A FATALITY CAUSED BY HYDROGEN SULFIDE PRODUCED FROM AN ACCIDENTAL TRANSFER OF SODIUM HYDROGEN SULFIDE INTO A TANK CONTAINING DILUTE SULFURIC ACID
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. Since a potential exposure to H2S was involved, blood was analyzed for sulfide (S(2-)) The analysis entailed isolating S(2-) 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 microg/mL of blood was found, and metoprolol was detected in the blood, liver, and kidney samples. Analysis further revealed the presence of S(2-). in blood at the level of 1.68 microg/mL. This S(2-). concentration is approximately 2 times higher than that reported in the blood of 2 separate fatalities associated with accidental exposures to H2S. The blood S(2-). value in the present case was about 34 times higher than the blood S(2-) concentration (<0.05 microg/mL) in normal subjects.
Hydrogen sulfide poisoning: clarification of some controversial issues.
BACKGROUND
Hydrogen sulfide is a toxic gas about which much has been written. We discuss here several issues we believe would benefit from further clarification.


CONCLUSIONS
We conclude that: 1) Certain neurotoxic effects of exposure are probably due to a direct toxic effect on the brain, while others are almost certainly a result of hypoxia secondary to H2S-induced respiratory insufficiency; 2) pulmonary edema is a common consequence of poisoning and there is suggestive evidence of hyperactive airway responses in some individuals following brief H2S-induced unconsciousness (knockdown); 3) criteria for acceptable community levels are very different than those governing occupational standards; 4) urinary thiosulfate determinations can be useful for monitoring occupational exposure; and 5) determination of sulfide ion concentrations in blood or major organs can be useful in corroborating a diagnosis of fatal H2S toxicity, but there are many pitfalls in collecting, storing, and analyzing tissue and fluid samples.
Fundamentals of Combustion Toxicology in Fire Hazard Assessment
This paper discusses fundamental principles of combustion toxicology and the application of those principles in formulating test protocols and research strategies aimed ultimately toward smoke toxicity hazard assessment and the influence of materials thereupon. It offers a review of principles basic to combustion toxicology to serve as introductory reading for fire technology professionals not generally familiar with the biological aspects of applied fire research and testing. While some methods of contemporary significance are referred to or discussed, this paper is not intended to be an exhaustive review or analysis of laboratory methods that have been applied in evaluating toxicological properties of smoke. This paper also addresses the basic issues of the assessment of toxic hazards to life and how laboratory methods may be applied in determining whether the choice of one material over another would significantly alter potential toxicological threats to life. Some approaches to laboratory assessments are given involving time-dependent bioassays of toxicological effects caused by allowing materials to perform as they would in a real fire. This paper is intended to open the way to the complex area of smoke toxicity hazard assessment in the laboratory in a relevant and practical manner.