -1982. A major cause of death from fires is cyanide from the combustion products of plastics and other man made material. Cassava, low grade CN poisoning, causes tropical ataxic neuropathy.

85 84 Additional History Who will forget the Jonestown massacre or the Tylenol deaths? Cause of toxic amblyopia for tobacco originated cyanide. Congenital flaw in cyanide metabolism lead to Lebers Optic Atrophy.

86 85 Facts About Cyanides 50 mg of the gas and 500mg of the sodium or potassium salts is lethal. Cigarette smoke contains 0.041 g/ml whole blood. 0.016 g/ml in Controls. Inhalation of gas kills in seconds. Longer period with the soluble > insoluble> cyanogen salts. Skin absorption is possible with this agent. Italian authorities arrested a Al Quaeda Cell it Italy with 9 lbs of potassium cyanide intending to poison the water of the US Embassy.

87 86 Pathophysiology Rapidly enters the blood through breath, intestine or skin. Cases histotoxic hypoxia by interfering with the respiratory cytochrome oxidase system. Greatest affinity for oxidized Iron at the cytochrome a-a3 complex. TWA 8 hours in US is 10 ppm. 100 ppm will kill in one hour. 300 ppm will kill in minutes. CN is an important killer in fires.

88 87 Clinical Aspects of Cyanide Poisoning If not fatal, we see weakness of the legs, vertigo, headache and nausea. This may be followed by convulsions and death. At a high Ct, death will occur in 20 seconds. It is unlikely that you will encounter any of those cases. The survivors should be observed and if symptomatic treated.

89 88 Clinical Manifestations of Cyanide Poisoning Gasping for air, hypertensive, bradycardic. Bulging eyes. Odor of bitter almonds - faint. 20-40% cant smell it. Cold clammy skin May have cherry red skin. Cyanosis late. Venous blood the same color as arterial blood – bright red or cherry pink. May look inebriated, confused, dizzy, nauseated. Chest pain.

90 89 Diagnosis of Cyanide Poisoning Clinical diagnosis mainly. CYANTOSNO paper. Blood cyanide of 0.2 g/ml –Clinical toxicity begins. Blood cyanide of 1.0 to 2.5 g/ml stupor and agitation. Levels over 2.5 g/ml potentially fatal. Pulse oximetry not useful. Draw arterial and venous oxygen saturation. If less than 10 mm Hg suspect cyanide. Look for elevated lactate and metabolic acidosis. Plasma lactate > 6 mmol/L.

91 90 Treatment of Cyanide Poisoning Use Lilly cyanide antidote kit. Manage ABC of emergency care. Remove from agent and remove any liquid cyanide that is present. But skin contamination is not required for the gas.

92 91 Treatment of Cyanide Poisoning First you must rapidly bind or fixate the cyanide ion either by creating methemoglobin or fixing it with cobalt compounds. Any person who is conscious and breathing normally more than 5 minutes after being exposed to and removed from cyanide agents will recover without any treatment as this substance is rapidly detoxified by the body.

93 92 Treatment of Cyanide Poisoning Amyl nitrite is often used if there is a respiratory positive pressure present. Do not use amyl nitrate with oxygen as an explosion may occur. Follow this with sodium thiosulphate. In the military, amyl nitrate is used less than in the civilian sector. More meaningful and predictable levels of methemoglobin can be produced by sodium nitrate.

94 93 Treatment of Cyanide Poisoning If there is impairment with breathing, IV sodium nitrate should be used (10 cc of a 3% solution, 300mg over 3 minutes). This will produce methemoglobin, which binds the cyanide. Keep the patient flat or their blood pressure will fall from the nitrite. Try to obtain a little cyanosis to indicate methemoglobinemia.

95 94 Treatment of Cyanide Poisoning Administer the sodium thiosulphate at a dose of 12.5 Gms (50 cc of a 50% solution over a 10 minute period of time. Remember that methemoglobin levels higher than 10% usually indicate that further nitrates are not needed. Cardiac complications with higher doses.

96 95 Treatment of Cyanide Poisoning Remember that sodium thiosulphate must always be given to complete the medical detoxification of cyanate by converting the free and bound cyanide to thiocyanates under the influence of the enzyme rhodenase. The relatively nontoxic thiocyanates can be metabolized.

97 96 Summary of Cyanides There is generally a favorable prognosis for survivors of a cyanide attack who have residual symptoms. Aggressive care is required to ensure a good outcome including cobaltous agents or nitrates followed by sodium thiocyanate.

98 97 Odors of Some Chemical Weapons Nerve gas – None to fruity or paint- like. Mustard –Garlic or Horseradish. Lewisite – Fruity to germanium. Phosgene – New mown hay or green corn. Cyanide – Bitter almond (faint).

99 98 If In Doubt Regional poison control center (1-800-222-1222) Centers for Disease Control and Prevention Public Response Hotline (CDC) English (888) 246-2675 Español (888) 246-2857 TTY (866) 874-2646

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