DOT/FAA/AM-00/34

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.

A Fatality Caused by Hydrogen

Sulfide Produced From an

Accidental Transfer of Sodium

Hydrogen Sulfide Into a Tank

Containing Dilute Sulfuric Acid

Office of Aviation Medicine

Washington, D.C. 20591

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.
i

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 (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 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

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 H2S 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.

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

1

A FATALITY 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

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, biological samples collected at autopsy from an

industrial fatality caused by an accidental inhalation

of hydrogen sulfide were submitted to CAMI for

toxicological evaluation.

Hydrogen sulfide, a powerful rapidly acting poisonous gas (1,2), is produced and used in industry for

the manufacturing of chemicals (3). This gas is also

naturally generated during the putrefaction of organic substances (4,5). The presence of this gas can be

identified by the characteristic odor of rotten eggs

(5), but its detection by the odor is not always

possible because this gas in higher concentrations

paralyzes the olfactory nerves (4).

Hydrogen sulfide has been the primary source of

sulfide (S2-) in several human poisonings, and numerous acute poisonings and fatalities have been reported from exposure to hydrogen sulfide in industrial

settings, sewers, wells, and septic tanks

(4-7). However, blood sulfide levels in the literature

are reported in only a limited number of hydrogen

sulfide fatalities-one paper describing a fatality with

0.92 μg/mL of sulfide in blood was published in 1968

by Winek et al. (6); another paper describing 5

fatalities with blood sulfide concentrations of 1.70-

3.75 μg/mL was published in 1979 by McAnalley et

al. (7). Additionally, 3 fatalities with blood sulfide

levels of 0.8, 3.6, and 5.0 μg/mL were reported in

1981 by Osbern and Crapo (2,8). Sulfide, similar to

cyanide (CN-

), produces acute systemic toxicity by

inhibiting the cytochrome oxidase system (1,2). In

the present study, we report toxicological findings,

along with the blood sulfide value, of the unique

industrial fatality caused by an accidental production

of, and exposure to, hydrogen sulfide.

Case History

A 55-year-old, healthy Caucasian male truck driver,

1.83 m in height and 88.5 kg in weight, was found

dead at the scene where he had accidentally transferred sodium hydrogen sulfide (NaHS) from his

tanker truck into a tank containing 4% sulfuric acid

(H2

SO4) and iron(II) sulfate (FeSO4). He had been

quickly overpowered by the chemically produced

hydrogen sulfide gas and had collapsed. This incident was not discovered for several minutes, when

another employee entering the area smelled the gas,

immediately evacuated the area, and called for help.

The death had occurred at 4:30 a.m., and the autopsy

was conducted about 8 hr later. The body was well

preserved, unembalmed, and refrigerated.

Pathology

External examination of the body revealed normal

features. Internal examination of organs disclosed no

significant anatomic abnormalities, except prevalence

of pulmonary edema and congestion in lungs and

kidneys. Microscopically, passive congestion was evident in lungs, spleen, kidneys, and adrenal glands.

The cause of death was determined to be hydrogen

sulfide poisoning. Blood, brain, kidney, liver, urine,

and vitreous humor samples collected during necropsy

were submitted for toxicological evaluation.

MATERIALS AND METHODS

Materials

All reagents and solvents were of analytical grade

and were of the highest available purity. These chemicals, drug standards, and other agents were obtained

from commercial sources. All calibrators, open controls, and negative controls were prepared in human

blood obtained from the local blood bank (Oklahoma Blood Institute, Oklahoma City, OK).
2

Toxicological Evaluation

Carbon monoxide in blood was analyzed spectrophotometrically as carboxyhemoglobin (9) and hydrogen cyanide colorimetrically as CN-

 (10). Alcohols

and drugs were analyzed according to the laboratory’s

standard analytical procedures.

Hydrogen Sulfide Determination

Hydrogen sulfide in blood was determined as

sulfide (S2-) by adopting a modified literature procedure (11), using a sulfide ion specific electrode (Model

9616; Orion Research, Inc., Beverly, MA). Sulfide

from blood was isolated as the hydrogen sulfide gas

by mixing 2.0 mL of blood with 2.0 mL of 0.5M

H3

PO4 in the outer ring of a Conway microdiffusion

dish. The evolved gas was absorbed in 1.5 mL of 1.0

M NaOH in the center well of the dish. After incubating the covered dish for 4 hr at ambient temperature, a 1.5-mL portion of Sulfide Antioxidant Buffer

(Orion Research, Inc., Beverly, MA) was added into

the central well. The chemical solutions in the well

were mixed, and the entire mixture was transferred

into a 5-mL beaker containing a magnetic stirrer. To

this 3-mL mixture, 100 μL of a standard sulfide

solution (1 μg/mL) was added. The addition of the

standard sulfide solution to each sample was necessary to minimize the fluctuation in the electromotive

force (EMF; -mV) readings, particularly at low sulfide concentrations. The EMF reading of each sample,

including calibrators, open controls, and negative

controls, was determined using the ion specific electrode and a digital pH/mV meter (Model 801; Orion

Research Inc., Beverly, MA). Calibrators were prepared in human blood by serial dilution of a stock

sulfide solution (1 mg/mL), which was prepared in

deionized water using Na2

S·9H2O. All samples were

analyzed sequentially, and the EMF readings were

taken within an hour. A linear blood calibration

curve was obtained by using 0.0, 1.0, 2.0, 4.0, and

8.0 μg/mL sulfide (Figure 1). Although the added

amount of sulfide (100 ng) is excluded from the

calibrator concentrations (see the figure), the EMF

values represented the readings from the added sulfide and the sulfide originally present in the respective samples.

RESULTS AND DISCUSSION

Toxicological evaluation of the blood sample failed

to disclose the presence of carbon monoxide, cyanide, or ethanol in a detectable amount. However,

14.3 μg/mL of acetaminophen was present in the

blood sample. Metoprolol was also detected in the

blood, liver, and kidney samples. Acetaminophen is

an over-the-counter analgesic/antipyretic medication

(12,13) and metoprolol is a ß-adrenergic blocking

prescription drug (14,15). The level of acetaminophen

found in the decedent’s blood was within the therapeutic range (10-20 μg/mL) (13,16). The presence of

metoprolol suggests that the victim was being treated

for hypertension.

Further analytical toxicology of the blood sample

revealed the presence of sulfide at the concentration

of 1.68 μg/mL (Table 1). The sulfide concentration

found in the blood of the victim was approximately

2 times higher than that reported in 2 separate fatal

cases (2,4,6-8) and falls well within the range of 0.8-

5.0 μg/mL in the postmortem blood of the individuals who have died in hydrogen sulfide related accidents

(6-8). The observed sulfide value in the present case

was about 34 times higher than the sulfide concentration (< 0.05 μg/mL) expected in blood from normal

subjects (7), which is consistent with the sulfide

values determined in the normal control (Table 1).

Since the victim’s body was well preserved and refrigerated, the autopsy was performed within about 8 hr,

and the blood sample storage temperature was 6°C or

less, the postmortem production of sulfide was presumably suppressed (4,17,18).

It is evident from the case history that the victim

was exposed to a lethal concentration of hydrogen

sulfide generated by the chemical reaction between

sodium hydrogen sulfide (NaHS) and sulfuric acid

(H2

SO4), as represented by the chemical equation:

NaHS (aq) + H2SO4 (aq) à NaHSO4 (aq)+ ↑ H2S(g)

The potential for other chemical reactions in the

mixture is negligible. Therefore, the gaseous material

generated during the accidental transfer of sodium

hydrogen sulfide was the hydrogen sulfide gas. Since
3

hydrogen sulfide toxicity manifests rapidly similar to

hydrogen cyanide poisoning by inhibiting the cytochrome oxidase system, causing histotoxic cellular

hypoxia (1,2), death occurs quickly. The pulmonary

edema and the passive congestion in various organs

observed during the pathological examination of the

Table 1. The Blood Sulfide (S2-) Concentration in the Fatality Resulting from Exposure

to Hydrogen Sulfide

Sample Description

Mean (SDn) Sulfide (S2-) Concentration

(μg/mL; n = 4)

Normal Subject Blood 0.03 (0.015)

Decedent Blood 1.68 (0.206)

victim’s body were consistent with the pathological

characteristics of hydrogen sulfide poisoning (1,2,6).

In view of the findings, it is concluded that the cause

of death was hydrogen sulfide poisoning associated

with a hazardous material accident in an industrial

situation.

Figure 1. The calibration curve of sulfide (S2-) in blood. Details are given in the text

of the Materials and Methods section.

y = 12.34x + 358

300

340

380

420

460

0.0 2.0 4.0 6.0 8.0

Sulfide (μg/mL)

EMF (-mV)

r = 0.9889
4

REFERENCES

1. R.P. Smith. Toxic responses of the blood. In

Casarett and Doull’s Toxicology—The Basic Science

of Poisons, 3rd ed., C.D. Klaassen, M.O. Amdur,

and J.Doull, Eds. Macmillan Publishing Company, New York, NY, 1986, pp 223-44.

2. T.A. Gossel and J.D. Bricker. Principles of Clinical Toxicology, 3rd Ed. Raven Press, New York,

NY, 1994, pp 109-34.

3. M. Windholz, S. Budavari, R.F. Blumetti, and

E.S. Otterbein, Eds. The Merck Index: An Encyclopedia of Chemicals, Drugs, and Biologicals,

10th Ed. Merck & Co., Inc., Rahway, NJ, 1983,

pp 4709-10.

4. R.C. Baselt. Disposition of Toxic Drugs and Chemicals in Man, 5th Ed. Chemical Toxicology Institute, Foster City, CA, 2000, pp 424-6.

5. M.N. Gleason, R.E. Gosselin, H.C. Hodge, and

R.P. Smith. Clinical Toxicology of Commercial Products-Acute Poisoning, 3rd Ed. The Williams &

Wilkins Co., Baltimore, 1969, pp 120-4.

6. C.L. Winek, W.D. Collom, and C.H. Wecht.

Death from hydrogen-sulphide fumes. Lacent 1:

1096 (1968).

7. B.H. McAnalley, W.T. Lowry, R.D. Oliver, and

J.C. Garriott. Determination of inorganic sulfide

and cyanide in blood using specific ion electrodes:

application to the investigation of hydrogen sulfide and cyanide poisoning. J. Anal. Toxicol. 3:

111-4 (1979).

8. L.N. Osbern and R.O. Crapo. Dung lung: a report

of toxic exposure to liquid manure. Ann. Intern.

Med. 95: 312-4 (1981).

9. D.V. Canfield, M. Smith, R.M. Ritter, and

A.K. Chaturvedi. Preparation of carboxyhemoglobin standards and calculation of spectrophotometric quantitation constants. J. Forensic

Sci. 44:409-12 (1999).

10. A.K. Chaturvedi, D.C. Sanders, B.R. Endecott,

and R.M. Ritter. Exposures to carbon monoxide,

hydrogen cyanide and their mixtures: interrelationship between gas exposure concentration, time

to incapacitation, carboxyhemoglobin and blood

cyanide in rats. J. Appl. Toxicol. 15:357-63 (1995).

11. R.C. Baselt. Analytical Procedures for Therapeutic Drug Monitoring and Emergency Toxicology.

Biomedical Publications, Davis, CA, 1980, pp

266-7.

12. Physician’s Desk Reference for Nonprescription Drugs

and Dietary Supplements. Medical Economics

Company, Inc., Montvale, NJ, 1999.

13. R.C. Baselt. Disposition of Toxic Drugs and Chemicals in Man, 5th Ed. Chemical Toxicology Institute, Foster City, CA, 2000, pp 4-8.

14. Physician’s Desk Reference. Medical Economics

Company, Inc., Montvale, NJ, 1999.

15. R.C. Baselt. Disposition of Toxic Drugs and Chemicals in Man, 5th Ed. Chemical Toxicology Institute, Foster City, CA, 2000, pp 573-5.

16. C.L. Winek. Drug & Chemical Blood-Level Data

1985. Fisher Scientific, Pittsburgh, PA, 1985.

17. T. Nagata, S. Kage, K. Kimura, K. Kudo, and M.

Noda. Sulfide concentrations in postmortem

mammalian tissues. J. Forensic Sci. 35:706-12

(1990).

18. T.H. Milby and R.C. Baselt. Hydrogen sulfide

poisoning: clarification of some controversial issues. Am. J. Ind. Med. 35:192-5 (1999).