- Arsenic Poisoning
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Yang Ho Kim, Ji Ho Lee, Chang Sun Sim, Kyoung Sook Jeong
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J Korean Soc Clin Toxicol. 2004;2(2):67-71. Published online December 31, 2004
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 Abstract
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- Arsenic poisoning has three types of poisoning. First, acute arsenic poisoning is usually caused by oral intake of large amount of arsenic compound with purpose of homicide or suicide. Second, chronic arsenic poisoning is caused by inhalation of arsenic in the occupational setting or by long-term oral intake of arsenic-contaminated well water. Third, arsine poisoning occurs acutely when impurities of arsenic in non-ferrous metal react with acid. Clinical manifestation of acute arsenic poisoning is mainly gastrointestinal symptoms and cardiovascular collapse. Those of chronic poisoning are skin disorder and cancer. Arsine poisoning shows massive intravascular hemolysis and hemoglobinuria with acute renal failure. Exposure evaluation is done by analysis of arsenic in urine, blood, hair and nail. Species analysis of arsenic is very important to evaluate inorganic arsenic acid and mono methyl arsenic acid (MMA) separated from dimethyl arsenic acid (DMA) and trimethyl arsenic acid (TMA) which originate from sea weed and sea food. Treatment with dimercaprol (BAL) is effective in acute arsenic poisoning only.
- Chemical Asphyxiants - Cyanides and Hydrogen Sulfides
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Yang Ho Kim, Young Hee Choi, Choong Ryeol Lee, Ji Ho Lee, Cheolln Yoo, Hun Lee
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J Korean Soc Clin Toxicol. 2003;1(1):12-20. Published online June 30, 2003
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Abstract
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- Cyanides and hydrogen sulfide ($H_2S$) are major chemical asphyxiants. They have common mechanism of action which inhibit cellular respiration and induce histotoxic hypoxia. They do not generate ATP, and all processes dependent on ATP are stopped. No extraction of $O_2$ from blood decreases AV $O_2$ differences, and the shift to anaerobic glycolysis brings about lactic acidosis with high anion gap. The mainstay of the treatment is rapid treatment with appropriate use of antidotes. However, there are several differences between cyanides and $H_2S$. First, $H_2S$ is not metabolized by enzymes such as thiosulfate. Thus thiosulfate does not play any role in treatment of $H_2S$. Second, $H_2S$ is a more potent inhibitor of cytochrome aa3 than cyanide. Third, $H_2S$ induces more divergent neurologic sequele than cyanide. Finally, $H_2S$ is not absorbed via skin.
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KSCT
Korean Society of Clinical Toxicology