Fatality Caused by Hydrogen Sulfide Produced from an Accidental Transfer of Sodium Hydrogen Sulfide into a Tank Containing Dilute Sulfuric Acid
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Fatality Caused by Hydrogen Sulfide Produced from an Accidental Transfer of Sodium Hydrogen Sulfide into a Tank Containing Dilute Sulfuric Acid

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      The National Transportation Safety Board has an agreement with the Federal Aviation Administration (FAA) that the FAA's Civil Aeromedical Institute (CAMI) provide toxicological services for selected surface transportation accidents. Under this agreement, postmortem bio samples from a hazardous chemical accident fatality were submitted to CAMI for toxicological evaluation. The victim succumbed from breathing the hydrogen sulfide (H2 S) gas produced by an accidental transfer of sodium hydrogen sulfide (NaHS) from a tanker truck to a tank containing 4% sulfuric acid (H2 SO4 ) and iron(II) sulfate (FeSO4 ). After inhaling the gas, the 55-year old male Caucasian truck driver was dead at the scene. Autopsy examination of the decedent's body revealed pulmonary edema and passive congestion in lungs, spleen, kidneys, and adrenal glands. The submitted samples were analyzed for carbon monoxide, cyanide, alcohols, and drugs. Since a potential exposure to H2 S was involved, blood was also analyzed for sulfide (S2-). The analysis entailed isolating S 2- from blood as H2 S using 0.5 M H3 PO4 , trapping the gas in 0.1 M NaOH, and determining the electromotive force using a sulfide ion specific electrode. Carbon monoxide, cyanide, or ethanol was not detected in blood, but acetaminophen at a therapeutic concentration of 14.3 µg/mL of blood was found, and metoprolol was detected in the blood, liver, and kidney samples. Analysis further revealed the presence of S2- in blood at the level of 1.68 µg/mL. This S2- concentration is approximately 2 times higher than that reported in the blood of 2 separate fatalities associated with accidental exposures to H2 S. The blood S2- value in the present case was about 34 times higher than the blood S2- concentration (< 0.05 µg/mL) in normal subjects. The observed pulmonary edema and the passive congestion in various organs were also in agreement with the pathological characteristics of H2 S poisoning. Since H2 S toxicity manifests rapidly by inhibiting the cytochrome oxidase system, causing histotoxic cellular hypoxia, death occurs quickly. Based on the case history, pathological findings, and blood S2- concentration, it is concluded that the cause of death was H2 S poisoning associated with a hazardous material accident in an industrial situation.
    • Content Notes:
      This work was accomplished under the approved tasks AM-B-99-TOX-202 and AM-B-00-TOX-202.
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