Industrial Toxins Acute Toxic Lung Injury Caused by Inhalation of Chemical Agents? Clin Toxicol (Phila) 49: 61, 2011

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Industrial Toxins Acute Toxic Lung Injury Caused by Inhalation of Chemical Agents? Clin Toxicol (Phila) 49: 61, 2011 31. de Lange DW, Meulenbelt J: Do corticosteroids have a role in preventing or reducing CHAPTER Industrial Toxins acute toxic lung injury caused by inhalation of chemical agents? Clin Toxicol (Phila) 49: 61, 2011. [PMID: 21370942] Chip Gresham 32. Pavelchak N, Church L, Roerig S, et al: Silo gas exposure in New York State following the 204 dry growing season of 1995. Appl Occup Environ Hyg 14: 34, 1999. [PMID: 10730136] Frank LoVecchio 33. Centers for Disease Control and Prevention (CDC): Exposure to nitrogen dioxide in an indoor ice arena—New Hampshire, 2011. MMWR Morb Mortal Wkly Rep 61: 139, 2012. [PMID: 22377844] 34. Hesterberg TW, Bunn WB, McClellan RO, Hamade AK, Long CM, Valberg PA: Critical REFERENCES review of the human data on short-term nitrogen dioxide (NO2) exposures: evidence for NO2 no-effect levels. Crit Rev Toxicol 39: 743, 2009. [PMID: 19852560] 1. Levitin HW, Siegelson HJ: Hazardous materials. Disaster medical planning and response. 35. Elsayed NM: Toxicity of nitrogen dioxide: an introduction. Toxicology 89: 161, 1994. Emerg Med Clin North Am 14: 327, 1996. [PMID: 8635411] [PMID: 8023327] 2. Levitin HW, Siegelson HJ, Dickinson S, et al: Decontamination of mass casualties— 36. Persinger RL, Poynter ME, Ckless K, Janssen-Heininger YM: Molecular mechanisms of re-evaluating existing dogma. Prehosp Disaster Med 18: 200, 2003. [PMID: 15141859] nitrogen dioxide induced epithelial injury in the lung. Mol Cell Biochem 234–235: 71, 3. Rotenberg JS, Newmark J: Nerve agent attacks on children: diagnosis and management. 2002. [PMID: 12162462] Pediatrics 112: 648, 2003. [PMID: 12949297] 37. Tanaka N, Emoto T, Matsumoto T, Matsunaga N, Tsuruta R, Lynch DA: Inhalational lung 4. Henretig FM, Cieslak TJ, Eitzen EM: Biological and chemical terrorism. J Pediatr 141: injury due to nitrogen dioxide: high-resolution computed tomography findings in 311, 2002. [PMID: 12219050] 3 patients. J Comput Assist Tomogr 31: 808, 2007. [PMID: 17895797] 5. Committee on Environmental Health; Committee on Infectious Diseases, Michael WS, 38. Pelham TW, Holt LE, Moss MA: Exposure to carbon monoxide and nitrogen dioxide in Julia AM: Chemical-biological terrorism and its impact on children. Pediatrics 118: 1267, enclosed ice arenas. Occup Environ Med 59: 224, 2002. [PMID: 11934949] 2006. [PMID: 16951026] 39. Aggarwal AN, Ramanathan RM, Jindal SK: Acute respiratory distress syndrome follow- 6. Teran-Maciver M, Larson K: Implications of chemical biological terrorist events for ing nitrogen dioxide exposure. Indian J Chest Dis Allied Sci 40: 275, 1998. [PMID: children and pregnant women. MCN Am J Matern Child Nurs 33: 224, 2008. [PMID: 10091468] 18664903] 40. Lalić H, Djindjić-Pavicić M, Kukuljan M: Ammonia intoxication on workplace—case 7. Collins JJ, Molenaar DM, Bowler LO, et al: Results from the US industry-wide phosgene report and a review of literature. Coll Antropol 33: 945, 2009. [PMID: 19860130] surveillance: the Diller Registry. J Occup Environ Med 53: 239, 2011. [PMID: 21293301] 41. Pirjavec A, Kovic I, Lulic I, Zupan Z: Massive anhydrous ammonia injury leading to lung 8. Gutch M, Jain N, Agrawal A, Consul S: Acute accidental phosgene poisoning. BMJ Case transplantation. J Trauma 67: E93, 2009. [PMID: 19820568] Rep Apr 2: 2012 [PMID: 22602834] 42. Bhalia A, Mahi S, Sharma N, Singh S: Glycopyrrolate in toxic exposure to ammonia gas. 9. McKeown NJ, Burton BT: Acute lung injury following refrigeration coil deicing. J Emerg Trauma Shock 4: 140, 2001. [PMID: 21633586] Clin Toxicol (Phila) 50: 218, 2012. [PMID: 22372791] 43. Borron SW, Baud FJ: Acute cyanide poisoning: clinical spectrum, diagnosis, and 10. Borak J, Diller WF: Phosgene exposure: mechanisms of injury and treatment strategies. treatment. Arh Hig Rada Toksikol 47: 307, 1996. [PMID: 8989894] J Occup Environ Med 43: 110, 2001. [PMID: 11227628] 44. Beasley DM, Glass WI: Cyanide poisoning: pathophysiology and treatment recommen- 11. Sciuto AM, Hurt HH: Therapeutic treatments of phosgene-induced lung injury. Inhal dations. Occup Med (Lond) 48: 427, 1998. [PMID: 10024740] Toxicol 16: 565, 2004. [PMID: 15204747] 45. Geller RJ, Barthold C, Saiers JA, Hall AH: Pediatric cyanide poisoning: causes, manifesta- 12. Grainge C, Rice P: Management of phosgene-induced acute lung injury. Clin Toxicol tions, management, and unmet needs. Pediatrics 118: 2146, 2006. [PMID: 17079589] (Phila) 48: 497, 2010. [PMID: 20849339] 46. Osuntokun BO: Epidemiology of tropical nutritional neuropathy in Nigerians. Trans R 13. Grainge C, Jugg BJ, Smith AJ, et al: Delayed low-dose supplemental oxygen improves Soc Trop Med Hyg 65: 454, 1971. [PMID: 5097851] survival following phosgene-induced acute lung injury. Inhal Toxicol 22: 552, 2010. 47. Cliff J, Muquingue H, Nhassico D, Nzwalo H, Bradbury JH: Konzo and continuing cya- [PMID: 20384554] nide intoxication from cassava in Mozambique. Food Chem Toxicol 49: 631, 2011. 14. Hardison L Jr, Wright E, Pizon AF: Phosgene exposure: a case of accidental industrial [PMID: 20654676] exposure. J Med Toxicol 10: 51, 2014. [PMID: 23842907] 48. Sang-A-Gad P, Guharat S, Wananukul W: A mass cyanide poisoning from pickling bam- 15. Grainge C, Brown R, Jugg BJ, et al: Early treatment with nebulised salbutamol worsens boo shoots. Clin Toxicol (Phila) 49: 834, 2011. [PMID: 21972937] physiological measures and does not improve survival following phosgene induced acute 49. Hall AH, Rumack BH: Clinical toxicology of cyanide. Ann Emerg Med 15: 1067, 1986. lung injury. J R Army Med Corps 155: 105, 2009. [PMID: 20095175] [PMID: 3526995] 16. Parkhouse DA, Brown RF, Jugg BJ, et al: Protective ventilation strategies in the manage- 50. Reade MC, Davies SR, Morley PT, Dennett J, Jacobs IC; the Australian Resuscitation ment of phosgene-induced acute lung injury. Mil Med 172: 295, 2007. [PMID: 17436775] Council: Review article: Management of cyanide poisoning. Emerg Med Australas 24: 22, 17. Del Sorbo L, Goffi A, Ranieri VM: Mechanical ventilation during acute lung injury: cur- 2012. [PMID: 22672162] rent recommendations and new concepts. Presse Med 40: e569, 2011. [PMID: 22104487] 51. Parker-Cote JL, Rizer J, Vakkalanka JP, et al: Challenges in the diagnosis of acute cyanide 18. Centers for Disease Control and Prevention (CDC): Ocular and respiratory illness asso- poisoning. Clin Toxicol (Phila) 56: 609, 2018. [PMID: 29417853] ciated with an indoor swimming pool—Nebraska, 2006. MMWR Morb Mortal Wkly Rep 52. Baud FJ, Barriot P, Toffis V, et al: Elevated blood cyanide concentrations in victims of 56: 929, 2007. [PMID: 17851445] smoke inhalation. N Engl J Med 325: 1761, 1991. [PMID: 1944484] 19. Babu RV, Cardenas V, Sharma G: Acute respiratory distress syndrome from chlorine 53. Garlich FM, Alsop JA, Anderson DL, et al: Poisoning and suicide by cyanide jewelry inhalation during a swimming pool accident: a case report and review of the literature. cleaner in the US Hmong community: a case series. Clin Toxicol (Phila) 50: 136, 2012. J Intensive Care Med 23: 275, 2008. [PMID: 18508837] [PMID: 22292976] 20. Cevik Y, Onay M, Akmaz I, Sezigen S: Mass casualties from acute inhalation of chlorine 54. Akyildiz BN, Kurtoğlu S, Kondolot M, Tunç A: Cyanide poisoning caused by ingestion gas. South Med J 102: 1209, 2009. [PMID: 20016425] of apricot seeds. Ann Trop Paediatr 30: 39, 2010. [PMID: 20196932] 21. Centers for Disease Control and Prevention (CDC): Chlorine gas exposure at a metal 55. Curry SC, Arnold-Capell P: Toxic effects of drugs used in the ICU: nitroprusside, nitro- recycling facility–California, 2010. MMWR Morb Mortal Wkly Rep 60: 951, 2011. glycerin, and angiotensin-converting enzyme inhibitors. Crit Care Clin 7: 555, 1991. [PMID: 21775949] [PMID: 1907524] 22. Jones R, Wills B, Kang C: Chlorine gas: an evolving hazardous material threat and uncon- 56. Bebarta VS, Pitotti RL, Dixon PS, et al: Hydroxocobalamin and epinephrine both ventional weapon. West J Emerg Med 11: 151, 2010. [PMID: 20823965] improve survival in a swine model of cyanide-induced cardiac arrest. Ann Emerg Med 60: 23. Urbanetti JS: Toxic inhalational injury, in Sidell FR, Takafuji ET, Franz DR (eds): Medical 415, 2012. [PMID: 22424656] Aspects of Chemical and Biological Warfare. Washington, DC: Office of the Surgeon 57. Cummings TF: The treatment of cyanide poisoning. Occup Med (Lond) 54: 82, 2004. General; 1997, p. 247. [PMID: 15020725] 24. White CW, Martin JG: Chlorine gas inhalation: human clinical evidence of toxicity and 58. Hall AH, Saiers J, Baud F: Which cyanide antidote? Crit Rev Toxicol 39: 541, 2009. experience in animal models. Proc Am Thorac Soc 7: 257, 2010. [PMID: 20601629] [PMID: 19650716] 25. Server M, Mordeniz C, Server F, Dokur M: Accidental chlorine gas intoxication: evalua- 59. Borron SW, Baud FJ: Antidotes for acute cyanide poisoning. Curr Pharm Biotechnol 13: tion of 39 patients. J Clin Med Res 1: 274, 2009. [PMID: 22481989] 1940, 2012. [PMID: 22352728] 26. Govier P, Coulson JM: Civilian exposure to chlorine gas: a systematic review. Toxicol Lett 60. Borron SW, Baud FJ, Megarbane B, Bismuth C: Hydroxocobalamin for severe acute cyanide 293: 249, 2018. [PMID: 29355691] poisoning by ingestion or inhalation. Am J Emerg Med 25: 551, 2007. [PMID: 17543660] 27. Mohan A, Kumar SN, Rao MH, Bollineni S, Manohar IC: Acute accidental exposure to 61. Borron SW, Baud FJ, Barriot P, et al: Prospective study of hydroxocobalamin for acute chlorine gas: clinical presentation, pulmonary functions and outcomes. Indian J Chest cyanide poisoning in smoke inhalation. Ann Emerg Med 49: 794, 2007. [PMID: 17481777] Dis Allied Sci 52: 149, 2010. [PMID: 20949733] 62. Hamad E, Babu K, Bebarta VS: Case files of the University of Massachusetts Toxicology 28. Liu ZJ, Huang DJ, Wang ZQ, Wang ZG, Chang SH, Wu ZC: [Radiographic and computed Fellowship: does this smoke inhalation victim require treatment with cyanide antidote? tomographic manifestations of chest in patients with acute chlorine gas poisoning]. J Med Toxicol 12: 192, 2016. [PMID: 26831054] Zhonghua Yi Xue Za Zhi 90: 2740, 2010. [PMID: 21162908] 63. Levine M, Spyres M: Fire-related inhalation injury.
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