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.
Exposures to carbon monoxide, hydrogen cyanide and their mixtures: Interrelationship between gas exposure concentration, time to incapacitation, carboxyhemoglobin and blood cyanide in rats
Carbon monoxide (CO) and hydrogen cyanide (HCN) are generated during aircraft interior fires in sufficient amounts to incapacitate cabin occupants. For typical post‐crash and in‐flight fires, minimum protection periods of 5 and 35 min, respectively, have been suggested for breathing devices to protect the occupants from smoke. Relationships of blood carboxyhemoglobin (COHb) and cyanide (CN−) levels to incapacitation have not been well defined for these gases. Therefore, time to incapacitation (ti) and blood COHb and CN− at incapacitation were examined in rats exposed to CO (5706 ppm for 5‐min ti; 1902 ppm for 35‐min ti), HCN (184 ppm for 5‐min ti; 64 ppm for 35‐min ti) and their mixtures (equipotent concentrations of each gas that produced 5‐ and 35‐min ti). Blood CO and HCN uptakes were evaluated at the two concentrations of each gas. With either gas, variation in ti was higher for the 35‐min ti than the 5‐min ti. The COHb level reached a plateau prior to incapacitation at both CO concentrations, and COHb levels at the 5‐ and 35‐min ti were different from each other. Blood CN− increased as a function of both HCN concentration and exposure time, but CN− at the 5‐min ti was half of the 35‐min ti CN− level. The HCN uptake at the high concentration was about three times that at the low concentration. In the high concentration CO–HCN mixture, ti was shortened from 5 to 2.6 min; COHb dropped from 81 to 55% and blood CN− from 2.3 to 1.1 μg ml−1. At the low‐concentration CO–HCN mixture, where ti was reduced from 35 to 11.1 min, COHb decreased from 71 to 61% and blood CN− from 4.2 to 1.1 μg ml−1. Any alteration in the uptake of either gas by the presence of the other was minimal. Our findings suggest that specific levels of blood COHb and CN− cannot be correlated directly with the incapacitation onset and that post‐mortem blood COHb and CN− levels should be evaluated carefully in fire victims.
Interaction of Diclofop-Methyl and MCPA on Wild Oats (Avena fatua)
Diclofop-methyl {methyl 2-[4-(2,4-dichlorophenoxy)phenoxy] propanoate} loses part of its activity on wild oats (Avena fatua L.) when it is applied in combination with ester or amine formulations of MCPA {[4-chloro-o-tolyl)oxy] acetic acid.} Uptake of diclofop-methyl is reduced in the presence of commercial formulations of MCPA, particularly amine formulations, which are only partly compatible with the diclofop-methyl formulation. With added MCPA, regardless of formulation, hydrolysis of diclofop-methyl to the acid diclofop is slowed down, both in intact wild oat plants and in a crude leaf extract. At the same time, conversion of any acid formed to inactive conjugates is accelerated in the presence of MCPA. It is concluded that the loss of activity of diclofop-methyl by MCPA can be accounted for by the effects of MCPA on uptake and metabolic conversion of diclofop-methyl.