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A Fatality Caused by Hydrogen Sulfide Produced from an Accidental November 2000 Transfer of Sodium Hydrogen Sulfide Into a Tank Containing Dilute 6

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A Fatality Caused by Hydrogen Sulfide Produced from an Accidental November 2000 Transfer of Sodium Hydrogen Sulfide Into a Tank Containing Dilute 6 DOT/FAA/AM-00/34 A Fatality Caused by Hydrogen Office of Aviation Medicine Sulfide Produced From an Washington, D.C. 20591 Accidental Transfer of Sodium Hydrogen Sulfide Into a Tank Containing Dilute Sulfuric Acid Arvind K. Chaturvedi Dudley R. Smith Dennis V. Canfield Civil Aeromedical Institute Federal Aviation Administration Oklahoma City, Oklahoma 73125 November 2000 Final Report This document is available to the public through the National Technical Information Service, Springfield, Virginia 22161. U.S. Department of Transportation Federal Aviation Administration NOTICE This document is disseminated under the sponsorship of the U.S. Department of Transportation in the interest of information exchange. The United States Government assumes no liability for the contents thereof. Technical Report Documentation Page 1. Report No. 2. Government Accession No. 3. Recipient's Catalog No. DOT/FAA/AM-00/34 4. Title and Subtitle 5. Report Date A Fatality Caused by Hydrogen Sulfide Produced from an Accidental November 2000 Transfer of Sodium Hydrogen Sulfide into a Tank Containing Dilute 6. Performing Organization Code Sulfuric Acid 7. Author(s) 8. Performing Organization Report No. Chaturvedi, A.K., Smith, D.R., and Canfield, D.V. 9. Performing Organization Name and Address 10. Work Unit No. (TRAIS) FAA Civil Aeromedical Institute P.O. Box 25082 11. Contract or Grant No. Oklahoma City, Oklahoma 73125 12. Sponsoring Agency name and Address 13. Type of Report and Period Covered Office of Aviation Medicine Federal Aviation Administration 800 Independence Ave., S.W. Washington, D.C. 20591 14. Sponsoring Agency Code 15. Supplemental Notes This work was accomplished under the approved tasks AM-B-99-TOX-202 and AM-B-00-TOX-202. 16. Abstract 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 biosamples from a hazardous chemical accident fatality were submitted to CAMI for toxicological evaluation. The victim succumbed from breathing the hydrogen sulfide (H2S) gas produced by an accidental transfer of sodium hydrogen sulfide (NaHS) from a tanker truck to a tank containing 4% sulfuric acid (H2SO4) 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. 2- Since a potential exposure to H2S was involved, blood was also analyzed for sulfide (S ). The analysis entailed isolating 2- S from blood as H2S using 0.5 M H3PO4, 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 2- 2- accidental exposures to H2S. The blood S value in the present case was about 34 times higher than the blood S 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 H2S poisoning. Since H2S toxicity manifests rapidly by inhibiting the cytochrome oxidase system, causing histotoxic cellular hypoxia, death occurs quickly. Based on 2- the case history, pathological findings, and blood S concentration, it is concluded that the cause of death was H2S poisoning associated with a hazardous material accident in an industrial situation. 17. Key Words 18. Distribution Statement Forensic Sciences, Toxicology, Acetaminophen, Document is available to the public through the Metoprolol, Hydrogen Sulfide, Hazardous Material National Technical Information Service Accident Investigation Springfield, Virginia 22161 19. Security Classif. (of this report) 20. Security Classif. (of this page) 21. No. of Pages 22. Price Unclassified Unclassified 7 Form DOT F 1700.7 (8-72) Reproduction of completed page authorized i A FATA LIT Y CAUSED BY HYDROGEN SULFIDE PRODUCED FROM AN ACCIDENTAL TRANSFER OF SODIUM HYDROGEN SULFIDE INTO A TANK CONTAINING DILUTE SULFURIC ACID INTRODUCTION The National Transportation Safety Board has an Case History agreement with the Federal Aviation Administration A 55-year-old, healthy Caucasian male truck driver, (FAA) that the FAA’s Civil Aeromedical Institute 1.83 m in height and 88.5 kg in weight, was found (CAMI) provide toxicological services for selected dead at the scene where he had accidentally trans- surface transportation accidents. Under this agree- ferred sodium hydrogen sulfide (NaHS) from his ment, biological samples collected at autopsy from an tanker truck into a tank containing 4% sulfuric acid industrial fatality caused by an accidental inhalation (H2SO4) and iron(II) sulfate (FeSO4). He had been of hydrogen sulfide were submitted to CAMI for quickly overpowered by the chemically produced toxicological evaluation. hydrogen sulfide gas and had collapsed. This inci- Hydrogen sulfide, a powerful rapidly acting poi- dent was not discovered for several minutes, when sonous gas (1,2), is produced and used in industry for another employee entering the area smelled the gas, the manufacturing of chemicals (3). This gas is also immediately evacuated the area, and called for help. naturally generated during the putrefaction of or- The death had occurred at 4:30 a.m., and the autopsy ganic substances (4,5). The presence of this gas can be was conducted about 8 hr later. The body was well identified by the characteristic odor of rotten eggs preserved, unembalmed, and refrigerated. (5), but its detection by the odor is not always possible because this gas in higher concentrations Pathology paralyzes the olfactory nerves (4). External examination of the body revealed normal Hydrogen sulfide has been the primary source of features. Internal examination of organs disclosed no sulfide (S2-) in several human poisonings, and numer- significant anatomic abnormalities, except prevalence ous acute poisonings and fatalities have been re- of pulmonary edema and congestion in lungs and ported from exposure to hydrogen sulfide in industrial kidneys. Microscopically, passive congestion was evi- settings, sewers, wells, and septic tanks dent in lungs, spleen, kidneys, and adrenal glands. (4-7). However, blood sulfide levels in the literature The cause of death was determined to be hydrogen are reported in only a limited number of hydrogen sulfide poisoning. Blood, brain, kidney, liver, urine, sulfide fatalities-one paper describing a fatality with and vitreous humor samples collected during necropsy 0.92 µg/mL of sulfide in blood was published in 1968 were submitted for toxicological evaluation. by Winek et al. (6); another paper describing 5 fatalities with blood sulfide concentrations of 1.70- MATERIALS AND METHODS 3.75 µg/mL was published in 1979 by McAnalley et al. (7). Additionally, 3 fatalities with blood sulfide Materials levels of 0.8, 3.6, and 5.0 µg/mL were reported in All reagents and solvents were of analytical grade 1981 by Osbern and Crapo (2,8). Sulfide, similar to and were of the highest available purity. These chemi- cyanide (CN-), produces acute systemic toxicity by cals, drug standards, and other agents were obtained inhibiting the cytochrome oxidase system (1,2). In from commercial sources. All calibrators, open con- the present study, we report toxicological findings, trols, and negative controls were prepared in human along with the blood sulfide value, of the unique blood obtained from the local blood bank (Okla- industrial fatality caused by an accidental production homa Blood Institute, Oklahoma City, OK). of, and exposure to, hydrogen sulfide. 1 Toxicological Evaluation RESULTS AND DISCUSSION Carbon monoxide in blood was analyzed spectro- photometrically as carboxyhemoglobin (9) and hy- Toxicological evaluation of the blood sample failed drogen cyanide colorimetrically as CN- (10). Alcohols to disclose the presence of carbon monoxide, cya- and drugs were analyzed according to the laboratory’s nide, or ethanol in a detectable amount. However, standard analytical procedures. 14.3 µg/mL of acetaminophen was present in the blood sample. Metoprolol was also detected in the Hydrogen Sulfide Determination blood, liver, and kidney samples. Acetaminophen is Hydrogen sulfide in blood was determined as an over-the-counter analgesic/antipyretic medication sulfide (S2-) by adopting a modified literature proce- (12,13) and metoprolol is a ß-adrenergic blocking dure (11), using a sulfide ion specific electrode (Model prescription drug (14,15). The level of acetaminophen 9616; Orion Research, Inc., Beverly, MA). Sulfide found in the decedent’s blood was within the thera- from blood was isolated as the hydrogen sulfide gas peutic range (10-20 µg/mL) (13,16). The presence of by mixing 2.0 mL of blood with 2.0 mL of 0.5M metoprolol suggests that the victim was being treated H3PO4 in the outer ring of a Conway microdiffusion for hypertension. dish. The evolved gas was absorbed
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