TOXICOLOGICAL PROFILE FOR 

HYDROGEN SULFIDE 

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES 

Public Health Service 

Agency for Toxic Substances and Disease Registry
 

July 2006 
HYDROGEN SULFIDE ii 

DISCLAIMER 

The use of company or product name(s) is for identification only and does not imply endorsement by the 

Agency for Toxic Substances and Disease Registry. 

 


 


 


 


 


 

HYDROGEN SULFIDE iii 

UPDATE STATEMENT 

A Toxicological Profile for Hydrogen Sulfide, Draft for Public Comment was released in September, 

2004. This edition supersedes any previously released draft or final profile. 

Toxicological profiles are revised and republished as necessary. For information regarding the update 

status of previously released profiles, contact ATSDR at: 

Agency for Toxic Substances and Disease Registry
 

Division of Toxicology and Environmental Medicine/Applied Toxicology Branch 

1600 Clifton Road NE 

Mailstop F-32 

Atlanta, Georgia 30333 
HYDROGEN SULFIDE iv 

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v 

FOREWORD 

This toxicological profile is prepared in accordance with guidelines developed by the Agency for Toxic 

Substances and Disease Registry (ATSDR) and the Environmental Protection Agency (EPA). The 

original guidelines were published in the Federal Register on April 17, 1987. Each profile will be revised 

and republished as necessary. 

The ATSDR toxicological profile succinctly characterizes the toxicologic and adverse health effects 

information for the hazardous substance described therein. Each peer-reviewed profile identifies and 

reviews the key literature that describes a hazardous substance’s toxicologic properties. Other pertinent 

literature is also presented, but is described in less detail than the key studies. The profile is not intended 

to be an exhaustive document; however, more comprehensive sources of specialty information are 

referenced. 

The focus of the profiles is on health and toxicologic information; therefore, each toxicological profile 

begins with a public health statement that describes, in nontechnical language, a substance’s relevant 

toxicological properties. Following the public health statement is information concerning levels of 

significant human exposure and, where known, significant health effects. The adequacy of information to 

determine a substance’s health effects is described in a health effects summary. Data needs that are of 

significance to protection of public health are identified by ATSDR and EPA. 

Each profile includes the following: 

(A) The examination, summary, and interpretation of available toxicologic information and 

epidemiologic evaluations on a hazardous substance to ascertain the levels of significant human 

exposure for the substance and the associated acute, subacute, and chronic health effects; 

(B) A determination of whether adequate information on the health effects of each substance 

is available or in the process of development to determine levels of exposure that present a 

significant risk to human health of acute, subacute, and chronic health effects; and 

(C) Where appropriate, identification of toxicologic testing needed to identify the types or 

levels of exposure that may present significant risk of adverse health effects in humans. 

The principal audiences for the toxicological profiles are health professionals at the Federal, State, and 

local levels; interested private sector organizations and groups; and members of the public. 

This profile reflects ATSDR’s assessment of all relevant toxicologic testing and information that has been 

peer-reviewed. Staff of the Centers for Disease Control and Prevention and other Federal scientists have 

also reviewed the profile. In addition, this profile has been peer-reviewed by a nongovernmental panel 

and was made available for public review. Final responsibility for the contents and views expressed in 

this toxicological profile resides with ATSDR. 
vi 

*Legislative Background 

The toxicological profiles are developed in response to the Superfund Amendments and Reauthorization 

Act (SARA) of 1986 (Public Law 99 499) which amended the Comprehensive Environmental Response, 

Compensation, and Liability Act of 1980 (CERCLA or Superfund). This public law directed ATSDR to 

prepare toxicological profiles for hazardous substances most commonly found at facilities on the 

CERCLA National Priorities List and that pose the most significant potential threat to human health, as 

determined by ATSDR and the EPA. The availability of the revised priority list of 275 hazardous 

substances was announced in the Federal Register on December 7, 2005 (70 FR 72840). For prior 

versions of the list of substances, see Federal Register notices dated April 17, 1987 (52 FR 12866); 

October 20, 1988 (53 FR 41280); October 26, 1989 (54 FR 43619); October 17,1990 (55 FR 42067); 

October 17, 1991 (56 FR 52166); October 28, 1992 (57 FR 48801); February 28, 1994 (59 FR 9486); 

April 29, 1996 (61 FR 18744); November 17, 1997 (62 FR 61332); October 21, 1999 (64 FR 56792); 

October 25, 2001 (66 FR 54014), and November 7, 2003 (68 FR 63098). Section 104(i)(3) of CERCLA, 

as amended, directs the Administrator of ATSDR to prepare a toxicological profile for each substance on 

the list. 

 


 


 


 

HYDROGEN SULFIDE vii 

QUICK REFERENCE FOR HEALTH CARE PROVIDERS 

Toxicological Profiles are a unique compilation of toxicological information on a given hazardous 

substance. Each profile reflects a comprehensive and extensive evaluation, summary, and interpretation 

of available toxicologic and epidemiologic information on a substance. Health care providers treating 

patients potentially exposed to hazardous substances will find the following information helpful for fast 

answers to often-asked questions. 

Primary Chapters/Sections of Interest 

Chapter 1: Public Health Statement: The Public Health Statement can be a useful tool for educating 

patients about possible exposure to a hazardous substance. It explains a substance’s relevant 

toxicologic properties in a nontechnical, question-and-answer format, and it includes a review of 

the general health effects observed following exposure. 

Chapter 2: Relevance to Public Health: The Relevance to Public Health Section evaluates, interprets, 

and assesses the significance of toxicity data to human health. 

Chapter 3: Health Effects: Specific health effects of a given hazardous compound are reported by type 

of health effect (death, systemic, immunologic, reproductive), by route of exposure, and by length 

of exposure (acute, intermediate, and chronic). In addition, both human and animal studies are 

reported in this section. 

NOTE: Not all health effects reported in this section are necessarily observed in the clinical 

setting. Please refer to the Public Health Statement to identify general health effects observed 

following exposure. 

Pediatrics: Four new sections have been added to each Toxicological Profile to address child health 

issues: 

Section 1.6 How Can (Chemical X) Affect Children? 

Section 1.7 How Can Families Reduce the Risk of Exposure to (Chemical X)? 

Section 3.7 Children’s Susceptibility 

Section 6.6 Exposures of Children 

Other Sections of Interest: 

Section 3.8 Biomarkers of Exposure and Effect 

Section 3.11 Methods for Reducing Toxic Effects 

ATSDR Information Center 

Phone: 1-888-42-ATSDR or (404) 498-0110 Fax: (770) 488-4178 

E-mail: atsdric@cdc.gov Internet: http://www.atsdr.cdc.gov 

The following additional material can be ordered through the ATSDR Information Center: 

Case Studies in Environmental Medicine: Taking an Exposure History—The importance of taking an 

exposure history and how to conduct one are described, and an example of a thorough exposure 

history is provided. Other case studies of interest include Reproductive and Developmental 
HYDROGEN SULFIDE viii 

Hazards; Skin Lesions and Environmental Exposures; Cholinesterase-Inhibiting Pesticide 

Toxicity; and numerous chemical-specific case studies. 

Managing Hazardous Materials Incidents is a three-volume set of recommendations for on-scene 

(prehospital) and hospital medical management of patients exposed during a hazardous materials 

incident. Volumes I and II are planning guides to assist first responders and hospital emergency 

department personnel in planning for incidents that involve hazardous materials. Volume III— 

Medical Management Guidelines for Acute Chemical Exposures—is a guide for health care 

professionals treating patients exposed to hazardous materials. 

Fact Sheets (ToxFAQs) provide answers to frequently asked questions about toxic substances. 

Other Agencies and Organizations 

The National Center for Environmental Health (NCEH) focuses on preventing or controlling disease, 

injury, and disability related to the interactions between people and their environment outside the 

workplace. Contact: NCEH, Mailstop F-29, 4770 Buford Highway, NE, Atlanta, 

GA 30341-3724 • Phone: 770-488-7000 • FAX: 770-488-7015. 

The National Institute for Occupational Safety and Health (NIOSH) conducts research on occupational 

diseases and injuries, responds to requests for assistance by investigating problems of health and 

safety in the workplace, recommends standards to the Occupational Safety and Health 

Administration (OSHA) and the Mine Safety and Health Administration (MSHA), and trains 

professionals in occupational safety and health. Contact: NIOSH, 200 Independence Avenue, 

SW, Washington, DC 20201 • Phone: 800-356-4674 or NIOSH Technical Information Branch, 

Robert A. Taft Laboratory, Mailstop C-19, 4676 Columbia Parkway, Cincinnati, OH 45226-1998 

• Phone: 800-35-NIOSH. 

The National Institute of Environmental Health Sciences (NIEHS) is the principal federal agency for 

biomedical research on the effects of chemical, physical, and biologic environmental agents on 

human health and well-being. Contact: NIEHS, PO Box 12233, 104 T.W. Alexander Drive, 

Research Triangle Park, NC 27709 • Phone: 919-541-3212. 

Referrals 

The Association of Occupational and Environmental Clinics (AOEC) has developed a network of clinics 

in the United States to provide expertise in occupational and environmental issues. Contact: 

AOEC, 1010 Vermont Avenue, NW, #513, Washington, DC 20005 • Phone: 202-347-4976 

• FAX: 202-347-4950 • e-mail: AOEC@AOEC.ORG • Web Page: http://www.aoec.org/. 

The American College of Occupational and Environmental Medicine (ACOEM) is an association of 

physicians and other health care providers specializing in the field of occupational and 

environmental medicine. Contact: ACOEM, 25 Northwest Point Boulevard, Suite 700, Elk 

Grove Village, IL 60007-1030 • Phone: 847-818-1800 • FAX: 847-818-9266. 

 


 


 


 


 


 


 

	 

	 

	 

	 

HYDROGEN SULFIDE ix 

CONTRIBUTORS 

CHEMICAL MANAGER(S)/AUTHOR(S): 

Selene Chou, Ph.D. 

Mike Fay, Ph.D. 

Sam Keith, M.S. 

ATSDR, Division of Toxicology and Environmental Medicine, Atlanta, GA 

Lisa Ingerman, Ph.D. 

Lara Chappell, Ph.D. 

Syracuse Research Corporation, North Syracuse, NY 

THE PROFILE HAS UNDERGONE THE FOLLOWING ATSDR INTERNAL REVIEWS: 

1. Health Effects Review. The Health Effects Review Committee examines the health effects 

chapter of each profile for consistency and accuracy in interpreting health effects and classifying 

end points. 

2.	 Minimal Risk Level Review. The Minimal Risk Level Workgroup considers issues relevant to 

substance-specific Minimal Risk Levels (MRLs), reviews the health effects database of each 

profile, and makes recommendations for derivation of MRLs. 

3. Data Needs Review. The Research Implementation Branch reviews data needs sections to assure 

consistency across profiles and adherence to instructions in the Guidance. 

4. Green Border Review. Green Border review assures the consistency with ATSDR policy. 
HYDROGEN SULFIDE x 

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HYDROGEN SULFIDE xi 

PEER REVIEW 

A peer review panel was assembled for hydrogen sulfide. The panel consisted of the following members: 

1. Steven C. Lewis, Ph.D., DABT, President and Principal Scientist, Integrative Policy & Science, 

Inc.; Adjunct Professor, Robert Wood Johnson Medical School, Washington, New Jersey; 

2.	 John A. Pickrell, Ph.D., Associate Professor Environmental Toxicology, College of Veterinary 

Medicine, Kansas State University, Manhattan, Kansas; and 

3.	 Roger P. Smith, Ph.D., Irene Heinz Given Professor of Pharmacology and Toxicology, Emeritus, 

Dartmouth Medical School, Hanover, New Hampshire. 

These experts collectively have knowledge of hydrogen sulfide's physical and chemical properties, 

toxicokinetics, key health end points, mechanisms of action, human and animal exposure, and 

quantification of risk to humans. All reviewers were selected in conformity with the conditions for peer 

review specified in Section 104(I)(13) of the Comprehensive Environmental Response, Compensation, 

and Liability Act, as amended. 

Scientists from the Agency for Toxic Substances and Disease Registry (ATSDR) have reviewed the peer 

reviewers' comments and determined which comments will be included in the profile. A listing of the 

peer reviewers' comments not incorporated in the profile, with a brief explanation of the rationale for their 

exclusion, exists as part of the administrative record for this compound. 

The citation of the peer review panel should not be understood to imply its approval of the profile's final 

content. The responsibility for the content of this profile lies with the ATSDR. 
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HYDROGEN SULFIDE xiii 

CONTENTS 

DISCLAIMER ..............................................................................................................................................ii 

UPDATE STATEMENT .............................................................................................................................iii 

FOREWORD ................................................................................................................................................v 

QUICK REFERENCE FOR HEALTH CARE PROVIDERS....................................................................vii 

CONTRIBUTORS.......................................................................................................................................ix 

PEER REVIEW ...........................................................................................................................................xi 

CONTENTS...............................................................................................................................................xiii 

LIST OF FIGURES ..................................................................................................................................xvii 

LIST OF TABLES.....................................................................................................................................xix 

1. PUBLIC HEALTH STATEMENT..........................................................................................................1 

1.1 WHAT IS HYDROGEN SULFIDE? ..........................................................................................1 

1.2 WHAT HAPPENS TO HYDROGEN SULFIDE WHEN IT ENTERS THE 

ENVIRONMENT? ......................................................................................................................2 

1.3 HOW MIGHT I BE EXPOSED TO HYDROGEN SULFIDE? .................................................2 

1.4 HOW CAN HYDROGEN SULFIDE ENTER AND LEAVE MY BODY? .............................. 3 

1.5 HOW CAN HYDROGEN SULFIDE AFFECT MY HEALTH? ...............................................4 

1.6 HOW CAN HYDROGEN SULFIDE AFFECT CHILDREN?...................................................5 

1.7 HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO HYDROGEN 

SULFIDE?...................................................................................................................................6 

1.8 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN
 

EXPOSED TO HYDROGEN SULFIDE? ..................................................................................6 

1.9 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO 

PROTECT HUMAN HEALTH?.................................................................................................7 

1.10 WHERE CAN I GET MORE INFORMATION? .......................................................................8 

2. RELEVANCE TO PUBLIC HEALTH ...................................................................................................9 

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO HYDROGEN 

SULFIDE IN THE UNITED STATES .......................................................................................9 

2.2 SUMMARY OF HEALTH EFFECTS......................................................................................10 

2.3 MINIMAL RISK LEVELS (MRLs) .........................................................................................14 

3. HEALTH EFFECTS..............................................................................................................................21 

3.1 INTRODUCTION.....................................................................................................................21 

3.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE ..................................21 

3.2.1 Inhalation Exposure ..............................................................................................................22 

3.2.1.1 Death ............................................................................................................................22 

3.2.1.2 Systemic Effects...........................................................................................................26 

3.2.1.3 Immunological and Lymphoreticular Effects...............................................................61 

3.2.1.4 Neurological Effects.....................................................................................................62 

3.2.1.5 Reproductive Effects....................................................................................................68 

3.2.1.6 Developmental Effects .................................................................................................70 

3.2.1.7 Cancer...........................................................................................................................71 

3.2.2 Oral Exposure........................................................................................................................72 

3.2.2.1 Death ............................................................................................................................72 

3.2.2.2 Systemic Effects...........................................................................................................72 

3.2.2.3 Immunological and Lymphoreticular Effects...............................................................73 

 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

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3.2.2.4 Neurological Effects.....................................................................................................73 

3.2.2.5 Reproductive Effects....................................................................................................73 

3.2.2.6 Developmental Effects .................................................................................................73 

3.2.2.7 Cancer...........................................................................................................................73 

3.2.3 Dermal Exposure...................................................................................................................73 

3.2.3.1 Death ............................................................................................................................73 

3.2.3.2 Systemic Effects...........................................................................................................74 

3.2.3.3 Immunological and Lymphoreticular Effects...............................................................74 

3.2.3.4 Neurological Effects.....................................................................................................74 

3.2.3.5 Reproductive Effects....................................................................................................75 

3.2.3.6 Developmental Effects .................................................................................................75 

3.2.3.7 Cancer...........................................................................................................................75 

3.3 GENOTOXICITY .....................................................................................................................75 

3.4 TOXICOKINETICS..................................................................................................................75 

3.4.1 Absorption.............................................................................................................................76 

3.4.1.1 Inhalation Exposure......................................................................................................76 

3.4.1.2 Oral Exposure...............................................................................................................76 

3.4.1.3 Dermal Exposure ..........................................................................................................77 

3.4.2 Distribution ...........................................................................................................................77 

3.4.2.1 Inhalation Exposure......................................................................................................77 

3.4.2.2 Oral Exposure...............................................................................................................79 

3.4.2.3 Dermal Exposure ..........................................................................................................79 

3.4.2.4 Other Routes of Exposure ............................................................................................79 

3.4.3 Metabolism............................................................................................................................79 

3.4.4 Elimination and Excretion.....................................................................................................82 

3.4.4.1 Inhalation Exposure......................................................................................................82 

3.4.4.2 Oral Exposure...............................................................................................................82 

3.4.4.3 Dermal Exposure ..........................................................................................................83 

3.4.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models .............83 

3.5 MECHANISMS OF ACTION .................................................................................................. 84 

3.5.1 Pharmacokinetic Mechanisms...............................................................................................84 

3.5.2 Mechanisms of Toxicity........................................................................................................86 

3.5.3 Animal-to-Human Extrapolations.........................................................................................88 

3.6 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS ..........................88 

3.7 CHILDREN’S SUSCEPTIBILITY...........................................................................................89 

3.8 BIOMARKERS OF EXPOSURE AND EFFECT ....................................................................91 

3.8.1 Biomarkers Used to Identify or Quantify Exposure to Hydrogen Sulfide ............................92 

3.8.2 Biomarkers Used to Characterize Effects Caused by Hydrogen Sulfide ..............................93 

3.9 INTERACTIONS WITH OTHER CHEMICALS ....................................................................93 

3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE............................................... 95 

3.11 METHODS FOR REDUCING TOXIC EFFECTS...................................................................95 

3.11.1 Reducing Peak Absorption Following Exposure ..............................................................96 

3.11.2 Reducing Body Burden.....................................................................................................97 

3.11.3 Interfering with the Mechanism of Action for Toxic Effects ...........................................97 

3.12 ADEQUACY OF THE DATABASE........................................................................................98 

3.12.1 Existing Information on Health Effects of Hydrogen Sulfide ..........................................98 

3.12.2 Identification of Data Needs ...........................................................................................100 

3.12.3 Ongoing Studies..............................................................................................................107 

 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

HYDROGEN SULFIDE xv 

4. CHEMICAL AND PHYSICAL INFORMATION..............................................................................109 

4.1 CHEMICAL IDENTITY.........................................................................................................109 

4.2 PHYSICAL AND CHEMICAL PROPERTIES......................................................................109 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL..........................................................113 

5.1 PRODUCTION .......................................................................................................................113 

5.2 IMPORT/EXPORT .................................................................................................................113 

5.3 USE..........................................................................................................................................114 

5.4 DISPOSAL..............................................................................................................................114 

6. POTENTIAL FOR HUMAN EXPOSURE .........................................................................................115 

6.1 OVERVIEW............................................................................................................................115 

6.2 RELEASES TO THE ENVIRONMENT................................................................................118 

6.2.1 Air .......................................................................................................................................118 

6.2.2 Water...................................................................................................................................119 

6.2.3 Soil ......................................................................................................................................120 

6.3 ENVIRONMENTAL FATE....................................................................................................121 

6.3.1 Transport and Partitioning...................................................................................................121 

6.3.2 Transformation and Degradation ........................................................................................122 

6.3.2.1 Air...............................................................................................................................122 

6.3.2.2 Water ..........................................................................................................................122 

6.3.2.3 Sediment and Soil.......................................................................................................123 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT...............................123 

6.4.1 Air .......................................................................................................................................124 

6.4.2 Water...................................................................................................................................127 

6.4.3 Sediment and Soil ...............................................................................................................127 

6.4.4 Other Environmental Media................................................................................................128 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE .....................................129 

6.6 EXPOSURES OF CHILDREN...............................................................................................131 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES ...........................................132 

6.8 ADEQUACY OF THE DATABASE......................................................................................132 

6.8.1 Identification of Data Needs ...............................................................................................133 

6.8.2 Ongoing Studies ..................................................................................................................135 

7. ANALYTICAL METHODS ...............................................................................................................137 

7.1 BIOLOGICAL MATERIALS.................................................................................................137 

7.2 ENVIRONMENTAL SAMPLES............................................................................................ 143 

7.3 ADEQUACY OF THE DATABASE......................................................................................151 

7.3.1 Identification of Data Needs ...............................................................................................151 

7.3.2 Ongoing Studies ..................................................................................................................152 

8. REGULATIONS AND ADVISORIES ...............................................................................................153 

9. REFERENCES ....................................................................................................................................159 

10. GLOSSARY ......................................................................................................................................201 

 


 


 


 

HYDROGEN SULFIDE xvi 

APPENDICES 

A. ATSDR MINIMAL RISK LEVELS AND WORKSHEETS .............................................................A-1 

B. USER’S GUIDE.................................................................................................................................. B-1 

C. ACRONYMS, ABBREVIATIONS, AND SYMBOLS...................................................................... C-1 

D. INDEX ................................................................................................................................................D-1 

 


 


 


 


 


 


 

HYDROGEN SULFIDE xvii 

LIST OF FIGURES 

3-1. Levels of Significant Exposure to Hydrogen Sulfide—Inhalation..................................................... 41 

3-2. Metabolic Pathways of Hydrogen Sulfide..........................................................................................80 

3-3. Conceptual Representation of a Physiologically Based Pharmacokinetic (PBPK) Model for a 

Hypothetical Chemical Substance......................................................................................................85 

3-4. Existing Information on Health Effects of Hydrogen Sulfide ............................................................99 

6-1. Frequency of NPL Sites with Hydrogen Sulfide Contamination .....................................................116 
HYDROGEN SULFIDE xviii 

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HYDROGEN SULFIDE xix 

LIST OF TABLES 

3-1. Levels of Significant Exposure to Hydrogen Sulfide—Inhalation..................................................... 27 

4-1. Chemical Identity of Hydrogen Sulfide............................................................................................110 

4-2. Physical and Chemical Identity of Hydrogen Sulfide ......................................................................111 

7-1. Analytical Methods for Determining Hydrogen Sulfide, Sulfide, and Thiosulfate in 

Biological Samples...........................................................................................................................138 

7-2. Analytical Methods for Determining Hydrogen Sulfide and Sulfide in Environmental Samples....144 

8-1. Regulations and Guidelines Applicable to Hydrogen Sulfide ..........................................................154 
HYDROGEN SULFIDE xx 

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HYDROGEN SULFIDE 1 

1. PUBLIC HEALTH STATEMENT 

This public health statement tells you about hydrogen sulfide and the effects of exposure to it. 

The Environmental Protection Agency (EPA) identifies the most serious hazardous waste sites in 

the nation. These sites are then placed on the National Priorities List (NPL) and are targeted for 

long-term federal clean-up activities. Hydrogen sulfide has been found in at least 35 of the 

1,689 current or former NPL sites. Although the total number of NPL sites evaluated for this 

substance is not known, the possibility exists that the number of sites at which hydrogen sulfide 

is found may increase in the future as more sites are evaluated. This information is important 

because these sites may be sources of exposure and exposure to this substance may harm you. 

When a substance is released either from a large area, such as an industrial plant, or from a 

container, such as a drum or bottle, it enters the environment. Such a release does not always 

lead to exposure. You can be exposed to a substance only when you come in contact with it. 

You may be exposed by breathing, eating, or drinking the substance, or by skin contact. 

If you are exposed to hydrogen sulfide, many factors will determine whether you will be harmed. 

These factors include the dose (how much), the duration (how long), and how you come in 

contact with it. You must also consider any other chemicals you are exposed to and your age, 

sex, diet, family traits, lifestyle, and state of health. 

1.1 WHAT IS HYDROGEN SULFIDE? 

Hydrogen sulfide (H2S) is a flammable, colorless gas with a sweetish taste and characteristic 

odor of rotten eggs that can be poisonous at high concentrations. Other names for hydrogen 

sulfide include hydrosulfuric acid, sewer gas, hydrogen sulphide, and stink damp. People 

usually can smell hydrogen sulfide at low concentrations in air, ranging from 0.0005 to 0.3 parts 

per million (ppm) (0.0005–0.3 parts of hydrogen sulfide in 1 million parts of air); however, at 
	 

	 

HYDROGEN SULFIDE 2 

1. PUBLIC HEALTH STATEMENT 

high concentrations, a person might lose their ability to smell it. This can make hydrogen sulfide 

very dangerous. 

Hydrogen sulfide occurs both naturally and from human-made processes. It is in the gases from 

volcanoes, sulfur springs, undersea vents, swamps, and stagnant bodies of water and in crude 

petroleum and natural gas. Hydrogen sulfide also is associated with municipal sewers and 

sewage treatment plants, swine containment and manure-handling operations, and pulp and paper 

operations. Industrial sources of hydrogen sulfide include petroleum refineries, natural gas 

plants, petrochemical plants, coke oven plants, food processing plants, and tanneries. Bacteria 

found in your mouth and gastrointestinal tract produce hydrogen sulfide during the digestion of 

food containing vegetable or animal proteins. Hydrogen sulfide is one of the principal 

components in the natural sulfur cycle. You will find more about the properties, production, and 

use of hydrogen sulfide in Chapters 4 and 5. 

1.2 WHAT HAPPENS TO HYDROGEN SULFIDE WHEN IT ENTERS THE 

ENVIRONMENT? 

Hydrogen sulfide is released primarily as a gas and spreads in the air. However, in some 

instances, it may be released in the liquid waste of an industrial facility or as the result of a 

natural event. When hydrogen sulfide is released as a gas, it remains in the atmosphere for an 

average of 18 hours. During this time, hydrogen sulfide can change into sulfur dioxide and 

sulfuric acid. Hydrogen sulfide is soluble in water, and is a weak acid in water. You will find 

more about what happens to hydrogen sulfide when it enters the environment in Chapter 6. 

1.3 HOW MIGHT I BE EXPOSED TO HYDROGEN SULFIDE? 

Your body makes small amounts of hydrogen sulfide. Hydrogen sulfide is produced by the 

natural bacteria in your mouth and is a component of bad breath (halitosis). Breakdown of 

sulfur-containing proteins by bacteria in the human intestinal tract also produces hydrogen 

sulfide. The levels of hydrogen sulfide in air and water are typically low. The amount of 

hydrogen sulfide in the air in the United States is 0.11–0.33 parts per billion (ppb) (one 
HYDROGEN SULFIDE 3 

1. PUBLIC HEALTH STATEMENT 

thousandth of a ppm). In undeveloped areas of the United States, concentrations have been 

reported at 0.02–0.07 ppb. The amount of hydrogen sulfide in surface water is low because 

hydrogen sulfide readily evaporates from water. Groundwater concentrations of hydrogen 

sulfide generally are less than 1 ppm; however, measured sulfur concentrations in surface and 

waste waters have ranged from slightly less than 1 to 5 ppm. Household exposures to hydrogen 

sulfide can occur through misuse of drain cleaning materials. Hydrogen sulfide can be found in 

well water and formed in hot water heaters, giving tap water a rotten egg odor. Cigarette smoke 

and emissions from gasoline vehicles contain hydrogen sulfide. The general population can be 

exposed to lower levels from accidental or deliberate release of emissions from pulp and paper 

mills; from natural gas drilling and refining operations; and from areas of high geothermal 

activity, such as hot springs. 

People who work in certain industries can be exposed to higher levels of hydrogen sulfide than 

the general population. These industries include rayon textiles manufacturing, pulp and paper 

mills, petroleum and natural gas drilling operations, and waste water treatment plants. Workers 

on farms with manure storage pits or landfills can also be exposed to higher levels of hydrogen 

sulfide than the general population. As a member of the general public, you might be exposed to 

higher-than-normal levels of hydrogen sulfide if you live near a waste water treatment plant, a 

gas and oil drilling operation, a farm with manure storage or livestock confinement facilities, or a 

landfill. Exposure from these sources is mainly from breathing air that contains hydrogen 

sulfide. You will find further information about hydrogen sulfide exposure in Chapter 6. 

1.4 HOW CAN HYDROGEN SULFIDE ENTER AND LEAVE MY BODY? 

Hydrogen sulfide enters your body primarily through the air you breathe. Much smaller amounts 

can enter your body through the skin. Hydrogen sulfide is a gas, so you would not likely be 

exposed to it by ingestion. When you breathe air containing hydrogen sulfide or when hydrogen 

sulfide comes into contact with skin, it is absorbed into the blood stream and distributed 

throughout the body. In the body, hydrogen sulfide is primarily converted to sulfate and is 

excreted in the urine. Hydrogen sulfide is rapidly removed from the body. Additional 

information about how hydrogen sulfide can enter or leave your body is discussed in Chapter 3. 
HYDROGEN SULFIDE 4 

1. PUBLIC HEALTH STATEMENT 

1.5 HOW CAN HYDROGEN SULFIDE AFFECT MY HEALTH? 

Scientists use many tests to protect the public from harmful effects of toxic chemicals and to find 

ways for treating persons who have been harmed. 

One way to learn whether a chemical will harm people is to determine how the body absorbs, 

uses, and releases the chemical. For some chemicals, animal testing may be necessary. Animal 

testing may also help identify health effects such as cancer or birth defects. Without laboratory 

animals, scientists would lose a basic method for getting information needed to make wise 

decisions that protect public health. Scientists have the responsibility to treat research animals 

with care and compassion. Scientists must comply with strict animal care guidelines because 

laws today protect the welfare of research animals. 

Exposure to low concentrations of hydrogen sulfide may cause irritation to the eyes, nose, or 

throat. It may also cause difficulty in breathing for some asthmatics. Brief exposures to high 

concentrations of hydrogen sulfide (greater than 500 ppm) can cause a loss of consciousness. In 

most cases, the person appears to regain consciousness without any other effects. However, in 

some individuals, there may be permanent or long-term effects such as headaches, poor attention 

span, poor memory, and poor motor function. No health effects have been found in humans 

exposed to typical environmental concentrations of hydrogen sulfide (0.00011–0.00033 ppm). 

Deaths due to breathing in large amounts of hydrogen sulfide have been reported in a variety of 

different work settings, including sewers, animal processing plants, waste dumps, sludge plants, 

oil and gas well drilling sites, and tanks and cesspools. 

Very little information is available about health problems that could occur from drinking or 

eating something with hydrogen sulfide in it. Scientists have no reports of people poisoned by 

such exposures. Pigs that ate feed containing hydrogen sulfide experienced diarrhea for a few 

days and lost weight after about 105 days. 
HYDROGEN SULFIDE 5 

1. PUBLIC HEALTH STATEMENT 

Scientists have little information about what happens when you are exposed to hydrogen sulfide 

by getting it on your skin, although they know that care must be taken with the compressed 

liquefied product to avoid frostbite. Hydrogen sulfide will irritate your eyes if you are exposed 

to the gas. These types of exposures are more common in certain kinds of jobs. 

Hydrogen sulfide has not been shown to cause cancer in humans, and its possible ability to cause 

cancer in animals has not been studied thoroughly. Hydrogen sulfide has not been classified for 

its ability to cause or not cause cancer. 

1.6 HOW CAN HYDROGEN SULFIDE AFFECT CHILDREN? 

This section discusses potential health effects in humans from exposures during the period from 

conception to maturity at 18 years of age. 

Children are likely to be exposed to hydrogen sulfide in the same manner as adults, except for 

adults at work. However, because hydrogen sulfide is heavier than air and because children are 

shorter than adults, children sometimes are exposed to more hydrogen sulfide than adults. There 

is very little information on possible health problems in children who have been exposed to 

hydrogen sulfide. Exposed children probably will experience effects similar to those 

experienced by exposed adults. Whether children are more sensitive to hydrogen sulfide 

exposure than adults or whether hydrogen sulfide causes birth defects in people is not known. 

The results of studies in animals suggest that exposure to low concentrations of hydrogen sulfide 

during pregnancy does not cause birth defects. 

For more information about the potential health effects of hydrogen sulfide on children, see 

Sections 3.7 and 6.6. 
	 

	 

HYDROGEN SULFIDE 6 

1. PUBLIC HEALTH STATEMENT 

1.7 HOW CAN FAMILIES REDUCE THE RISK OF EXPOSURE TO HYDROGEN 

SULFIDE? 

If your doctor finds that you have been exposed to substantial amounts of hydrogen sulfide, ask 

whether your children might also have been exposed. Your doctor might need to ask your state 

health department to investigate. 

Hydrogen sulfide is part of the natural environment; the general population will have some 

exposure to hydrogen sulfide. Families can be exposed to more hydrogen sulfide than the 

general population if they live near natural or industrial sources of hydrogen sulfide, such as hot 

springs, manure holding tanks, or pulp and paper mills. However, their exposure levels are 

unlikely to approach those that sicken people exposed at work. Families can reduce their 

exposure to hydrogen sulfide by avoiding areas that are sources of hydrogen sulfide. For 

example, individuals of families that live on farms can avoid manure storage areas where high 

concentrations of hydrogen sulfide may be found. 

1.8 IS THERE A MEDICAL TEST TO DETERMINE WHETHER I HAVE BEEN 

EXPOSED TO HYDROGEN SULFIDE? 

Hydrogen sulfide can be measured in exhaled air, but samples must be taken within 2 hours after 

exposure to be useful. A more reliable test to determine if you have been exposed to hydrogen 

sulfide is the measurement of increased thiosulfate levels in urine. This test must be done within 

12 hours of exposure. Both tests require special equipment, which is not routinely available in a 

doctor’s office. Samples can be sent to a special laboratory for the tests. These tests can tell 

whether you have been exposed to hydrogen sulfide, but they cannot determine exactly how 

much hydrogen sulfide you have been exposed to or whether harmful effects will occur. 

Exposure to high levels of hydrogen sulfide can cause long-term effects on the nervous system. 

There are tests that can measure nervous system function. However, these tests are not specific 

for hydrogen sulfide and could indicate that you have been exposed to other chemicals that affect 

the nervous system. 

See Chapters 3 and 7 for more information on tests for exposure to hydrogen sulfide. 
	 

HYDROGEN SULFIDE 7 

1. PUBLIC HEALTH STATEMENT 

1.9 WHAT RECOMMENDATIONS HAS THE FEDERAL GOVERNMENT MADE TO 

PROTECT HUMAN HEALTH? 

The federal government develops regulations and recommendations to protect public health. 

Regulations can be enforced by law. The EPA, the Occupational Safety and Health 

Administration (OSHA), and the Food and Drug Administration (FDA) are some federal 

agencies that develop regulations for toxic substances. Recommendations provide valuable 

guidelines to protect public health, but cannot be enforced by law. The Agency for Toxic 

Substances and Disease Registry (ATSDR) and the National Institute for Occupational Safety 

and Health (NIOSH) are two federal organizations that develop recommendations for toxic 

substances. 

Regulations and recommendations can be expressed as “not-to-exceed” levels, that is, levels of a 

toxic substance in air, water, soil, or food that do not exceed a critical value that is usually based 

on levels that affect animals; they are then adjusted to levels that will help protect humans. 

Sometimes these not-to-exceed levels differ among federal organizations because they used 

different exposure times (an 8-hour workday or a 24-hour day), different animal studies, or other 

factors. 

Recommendations and regulations are also updated periodically as more information becomes 

available. For the most current information, check with the federal agency or organization that 

provides it. Some regulations and recommendations for hydrogen sulfide include the following: 

OSHA has established an acceptable ceiling concentration of 20 ppm for hydrogen sulfide in the 

workplace, with a maximum level of 50 ppm allowed for 10 minutes maximum duration if no 

other measurable exposure occurs. NIOSH has set a maximum Recommended Exposure Limit 

(REL) ceiling value of 10 ppm for 10 minutes maximum duration. A more complete listing of 

federal and state regulations and recommendations is found in Chapter 8. 

 


 

HYDROGEN SULFIDE 8 

1. PUBLIC HEALTH STATEMENT 

1.10 WHERE CAN I GET MORE INFORMATION? 

If you have any more questions or concerns, please contact your community or state health or 

environmental quality department, or contact ATSDR at the address and phone number below. 

ATSDR can also tell you the location of occupational and environmental health clinics. These 

clinics specialize in recognizing, evaluating, and treating illnesses that result from exposure to 

hazardous substances. 

Toxicological profiles are also available on-line at www.atsdr.cdc.gov and on CD-ROM. You 

may request a copy of the ATSDR ToxProfilesTM CD-ROM by calling the toll-free information 

and technical assistance number at 1-888-42ATSDR (1-888-422-8737), by e-mail at 

atsdric@cdc.gov, or by writing to: 

Agency for Toxic Substances and Disease Registry 

 Division of Toxicology and Environmental Medicine 

1600 Clifton Road NE 

 Mailstop F-32 

 Atlanta, GA 30333 

 Fax: 1-770-488-4178 

Organizations for-profit may request copies of final Toxicological Profiles from the following: 

National Technical Information Service (NTIS) 

5285 Port Royal Road 

 Springfield, VA 22161 

 Phone: 1-800-553-6847 or 1-703-605-6000 

 Web site: http://www.ntis.gov/ 

 

	 

HYDROGEN SULFIDE 9 

2. RELEVANCE TO PUBLIC HEALTH 

2.1 BACKGROUND AND ENVIRONMENTAL EXPOSURES TO HYDROGEN SULFIDE IN 

THE UNITED STATES 

Hydrogen sulfide (H2S) is a poisonous, colorless gas with a characteristic odor of rotten eggs. It naturally 

occurs in the gases from volcanoes, sulfur springs, undersea vents, swamps and stagnant bodies of water 

and in crude petroleum and natural gas. Additionally, bacteria, fungi, and actinomycetes release 

hydrogen sulfide during the decomposition of sulfur-containing proteins and by the direct reduction of 

sulfate (SO4

2-). Hydrogen sulfide is frequently encountered in various industries and may be released to 

the environment as a result of their operations. Some of these industries include natural gas production, 

municipal sewage pumping and treatment plants, landfilling, swine containment and manure handling, 

pulp and paper production, construction in wetlands, asphalt roofing, pelt processing, animal slaughter 

facilities, tanneries, petroleum refining, petrochemical synthesis, coke production plants, viscose rayon 

manufacture, sulfur production, iron smelting, and food processing. 

Ambient air concentrations of hydrogen sulfide from natural sources range between 0.11 and 0.33 ppb. 

Concentrations of hydrogen sulfide in urban areas are generally <1 ppb. Much higher levels (often 

exceeding 90 ppb) have been detected in communities living near natural sources of hydrogen sulfide or 

near industries releasing hydrogen sulfide. 

Humans may be exposed to hydrogen sulfide both from its endogenous production or from exogenous 

sources. Most endogenous production apparently results from the metabolism of sulfhydryl-containing 

amino acids (e.g., cysteine) by bacteria present in both the intestinal tract and the mouth; however, it is 

also produced in the brain and several smooth muscles (e.g., thoracic aorta) by enzymes found in these 

tissues. In the brain, hydrogen sulfide produced from reactions catalyzed by the cystathionine β-synthase 

enzyme from the desulfhydration of cysteine acts as a neuromodulator. Physiological concentrations of 

hydrogen sulfide enhance the N-methyl-D-asparate (NMDA) receptor mediated response and can 

facilitate the induction of hippocampal long-term potentiation. Hydrogen sulfide produced in the mouth 

is a component of bad breath (halitosis); concentrations between 1 and 100 ppb have been measured in 

mouth air. It is generated in the large intestine by the bacterial reduction of inorganic sulfate and sulfite, 

and by fermentation of sulfur-containing amino acids. It can compose up to 10% of intestinal gases. In 

flatus, hydrogen sulfide concentrations as high as 18 ppm were recorded in individuals on a normal diet. 
HYDROGEN SULFIDE 10 

2. RELEVANCE TO PUBLIC HEALTH 

In these experiments, between 40 and 90% of normal individuals produced hydrogen sulfide; mean values 

over a 4-year period were between 1 and 4 ppm. Sulfide concentrations in whole blood samples from six 

healthy adults were found to range from 10 to 100 μmol/L. 

There is considerable individual variability in the odor threshold for hydrogen sulfide in humans; the 

thresholds can range from 0.0005 to 0.3 ppm. However, at concentrations of 100 ppm and higher, 

individuals may not detect hydrogen sulfide odor due to damage to olfactory tissue. 

2.2 SUMMARY OF HEALTH EFFECTS 

The general population is primarily exposed to hydrogen sulfide via the inhalation route. Although oral 

and dermal absorption can also occur, these routes only contribute small amounts to the overall body 

burden. Information on the toxicity of hydrogen sulfide in humans comes from case reports, occupational 

studies, and community studies. Hydrogen sulfide tends to be a problem in communities located near 

certain types of industrial sites, including pulp and paper mills, natural gas production, swine containment 

and manure handling, or geothermal power plants. The interpretation of the community studies is often 

limited by exposure to other chemicals. The human data suggest that the respiratory tract and nervous 

system are the most sensitive targets of hydrogen sulfide toxicity. The most commonly reported 

nonlethal effect found in individuals acutely exposed to high concentrations of hydrogen sulfide is 

unconsciousness followed by apparent recovery, colloquially referred to as knockdown. In most cases, 

actual exposure concentrations and durations are not known; estimates suggest that the concentrations 

exceed 500 ppm and the durations are short, typically <1 hour. Although there is an apparent recovery, 

many individuals report permanent or persistent neurological effects including headaches, poor 

concentration ability and attention span, impaired short-term memory, and impaired motor function. 

Respiratory distress or arrest and pulmonary edema are also associated with exposure to very high 

concentrations of hydrogen sulfide; it is believed that these respiratory effects are secondary to central 

nervous system depression or due to tissue hypoxia. Cardiovascular effects (e.g., cardiac arrhythmia and 

tachycardia) have also been observed following an acute exposure to high concentrations of hydrogen 

sulfide. 

Exposure to lower concentrations of hydrogen sulfide can result in less severe neurological and 

respiratory effects. Reported neurological effects include incoordination, poor memory, hallucinations, 

personality changes, and anosmia (loss of sense of smell); the respiratory effects include nasal symptoms, 

sore throat, cough, and dyspnea. Impaired lung function has also been observed in asthmatics acutely 
HYDROGEN SULFIDE 11 

2. RELEVANCE TO PUBLIC HEALTH 

exposed to 2 ppm hydrogen sulfide; no alterations in lung function were observed in studies of nonasthmatic workers. 

Animal studies confirm the human data suggesting that the respiratory tract and the nervous system are 

the most sensitive targets of hydrogen sulfide toxicity. As with humans, unconsciousness was observed 

in rats exposed to very high concentrations of hydrogen sulfide (800 ppm); central nervous system 

depression, as evidenced by lethargy, and pulmonary edema were observed in rats exposed to 400 ppm 

hydrogen sulfide for 4 hours. Decreased performance in neurological tests has been observed in rats 

exposed to 80–200 ppm hydrogen sulfide for 5 days to 11 weeks. Damage to the nasal olfactory 

epithelium is also observed in rats exposed to lower levels of hydrogen sulfide for an acute or 

intermediate duration; the adverse effect levels are 80 ppm (3 hours/day for 5 days) and 30 ppm 

(6 hours/day, 7 days/week for 10 weeks) following acute- or intermediate-duration exposure, respectively. 

Information on the toxicity of hydrogen sulfide following oral or dermal/ocular exposure is limited. Oral 

exposure data are limited to a single pig study examining the effects of hydrogen sulfide in feed. 

Observed effects included a diarrheic digestive disorder and decreased body weight gain. Exposure to 

hydrogen sulfide gas can result in a number of ocular effects, including keratoconjunctivitis, punctuate 

corneal erosion, blepharospasm, lacrimation, and photophobia in humans. A community exposure study 

found a concentration-related increase in the prevalence of eye symptoms in residents exposed to low 

(daily mean of total reduced sulfur <10 μg/m3

), medium (10–30 μg/m3), or high (>30 μg/m3) levels. 

Although hydrogen sulfide was the primary constituent of the total reduced sulfur levels, other sulfur 

compounds, as well as other air pollutants, may have contributed to the eye irritation. 

There are limited human data suggesting that maternal or paternal exposure to hydrogen sulfide can 

increase the risk of spontaneous abortion among rayon textile, paper produces, or petrochemical workers 

(or their spouses). However, the subjects (or their spouses) were exposed to a number of other hazardous 

chemicals, which may have contributed to the increased risk. No significant alterations in reproductive 

performance were observed in rats exposed to 10–80 ppm hydrogen sulfide for an intermediate duration. 

The available animal data suggest that hydrogen sulfide is not a developmental toxicant at concentrations 

of 80 ppm and lower. No structural anomalies, developmental delays, performance in developmental 

neurobehavioral tests, or brain histology were observed in a well-conducted rat study. Another study 

found alterations in Purkinje cell growth in the offspring of rats exposed to 20 or 50 ppm hydrogen 

sulfide during the gestation and lactation periods; the toxicological significance of this finding in the 

absence of alterations in neurobehavioral performance is not known. 
HYDROGEN SULFIDE 12 

2. RELEVANCE TO PUBLIC HEALTH 

There are limited data on the potential of hydrogen sulfide to induce cancer in humans. One study found 

significant increases in the risk of developing cancers of the trachea, bronchus, and lung among residents 

exposed to high levels of naturally occurring hydrogen sulfide. However, the authors noted that the 

elevated disease rates were consistent with exposure to high concentrations of hydrogen sulfide and 

mercury; the contribution of mercury to the overall respiratory tract cancer rates cannot be determined 

from these data. Another study did not find significant alterations in cancer incidences among residents 

living near natural gas refineries. The carcinogenicity of hydrogen sulfide has not been assessed in 

animal studies. 

A greater detailed discussion of the hydrogen sulfide-induced respiratory effects and neurological effects 

follows. The reader is referred to Section 3.2, Discussion of Health Effects by Route of Exposure, for 

additional information of these effects and other health effects. 

Respiratory Effects. Exposure to very high concentrations of hydrogen sulfide can result in 

respiratory arrest and/or pulmonary edema. Numerous case reports suggest that these effects can occur 

after a brief exposure to hydrogen sulfide. Although the exact mechanism is not known, there is strong 

evidence to suggest that the rapid respiratory failure and possibly the pulmonary edema are secondary to 

the action of hydrogen sulfide on the respiratory center of the brain. There is also some evidence that the 

respiratory failure and pulmonary edema may be due to a dose-dependent inhibition of cytochrome 

oxidase in lung mitochondria, the terminal step in oxidative metabolism, resulting in tissue hypoxia. At 

low concentrations, hydrogen sulfide is a respiratory irritant. Residents living near industries emitting 

hydrogen sulfide, such as paper mills, animal slaughter facilities, or tanneries, reported nasal symptoms, 

cough, or increased visits to the hospital emergency room due to respiratory symptoms (including 

asthma). In general, exposure to hydrogen sulfide has not resulted in significant alterations in lung 

function. No alterations in lung function were observed in workers chronically exposed to 1–11 ppm 

hydrogen sulfide. However, there is some evidence to suggest that asthmatics may be a sensitive 

subpopulation. No statistical alterations in lung function were observed in a group of 10 asthmatics 

exposed to 2 ppm hydrogen sulfide for 30 minutes, as compared with pre-exposure values. However, 

increased airway resistance and decreased specific airway conductance, implying bronchial obstruction, 

were observed in 2 out of the 10 subjects. 

Although the human data are useful in establishing the respiratory tract as a target of toxicity, 

concentration-response relationships cannot be established for most of these studies because exposure 
HYDROGEN SULFIDE 13 

2. RELEVANCE TO PUBLIC HEALTH 

levels were not monitored or the subjects were exposed to several sulfur compounds. Animal data 

provide strong evidence that the respiratory tract is a sensitive target of hydrogen sulfide toxicity and can 

be used to establish concentration-response relationships. Damage to the nasal olfactory epithelium has 

been observed in rats exposed to hydrogen sulfide for acute or intermediate durations. Loss of olfactory 

neurons and basal cell hyperplasia were observed in rats exposed to 30 ppm and higher for 6 hours/day, 

7 days/week for 10 or 13 weeks. The severity of the olfactory neuron loss was concentration-related; 

however, an inverse relationship between severity and concentration was observed for the basal cell 

hyperplasia suggesting that as the concentration increased, the ability of the olfactory epithelium to 

regenerate decreased. Similar effects were observed in rats exposed to hydrogen sulfide once or 

repeatedly for 5 days; however, higher concentrations were needed to elicit a significant response. 

Intermediate-duration exposure (6 hours/day, 5 days/week for 13 weeks) resulted in inflammation of the 

squamous portion of the nasal mucosa in mice exposed to 80 ppm and loss of olfactory neurons in mice 

exposed to 30 ppm and higher. 

Neurological Effects. A brief exposure to very high concentrations of hydrogen sulfide can result in 

unconsciousness in humans and animals followed by an apparent full recovery upon exposure termination 

(some human case reports note that the subjects recovered after administration of oxygen). Human data 

are not reliable for establishing the threshold for this effect. In rats, the threshold for severe central 

nervous system depression is between 400 and 800 ppm; exposure to 400 ppm was associated with 

lethargy. As noted previously, persistent neurological effects have been reported in humans recovering 

from hydrogen-sulfide induced unconsciousness. These effects include headaches, poor concentration 

ability and attention span, impaired short-term memory, and impaired motor function. 

Exposure to hydrogen sulfide can also result in neurobehavioral effects in humans and animals. 

Alterations in balance, reaction time, visual field, and verbal recall were observed in individuals exposed 

to high concentrations of hydrogen sulfide for an acute duration and in individuals exposed to lower 

levels of hydrogen sulfide for a chronic duration; no monitoring data were provided. The severity of 

effects appeared to be related to the duration of exposure as well as the exposure concentration. Several 

animal studies provide suggestive evidence that hydrogen sulfide exposure results in a decrease in motor 

activity and task response rate; the lowest adverse effect level for altered neurobehavioral performance is 

the decreased spontaneous motor activity observed in rats receiving nose-only exposure to 80 ppm, 

3 hours/day for 5 days. A rat study found that intermediate-duration exposure to hydrogen sulfide did not 

adversely affect memory; however, learning a new complex task was adversely affected at 125 ppm 

(4 hours/day, 5 days/week). 
HYDROGEN SULFIDE 14 

2. RELEVANCE TO PUBLIC HEALTH 

2.3 MINIMAL RISK LEVELS (MRLs) 

Estimates of exposure levels posing minimal risk to humans (MRLs) have been made for hydrogen 

sulfide. An MRL is defined as an estimate of daily human exposure to a substance that is likely to be 

without an appreciable risk of adverse effects (noncarcinogenic) over a specified duration of exposure. 

MRLs are derived when reliable and sufficient data exist to identify the target organ(s) of effect or the 

most sensitive health effect(s) for a specific duration within a given route of exposure. MRLs are based 

on noncancerous health effects only and do not consider carcinogenic effects. MRLs can be derived for 

acute, intermediate, and chronic duration exposures for inhalation and oral routes. Appropriate 

methodology does not exist to develop MRLs for dermal exposure. 

Although methods have been established to derive these levels (Barnes and Dourson 1988; EPA 1990), 

uncertainties are associated with these techniques. Furthermore, ATSDR acknowledges additional 

uncertainties inherent in the application of the procedures to derive less than lifetime MRLs. As an 

example, acute inhalation MRLs may not be protective for health effects that are delayed in development 

or are acquired following repeated acute insults, such as hypersensitivity reactions, asthma, or chronic 

bronchitis. As these kinds of health effects data become available and methods to assess levels of 

significant human exposure improve, these MRLs will be revised. 

Inhalation MRLs 

• An MRL of 0.07 ppm has been derived for acute-duration inhalation exposure to hydrogen sulfide. 

A small number of controlled exposure studies have examined the acute toxicity of hydrogen sulfide in 

humans; most of these have focused on potential respiratory and metabolic effects. No significant 

alterations in lung function (forced lung vital capacity, forced expiratory volume, bronchial 

responsiveness to a histamine challenge, airway resistance, and specific airway conductance) were 

observed in asthmatics exposed to 2 ppm for 30 minutes (Jappinen et al. 1990). However, 2 of the 

10 subjects had >30% changes in airway resistance and specific airway conductance, implying bronchial 

obstruction. Three of the subjects also reported headaches. A series of studies conducted by Bhambhani 

and associates examined the potential of hydrogen sulfide to induce respiratory and metabolic effects in 

exercising adults. No significant alterations in lung function were observed in individuals exposed to 

10 ppm for 15 minutes (Bhambhani et al. 1996a), but increases in blood lactate levels were observed in 
HYDROGEN SULFIDE 15 

2. RELEVANCE TO PUBLIC HEALTH 

subjects exposed to 5 or 10 ppm (Bhambhani and Singh 1991; Bhambhani et al. 1997). The study authors 

noted that the increase in lactate levels suggested an increased dependence on anaerobic metabolism, 

which may have resulted from reduced oxygen availability due to detoxification of hydrogen sulfide by 

oxyhemoglobin or inhibition of cytochrome oxidase in exercising tissue (Bhambhani 1999). 

Animal studies have reported a variety of respiratory effects following acute-duration exposure to 

hydrogen sulfide. Damage to the nasal olfactory epithelium was observed in rats exposed to 400 ppm for 

4 hours (Lopez et al. 1988b), 200 ppm for 3 hours (Brenneman et al. 2002), or 80 ppm 3 hours/day for 

5 days (Brenneman et al. 2002). Pulmonary edema has been observed in rats exposed to 83 or 375 ppm 

for 4 hours (Lopez et al. 1988a; Prior et al. 1990). Neurological effects include decreased spontaneous 

motor activity in rats exposed to 80 ppm, 3 hours/day for 5 days (Struve et al. 2001), impaired 

performance on a discriminated avoidance task in rats exposed to 200 ppm for 2 hours (Higuchi and 

Fukamachi 1977), lethargy in rats exposed to 400 ppm for 4 hours (Lopez et al. 1988b), and 

unconsciousness in rats exposed to 800 ppm for 20 minutes (Beck et al. 1979). 

The Jappinen et al. (1990) study, which found suggestive evidence of bronchial obstruction among 

asthmatics exposed to 2 ppm hydrogen sulfide for 30 minutes, was selected as the basis of the MRL. The 

2 ppm concentration was considered a minimally adverse effect level because the changes in airway 

resistance and specific airway conductance were only observed in 2 of the 10 subjects. The lowestobserved-adverse-effect level (LOAEL) from the Jappinen et al. (1990) study is supported by the LOAEL 

of 5 ppm for increased blood lactate levels observed in exercising subjects (Bhambhani et al. 1996b). The 

Jappinen et al. (1990) study was selected over the Bhambhani et al. (1996b) study because the Bhambhani 

studies involved mouth-only exposure so that the subjects could not smell the hydrogen sulfide. The 

MRL was calculated by dividing the unadjusted LOAEL by an uncertainty factor of 27 (3 for use of a 

minimal LOAEL, 3 for human variability, and 3 for database deficiencies). A partial uncertainty factor of 

3 was used for human variability because the study was conducted in asthmatics who are likely to be a 

sensitive subpopulation. Further details on the derivation of this MRL can be found in the MRL 

worksheets in Appendix A of this profile. 

•	 An MRL of 0.02 ppm has been derived for intermediate-duration inhalation exposure to hydrogen 

sulfide. 

There are limited data on the toxicity of hydrogen sulfide in humans following intermediate-duration 

exposure. Acute- and chronic-duration studies suggest that the respiratory tract and nervous system are 

sensitive targets of hydrogen sulfide. 
HYDROGEN SULFIDE 16 

2. RELEVANCE TO PUBLIC HEALTH 

Intermediate-duration animal studies support the identification of the respiratory tract and nervous system 

as sensitive targets. Exposure of rats and mice to low hydrogen sulfide concentrations have resulted in 

histological damage to the upper respiratory tract. Brenneman et al. (2000) reported significant 

concentration-related increases in the incidence and severity of lesions to the nasal olfactory epithelium in 

rats exposed to hydrogen sulfide for 10 weeks. The effects consisted of olfactory neuron loss and basal 

cell hyperplasia in rats exposed to 30 or 80 ppm, 6 hours/day, 7 days/week for 10 weeks; no adverse 

effects were observed at 10 ppm. In contrast, earlier studies conducted by CIIT (1983b, 1983c) did not 

find significant alterations in the nasal turbinates of Sprague-Dawley or Fischer-344 (F-344) rats exposed 

to 80 ppm or less hydrogen sulfide, 6 hours/day, 5 days/week for 13 weeks. Inflammation of the 

squamous portion of the nasal mucosa was observed in mice exposed to 80 ppm hydrogen sulfide, 

6 hours/day, 5 days/week for 13 weeks (CIIT 1983a); the no-observed-adverse-effect level (NOAEL) for 

this effect is 30 ppm. However, a re-examination of the histological specimens from this study (Dorman 

et al. 2004) revealed a statistically significant increase in the incidence of olfactory neuron loss in 

Sprague-Dawley rats, F-344 rats, and B6C3F1 mice exposed to 30 or 80 ppm; no lesions were observed at 

10 ppm. In addition, increases in the incidence of bronchiolar epithelial hyperplasia and hypertrophy 

were observed in female Sprague-Dawley rats exposed to 30 or 80 ppm and male Sprague-Dawley and 

F-344 rats exposed to 80 ppm. The sensitivity of the olfactory epithelium has also been confirmed by 

acute-duration studies; degeneration of the olfactory epithelium was observed in rats exposed to 400 ppm 

hydrogen sulfide for 4 hours (Lopez et al. 1988b), rats exposed to 200 ppm for 3 hours (Brenneman et al. 

2002), and rats exposed to 80 ppm, 3 hours/day for 5 days (Brenneman et al. 2002). Additionally, data 

collected using a computational fluid dynamics model of the rat nasal epithelium (Moulin et al. 2002) 

suggest that the olfactory epithelium is more sensitive than the nasal respiratory epithelium despite the 

higher hydrogen sulfide flux (a surrogate for dose) to the regions lined with respiratory epithelium 

compared to regions lined with olfactory epithelium. Within the areas of the nose lined with olfactory 

epithelium, a high correlation between predicted hydrogen sulfide flux and the incidence of olfactory 

lesion was found. 

The neurotoxicity of hydrogen sulfide in mature animals following intermediate-duration exposure has 

been assessed in studies examining brain weight, neurological function (posture, gait, tone of facial 

muscles, and pupillary reflexes), and histopathology; neurobehavioral performance has not been 

adequately assessed in longer duration studies. A 5% decrease in absolute brain weight was observed in 

Sprague-Dawley rats exposed to 80 ppm hydrogen sulfide 6 hours/day, 5 days/week for 13 weeks; no 

alterations were observed at 30 ppm (CIIT 1983c). No alterations in histopathology or neurological 
HYDROGEN SULFIDE 17 

2. RELEVANCE TO PUBLIC HEALTH 

function were observed in these rats (CIIT 1983c) or in similarly exposed F-344 rats (CIIT 1983b) or 

B6C3F1 mice (CIIT 1983a). Neurodevelopmental toxicity studies have found some alterations that are 

suggestive of neurotoxicity. The suggestive findings in the offspring of rats exposed for 7 hours/day on 

gestational day 5 through postnatal day 21 include alterations in the architecture and growth 

characteristics of Purkinje cell dendritic fields at 20 ppm (Hannah and Roth 1991), decreases in 

norepinephrine and increases in serotonin in the frontal cortex at 20 ppm (Skrajny et al. 1992), and 

decreases in brain amino acid levels at 75 ppm (Hannah et al. 1989, 1990). However, no alterations in 

neurobehavioral performance (assessed via motor activity, passive avoidance, acoustic startle, functional 

observation battery), delays in development (pinnae detachment, surface righting, incisor eruption, 

negative geotaxis, and eyelid detachment), or neuropathology were observed in the offspring of rats 

exposed 6 hours/day, 7 days/week for 2 weeks prior to mating, during mating, on gestational days 5–19, 

and on postnatal days 5–18 (Dorman et al. 2000). These data suggest that exposures of 20–80 ppm may 

result in subclinical alterations in neurochemistry and neuroanatomy. 

The Brenneman et al. (2000) study was selected as the basis of the intermediate-duration inhalation MRL. 

In this study, groups of 12 male Sprague-Dawley rats were exposed to 0, 10, 30, or 80 ppm hydrogen 

sulfide for 6 hours/day, 7 days/week for 10 weeks. Parameters used to assess toxicity were limited to 

extensive histopathological examination of the nasal cavity (six transverse sections examined via light 

microscopy; transverse sections form a series of circumferential slices [labeled levels 1–6], which allow 

for a thorough evaluation of all major structures and mucosae of the nasal cavity). Nasal lesions occurred 

only in the olfactory mucosa in rats exposed to 30 or 80 ppm and consisted of multifocal, bilaterally 

symmetrical olfactory neuron loss and basal cell hyperplasia affecting the lining of the dorsal medial 

meatus and the dorsal and medial regions of the ethmoid recess. The severity of the olfactory lesions was 

scored as 1 mild, 2 moderate, or 3 severe. For the olfactory neuron loss, the mild, moderate, or severe 

severity scores corresponded to 26–50, 51–75, and 76–100%, respectively, reduction in the normal 

thickness of the olfactory neuron layer; for the basal cell hyperplasia, mild, moderate, or severe severity 

scores corresponded to 1–33, 34–67, or 68–100% of the normal thickness of the olfactory neuron cell 

layer replaced by basal cells. No olfactory lesions were observed in the controls or rats exposed to 

10 ppm. At 30 ppm, olfactory neuron loss was observed at nasal levels 4 (11/12, severity 1.4) and 

5 (9/12, severity 1.1) and basal cell hyperplasia was observed at nasal levels 4 (10/12, severity 1.8) and 

5 (11/12, severity 1.3). At 80 ppm, olfactory neuron loss was observed at levels 3 (8/8, severity 2.4), 

4 (12/12, severity 2.4), 5 (11/12, severity 1.5), and 6 (5/12, severity 1.2—incidence not statistically 

significant) and basal cell hyperplasia was observed at nasal levels 4 (12/12, severity 1.2), 5 (11/12, 

severity 1.3), and 6 (6/12, severity 1.0). 
HYDROGEN SULFIDE 18 

2. RELEVANCE TO PUBLIC HEALTH 

The Brenneman et al. (2000) study was selected over the neurodevelopmental studies (Hannah and Roth 

1991; Skrajny et al. 1992), which identified a slightly lower LOAEL (20 ppm, 7 hours/day, gestation 

day 5 to postnatal day 21) because the respiratory tract effect has been confirmed by other studies 

(Brenneman et al. 2002; Lopez et al. 1988b) and the adversity of the alterations in neurochemistry and 

neuroanatomy in the absence of neurological performance alterations is not known. As discussed by 

Ferguson (1996), prenatal exposure to ionizing radiation can result in misalignment of Purkinje cells in 

the cerebellum; clinical signs associated with these neuroanatomical alterations include hypoactivity, 

ataxia, tremors, and learning deficits. Although a direct comparison of the Purkinje cell alterations 

reported in the Hannah and Roth (1991) study and those resulting from ionizing radiation exposure cannot 

be made because the Hannah and Roth study involved examination of a single Purkinje cell rather than 

cerebellar sections, it may be reasonable to predict that the clinical manifestations of the Purkinje cell 

damage would be similar. The similarity of the LOAELs for nasal effects and neurodevelopmental 

effects suggest that an MRL derived for one would be protective of the other. 

Because the dose-response for olfactory neuron loss and basal cell hyperplasia went from 0/12 to 10 or 

11/12 with no intermediate levels of response, the data were not considered suitable for benchmark dose 

analysis; thus, the MRL was derived using the NOAEL/LOAEL approach. The intermediate-duration 

inhalation MRL of 0.02 ppm was calculated by dividing the human equivalent NOAEL (NOAELHEC) of 

0.46 ppm by an uncertainty factor of 30 (3 for extrapolation from animals using dosimetric adjustments 

and 10 for human variability). The NOAELHEC was calculated using the following equation from EPA 

(1994b) for category 1 gases: 

NOAELHEC = NOAELADJ x RDGRET 

The duration-adjusted NOAEL (NOAELADJ) of 2.5 ppm was calculated as follows: 

NOAELADJ =10 ppm x 6 hour/24 hour x 7 days/7 days 
 

 

 

 

HYDROGEN SULFIDE 19 

2. RELEVANCE TO PUBLIC HEALTH 

The regional gas dose ratio for the extrathoracic region (RGDRET) of 0.184 was calculated using the 

following equation: 

⎛ V ⎞ E ⎜

⎜

SA ⎟

⎟

⎝ ET ⎠rat RGDRET = ⎛ V ⎞ E ⎜

⎜

SA ⎟

⎟

⎝ ET ⎠human 

Where: 

Ve is the minute volume and SAET is the surface area of the extrathoracic (ET) region of the respiratory 

tract. 

 Minute volume (Ve): 

Human: 13.8 L/minute (EPA 1994) 

Rat: 0.190 L/minute; calculated using the following EPA equation 

ln(Ve) = b0 + b1ln(BW) 

For rats, b0 equals -0.578 and b1 equals 0.821 

Because a limited amount of body weight data was reported in the study, a reference 

body weight of 0.267 kg (EPA 1988) was used. 

The rat and human respiratory surface area for the extrathoracic region reference values 

are 15.0 and 200 cm2

, respectively (EPA 1994b). 

NOAEL[HEC] = NOAELADJ x RGDR 

NOAEL[HEC] = 2.5 ppm x 0.184 

NOAEL[HEC] = 0.46 ppm 

The dosimetric model used to estimate a concentration for humans that would be equivalent to the 

exposure concentration in rats takes into account species differences in the surface area of the upper 

respiratory tract and inhalation rates. However, the model does not take into consideration that a larger 

portion of the rat nasal cavity is lined with olfactory epithelium compared to humans (50% in rats 

compared to 10% in humans) and differences in air flow patterns. A computational fluid dynamics model 

of the rat nasal epithelium developed for hydrogen sulfide (Moulin et al. 2002) found a strong correlation 

between the amount of hydrogen sulfide reaching the olfactory tissue and the severity of the lesions. A 

human computational fluid dynamics model has not been identified; thus, there is some uncertainty 

whether the dosimetric adjustments used to calculate the MRL over- or underestimates the risk to humans. 

Several human studies have examined the chronic toxicity of inhaled hydrogen sulfide (Ahlborg 1951; 

Deane et al. 1977; Hemminki and Niemi 1982; Jaakkola 1990; Jappinen et al. 1990; Kangas et al. 1984; 
HYDROGEN SULFIDE 20 

2. RELEVANCE TO PUBLIC HEALTH 

Schechter et al. 1989; Tenhunen et al. 1983). Most of these studies reported increases in the occurrence 

of subjective symptoms of respiratory irritation in workers or residents living near paper mills. 

Limitations, such as poor exposure characterization (including the lack of information on peak exposure 

levels) and co-exposure to other chemicals, limit the use of these studies for MRL derivation. No animal 

studies examined the chronic toxicity of hydrogen sulfide. Thus, a chronic-duration inhalation MRL was 

not derived. 

Oral MRLs 

Information on the toxicity of hydrogen sulfide following oral exposure is limited to a dietary exposure 

study in pigs (Wetterau et al. 1964). The observed effects include a 23% decrease in body weight gain at 

6.7 mg/kg/day in pigs exposed for 105 days and diarrheic digestive disturbance in pigs exposed to 

15 mg/kg/day for a few days. Interpretation of this study is limited because very few details are reported, 

(e.g., no information on strain, methods used, number of animals studied, or statistics). This study was 

considered inadequate for MRL derivation. 
HYDROGEN SULFIDE 21 

3. HEALTH EFFECTS 

3.1 INTRODUCTION 

The primary purpose of this chapter is to provide public health officials, physicians, toxicologists, and 

other interested individuals and groups with an overall perspective on the toxicology of hydrogen sulfide. 

It contains descriptions and evaluations of toxicological studies and epidemiological investigations and 

provides conclusions, where possible, on the relevance of toxicity and toxicokinetic data to public health. 

A glossary and list of acronyms, abbreviations, and symbols can be found at the end of this profile. 

3.2 DISCUSSION OF HEALTH EFFECTS BY ROUTE OF EXPOSURE 

To help public health professionals and others address the needs of persons living or working near 

hazardous waste sites, the information in this section is organized first by route of exposure (inhalation, 

oral, and dermal) and then by health effect (death, systemic, immunological, neurological, reproductive, 

developmental, genotoxic, and carcinogenic effects). These data are discussed in terms of three exposure 

periods: acute (14 days or less), intermediate (15–364 days), and chronic (365 days or more). 

Levels of significant exposure for each route and duration are presented in tables and illustrated in 

figures. The points in the figures showing no-observed-adverse-effect levels (NOAELs) or lowestobserved-adverse-effect levels (LOAELs) reflect the actual doses (levels of exposure) used in the studies. 

LOAELs have been classified into "less serious" or "serious" effects. "Serious" effects are those that 

evoke failure in a biological system and can lead to morbidity or mortality (e.g., acute respiratory distress 

or death). "Less serious" effects are those that are not expected to cause significant dysfunction or death, 

or those whose significance to the organism is not entirely clear. ATSDR acknowledges that a 

considerable amount of judgment may be required in establishing whether an end point should be 

classified as a NOAEL, "less serious" LOAEL, or "serious" LOAEL, and that in some cases, there will be 

insufficient data to decide whether the effect is indicative of significant dysfunction. However, the 

Agency has established guidelines and policies that are used to classify these end points. ATSDR 

believes that there is sufficient merit in this approach to warrant an attempt at distinguishing between 

"less serious" and "serious" effects. The distinction between "less serious" effects and "serious" effects is 
HYDROGEN SULFIDE 22 

3. HEALTH EFFECTS 

considered to be important because it helps the users of the profiles to identify levels of exposure at which 

major health effects start to appear. LOAELs or NOAELs should also help in determining whether or not 

the effects vary with dose and/or duration, and place into perspective the possible significance of these 

effects to human health. 

The significance of the exposure levels shown in the Levels of Significant Exposure (LSE) tables and 

figures may differ depending on the user's perspective. Public health officials and others concerned with 

appropriate actions to take at hazardous waste sites may want information on levels of exposure 

associated with more subtle effects in humans or animals (LOAELs) or exposure levels below which no 

adverse effects (NOAELs) have been observed. Estimates of levels posing minimal risk to humans 

(Minimal Risk Levels or MRLs) may be of interest to health professionals and citizens alike. 

A User's Guide has been provided at the end of this profile (see Appendix B). This guide should aid in 

the interpretation of the tables and figures for Levels of Significant Exposure and the MRLs. 

3.2.1 Inhalation Exposure 

3.2.1.1 Death 

There have been numerous case reports of human deaths after acute exposure to presumably high 

concentrations (≥500 ppm) of hydrogen sulfide gas (Beauchamp et al. 1984). NIOSH (1977a) reported 

that hydrogen sulfide was the primary occupational cause of unexpected death. Snyder et al. (1995), 

summarizing 10 years of data (1983–1992) from the Poison Control Centers National Data Collection 

system, indicated that at least 29 deaths and 5,563 exposures were attributed to hydrogen sulfide during 

that time period. Most fatal cases associated with hydrogen sulfide exposure occurred in relatively 

confined spaces, such as sewers (Adelson and Sunshine 1966), animal processing plants (Breysse 1961), 

waste dumps (Allyn 1931), sludge plants (NIOSH 1985a), tanks and cesspools (Campanya et al. 1989; 

Freireich 1946; Hagley and South 1983; Morse et al. 1981; Osbern and Crapo 1981), and other closed 

environments (Deng and Chang 1987; Parra et al. 1991). Almost all individuals described in these reports 

lost consciousness quickly after inhalation of hydrogen sulfide, sometimes after only one or two breaths 

(the so-called "slaughterhouse sledgehammer" effect). Many of the case studies involved accidental 

poisonings for which the concentrations and/or duration of exposure were not known (Allyn 1931; Arnold 

et al. 1985; Burnett et al. 1977; Deng and Chang 1987; Freireich 1946; Hagley and South 1983; Morse et 

al. 1981). In some cases, the victims were exposed for a period of time ranging from a few minutes to an 
HYDROGEN SULFIDE 23 

3. HEALTH EFFECTS 

hour and were unable to be revived (Adelson and Sunshine 1966; Deng and Chang 1987; NIOSH 1989; 

Osbern and Crapo 1981). 

Death occurring after acute exposure to hydrogen sulfide appears to be the result of respiratory failure or 

arrest, with most cases initially presenting with respiratory insufficiency, noncardiogenic pulmonary 

edema, coma, and cyanosis. Three men lost consciousness and died after entering a sewer containing 

high concentrations of hydrogen sulfide; all had the characteristic odor of hydrogen sulfide at autopsy and 

presented with cyanosis and pulmonary edema (Adelson and Sunshine 1966). After being exposed to 

hydrogen sulfide in a bathroom connected to a manure pit, a man developed nausea, vomiting, dizziness, 

and dyspnea, and died a few hours later; hemorrhagic bronchitis and asphyxiation were noted as the cause 

of death (Parra et al. 1991). 

Estimates of hydrogen sulfide exposure were available for some of the cases reported involving deaths. 

After developing decerebrate responses to painful stimuli and partial seizures, with subsequent indications 

of brain stem damage, a 16-year-old boy died (Hagley and South 1983). He was exposed to what was 

presumed to be hydrogen sulfide in a liquid manure tank; 2 weeks after exposure, hydrogen sulfide 

concentrations measured 30 cm below the tank manhole were >150 ppm, the detection limit of the 

equipment. In another incident, a 16-year-old boy was 10 meters away from an underground liquid 

manure storage tank, the contents of which had been agitating for 30–60 minutes; he began coughing, 

vomited, lost consciousness, and died (Morse et al. 1981). Autopsy showed tracheobronchial aspiration 

of stomach contents, focal pulmonary hemorrhages and edema, and small petechial brain hemorrhages. 

Hydrogen sulfide concentrations were found to be >60 ppm (equipment detection limit) under similar 

conditions in the vicinity of the accident 2 days later. Although some other gases common to this 

environment were not detected, it is possible that there was simultaneous exposure to other compounds. 

A boy and his father were overcome and died after inhaling hydrogen sulfide gas from a discarded drum 

at a manufacturing dump (Allyn 1931). Although the concentration of the gas inside the drum at the time 

of exposure was not known, a crude attempt was made to estimate exposure. Gas was collected from the 

drum 2 weeks after the accident and diluted 1:400 with air. A rat exposed to this dilution died after 

40 seconds of exposure. 

Three of five men, who lost consciousness within a few minutes of entering a partially drained 

underground liquid manure storage tank, died before reaching the hospital; autopsy showed that two had 

massive liquid manure pulmonary aspiration, while the third had fulminant pulmonary edema without 

manure aspiration (Osbern and Crapo 1981). Markedly elevated heart-blood sulfide-ion levels indicated 
HYDROGEN SULFIDE 24 

3. HEALTH EFFECTS 

significant hydrogen sulfide exposure. Air samples analyzed about a week after the accident detected 

only 76 ppm of hydrogen sulfide, but the study authors noted that the environmental conditions were 

probably different (e.g., warmer weather, less-concentrated manure). 

Two maintenance workers at an animal tanning company collapsed and died no more than 45 minutes 

after entering a sewer manhole; a hydrogen sulfide concentration of 200 ppm was obtained just inside the 

manhole 6 days after the accident (NIOSH 1989). A worker at a poultry feather processing plant died 

after being exposed to hydrogen sulfide gas for an estimated 15–20 minutes (Breysse 1961). Testing 

performed later in the area where the exposure occurred indicated that hydrogen sulfide concentrations 

ranged from 2,000 to 4,000 ppm. Pulmonary, intracranial, and cerebral edema and cyanosis were noted at 

autopsy. 

Claims for acute hydrogen sulfide exposure that occurred over a 5-year period (1969–1973) in Alberta, 

Canada, primarily among petrochemical workers, were reviewed by Burnett et al. (1977). Acute effects 

noted included coma, disequilibrium, and respiratory insufficiency with pulmonary edema. Of 221 cases, 

there were 14 deaths. A follow-up study of 250 workers’ claims for hydrogen sulfide exposure from 1979 

to 1983 in Alberta, Canada, found 7 fatalities that usually involved the central nervous and respiratory 

systems; hepatic congestion and cardiac petechiae were also noted (Arnold et al. 1985). The difference in 

fatality rate (6% down to 2.8%) was attributed to improved first aid training and an increased awareness 

of the dangers of hydrogen sulfide. 

Only very limited information is available on mortality in humans associated with chronic exposure to 

hydrogen sulfide. Bates et al. (1997), taking advantage of the fact that the New Zealand city of Rotorua is 

in a geothermally active area, conducted a retrospective ecological epidemiologic study in which they 

compared the mortality for selected diseases between residents in Rotorua and the rest of New Zealand. 

Rotorua uses geothermal energy for industrial and domestic heating purposes. Monitoring during the 

1970s found levels of hydrogen sulfide as high as 1 mg/m3

 (710 ppb); the most reliable data provided a 

median concentration of 20 μg/m3

 (14 ppb) with 35% of the measurements of 70 μg/m3 (50 ppb), and 

10% over 400 μg/m3 (284 ppb). Mortality data examined were limited to the main organ systems known 

to be at risk in hydrogen sulfide exposure (i.e., the nervous, respiratory and cardiovascular/circulatory 

systems, and birth defects). Among these four mortality categories, only deaths due to diseases of the 

respiratory system showed a significantly elevated standardized mortality ratio (SMR=1.18; p<0.001). 

Because the population in the Rotorua area has markedly more Maori than in the rest of New Zealand, 

and because Maori disease and mortality rates are relatively high compared with those of the non-Maori 
HYDROGEN SULFIDE 25 

3. HEALTH EFFECTS 

population, further analysis was carried out with an adjustment for ethnicity. When these data were 

stratified by sex and ethnicity, female Maoris had an SMR of 1.61 (p<0.001). Carrying the analysis to 

minor groupings of disease, significant increases in SMR were found for rheumatic fever and chronic 

rheumatic heart disease (SMR=1.51; p=0.01), hypertensive disease (SMR=1.61; p<0.001), pneumonia 

and influenza (SMR=1.20; p=0.008), and chronic obstructive respiratory disease and allied conditions 

(SMR=1.20; p=0.004). In their analysis of the data, the authors note the numerous issues that can be 

raised with regard to ecologic studies such as theirs; the two principal issues being confounded by other 

exposures (e.g., smoking) and by ethnicity misclassification. Despite the fact that the data indicate 

significant increases in SMRs, the study authors concluded that “no convincing evidence was found in 

this study of elevated rates of mortality in Rotorua compared with the rest of New Zealand.” They caveat 

this conclusion with three considerations: not all causes of deaths were considered, exposures were 

inadequately characterized, and ethnicity misclassification could have obscured important causes of 

mortality. 

Studies performed using laboratory animals exposed to high concentrations of hydrogen sulfide gas have 

yielded results similar to those observed in humans exposed at high levels. Exposure of Sprague-Dawley 

rats to 1,655 ppm killed all five animals within 3 minutes (Lopez et al. 1989). All male F-344 rats 

exposed to 500–700 ppm hydrogen sulfide gas for 4 hours died, while no rats died when exposed to 

concentrations up to 400 ppm under these conditions (Khan et al. 1990; Lopez et al. 1987, 1988a, 1988b). 

Ten of 10 male Wistar rats died after a 12-minute exposure (mean) to 800 ppm hydrogen sulfide (Beck et 

al. 1979). Concentrations of 335–587 ppm that cause death in 50% of the animals tested (LC50) have 

been reported in Sprague-Dawley, F-344, and Long Evans rats exposed to hydrogen sulfide gas for 2– 

6-hour periods (Prior et al. 1988; Tansy et al. 1981), although there were fewer deaths in approximately 

the same dose range in another study using F-344 rats (Prior et al. 1990). No mortality was reported 

when male Wistar rats were exposed to up to 500 ppm hydrogen sulfide for 2 hours (Higuchi and 

Fukamachi 1977). 

No deaths occurred among 30 adult female CB-20 mice exposed to 100 ppm hydrogen sulfide for 

2 hours/day for 1 day (Elovaara et al. 1978), nor in 20 adult female NMRI mice exposed for 1–4 days 

(Savolainen et al. 1980). All six mice exposed to 722 ppm hydrogen sulfide for 50 minutes died, while 

1,872 ppm hydrogen sulfide killed a group of six mice in 10 minutes (Smith and Gosselin 1964). Five 

Japanese white rabbits died within 30 minutes of exposure to 500–1,000 ppm hydrogen sulfide (Kage et 

al. 1992). 
HYDROGEN SULFIDE 26 

3. HEALTH EFFECTS 

No mortality was noted during 90-day studies in which male and female F-344 or Sprague-Dawley rats 

were exposed for 6 hours/day, 5 days/week, to up to 80 ppm hydrogen sulfide (CIIT 1983b, 1983c). 

Similar results were obtained at the same concentrations and conditions in a companion study using 

B6C3F1 mice; although two high-dose animals were killed in extremis, and two control animals were 

found dead in the cage (CIIT 1983a). 

All reliable LOAEL values for death in each species and duration category are recorded in Table 3-1 and 

plotted in Figure 3-1. 

3.2.1.2 Systemic Effects 

The highest NOAEL and all reliable LOAEL values for systemic effects in each species and duration are 

recorded in Table 3-1 and plotted in Figure 3-1. 

Respiratory Effects. With acute accidental hydrogen sulfide exposure, numerous respiratory effects 

are observed. Death usually occurs after respiratory distress or arrest from the disruption of oxidative 

metabolism in the brain. Respiratory distress has also been noted in individuals who survived after acute 

exposures (Osbern and Crapo 1981; Peters 1981; Spolyar 1951). Other respiratory effects of acute 

hydrogen sulfide exposure include noncardiogenic pulmonary edema (Arnold et al. 1985; Burnett et al. 

1977; Deng and Chang 1987; Thoman 1969; Tvedt et al. 1991a, 1991b), sore throat, cough (Burnett et al. 

1977; Jaakkola et al. 1990), and dyspnea (Arnold et al. 1985; Burnett et al. 1977; Krekel 1964; Osbern 

and Crapo 1981; Parra et al. 1991; Ravizza et al. 1982; Stine et al. 1976; Thoman 1969). Cyanosis has 

been reported in a number of case reports and is believed to result from respiratory distress (Arnold et al. 

1985; Tvedt et al. 1991a, 1991b). In most studies, exposure concentrations and/or durations were 

unknown. Among hydrogen sulfide exposure survivors, respiratory symptoms generally subsided within 

several weeks of exposure, but occasionally persisted for several months or longer (Duong et al. 2001; 

Parra et al. 1991). Acute exposure to >500 ppm hydrogen sulfide is considered to cause rapid respiratory 

failure (Beauchamp et al. 1984). 

Respiratory distress was noted in two workers exposed to >40 ppm hydrogen sulfide for <25 minutes 

(Spolyar 1951). Bhambhani and associates have conducted a number of studies of young healthy 

volunteers exposed to hydrogen sulfide via oral inhalation. Male volunteers were exposed to hydrogen 

sulfide concentrations up to 5 ppm for >16 minutes after graded exercise that was performed to 

exhaustion (Bhambhani and Singh 1991). No effects on expired ventilation or maximum power output 
201

800

039

500

212

1655

327

587

328

501

329

335

052

375

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation 

Exposure/ LOAEL 

Duration/ 

a 

Key to 

Figure 

Species 

(Strain) 

Frequency 

(Route) 

ACUTE EXPOSURE Death 

1 Rat 

(Wistar) 

12 min 

System 

NOAEL 

(ppm) 

Less Serious 

(ppm) 

Serious 

(ppm) 

800 M (10/10 died) 

2 Rat 

(Fischer- 344) 

4 hr 500 M (4-6 used; all died) 

3 Rat 

(SpragueDawley) 

3 min 1655 M (5/5 died) 

4 Rat 

(SpragueDawley, Fischer344, Long Evans) 

2 hr 587 (LC50 ) 

5 Rat 

(SpragueDawley, Fischer344, Long Evans) 

4 hr 501 (LC50) 

6 Rat 

(SpragueDawley, Fischer344, Long Evans) 

6 hr 335 (LC50) 

7 Rat 

(Fischer- 344) 

4 hr 375 M (2/12 died) 

Reference Chemical Form 

Beck et al. 1979 Khan et al. 1990 Lopez et al. 1989 Prior et al. 1988 Prior et al. 1988 Prior et al. 1988 Prior et al. 1990 
074

444

061

722

237

500

207

552

5

348

10

206

55

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued) 

a 

Key to Species 

Figure (Strain) 

8 Rat 

(SpragueDawley) 

9 Mouse 

(CD-1) 

10 Rabbit 

(Japanese white) 

Systemic 

11 Human 12 Human 13 Human 

Exposure/ 

Duration/ 

Frequency 

(Route) System NOAEL (ppm) Less Serious (ppm) 

LOAEL 

Serious 

(ppm) 

Reference Chemical Form 

4 hr 444 (LC50) Tansy et al. 1981 50 min 722 F (6/6 died) Smith and Gosselin 19614-30 min 500 (5/5 died) Kage et al. 1992 >16 min Resp 5 M Bhambhani and Singh 1

Cardio 

Metab 

5 M 

2 M 5 M (increased blood lactate 

during exercise) 

15 min Resp 10 Bhambhani et al. 1996a 

30 min Resp 5 Bhambhani et al. 1994 

Cardio 5 
1

5

1

10

10

038

2

356

80

200

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued) 

a 

Key to Species 

Figure (Strain) 

Exposure/ 

Duration/ 

Frequency 

(Route) System NOAEL (ppm) Less Serious (ppm) 

LOAEL 

Serious 

(ppm) 

Reference Chemical Form 

14 Human 2x 30 min Musc/skel 5 M (decrease in citrate 

synthase when exercising at 50% maximum aerobic power) 

Bhambhani et al. 1996b 

15 Human 2x30 min Cardio 10 Bhambhani et al. 1997 

Metab 10 (increase in blood lactate 

and decrease in oxygen uptake) 

16 Human 30 min Resp b2 (increased airway 

resistance and decreased specific airway conductance in 2/10 asthmatics) 

Jappinen et al. 1990 

17 Rat 

(SpragueDawley) 

3 hr Resp 80 M 200 M (necrosis of olfactory 

epithelium and regeneration of respiratory epithelium in nose) 

Brenneman et al. 2002 
357

30

80

026

200

339

100100

040

10

50

041

50

200

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued) 

Exposure/ LOAEL 

Duration/ 

a 

Key to Species Frequency NOAEL Less Serious Serious Reference (Route) Figure (Strain) System (ppm) (ppm) (ppm) Chemical Form 

18 Rat 

(SpragueDawley) 

3 hr 5 d Resp 30 M 80 M (necrosis of nasal olfactory epithelium in 5/5 

rats) 

Brenneman et al. 2002 

19 Rat 

(Fischer- 344) 

4 hr Resp 200 M (increase in protein and 

lactate dehydrogenase in lavage fluid; focal areas of perivascular edema; proteinaceous material in the alveoli) 

Green et al. 1991 

20 Rat 

(Wistar) 

1 hr Resp 100 M (increased respiration 

rate) 

Higuchi and Fukamachi 

Cardio 100 M (increased blood 

pressure, heart rate) 

21 Rat 

(Fischer- 344) 

4 hr Resp 10 M 50 M (15% reduction in lung 

cytochrome c oxidase activity) 

Khan et al. 1990 

22 Rat 

(Fischer- 344) 

4 hr Resp 50 M 200 M (decreased respiratory 

rate of pulmonary alveolar macrophages stimulated with zymosan) 

Khan et al. 1991 
342

75

75

219

10

256

83

218

400

336

200 400

053

375

066

20

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued) 

a 

Key to 

Figure 

Exposure/ 

Duration/ 

Species Frequency 

(Strain) (Route) System NOAEL (ppm) 

LOAEL 

Less Serious 

(ppm) 

Serious 

(ppm) 

Reference Chemical Form 

23 Rat 20-60 min 

(Wistar) Resp 75 M (slight congestion) Kohno et al. 1991 

Cardio 75 M (cardiac arrhythmia; 

decreased heart rate) 

24 Rat 4 hr 

(Fischer- 344) Resp 10 M (increased cellularity in nasal lavage fluid) Lopez et al. 1987 

25 Rat 4 hr 

(Fischer- 344) Resp 83 M (mild perivascular edema) Lopez et al. 1988a 

26 Rat 4 hr 

(Fischer- 344) Resp 400 M (severe inflammation and Lopez et al. 1988b necrosis of respiratory 

and olfactory epithelium) 

27 Rat 4 hr 

(Fischer- 344) Ocular 200 M 400 M (epiphora) Lopez et al. 1988b 

28 Rat 4 hr 

(Fischer- 344) Resp 375 M (moderate to massive pulmonary edema) Prior et al. 1990 

29 Gn Pig 11 d 

(NS) 1 hr/d Ocular 20 M (eye irritation) Haider et al. 1980 
047

72

266

50

200

336

2

200

800

346

100

200

220

200 400

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued) 

Exposure/ LOAEL 

Duration/ 

a 

Key to Species Frequency NOAEL Less Serious Serious Reference (Route) Figure (Strain) System (ppm) (ppm) (ppm) Chemical Form 

30 Rabbit 

(mixed breeds) 

Immuno/ Lymphoret 

31 Rat 

(Fischer- 344) 

Neurological 

32 Human 33 Rat 

(Wistar) 

34 Rat 

(Wistar) 

35 Rat 

(Fischer- 344) 

1.5 hr or 5 d 0.5hr/d 

Cardio 72 (changes in ventricular 

repolarization; cardiac arrhythmia) 

Kosmider et al. 1967 

4 hr 50 M 200 M (decreased respiratory 

rate of pulmonary alveolar macrophages stimulated with zymosan) 

Khan et al. 1991 

30 min 2 (headache in 3/10 

asthmatics) 

Jappinen et al. 1990 

20 min 800 M (unconsciousness) Beck et al. 1979 

2 hr 100 M 200 M (decreased response 

rate in conditioned 

Higuchi and Fukamachi 

avoidance task) 

4 hr 200 M 400 M (lethargy) Lopez et al. 1988b 
361

30

80

065

20

046

72

355

10

30

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued) 

a 

Key to Species 

Figure (Strain) 

Exposure/ 

Duration/ 

Frequency 

(Route) System NOAEL (ppm) Less Serious (ppm) 

LOAEL 

Serious 

(ppm) 

Reference Chemical Form 

36 Rat 

(CD) 

3 hr/d 5 d 30 M 80 M (decreased spontaneous motor activity) Struve et al. 2001 

37 Gn Pig 

(NS) 

11 d 1 hr/d 20 M (decreased cerebral hemisphere and brain 

stem total lipids and phospholipids) 

Haider et al. 1980 

38 Rabbit 

(mixed breeds) 

1.5 hr 

INTERMEDIATE EXPOSURE Systemic 

39 Rat 

(SpragueDawley) 

6 hr/d 7 d/wk 10 wk 

Resp 

c

10 M 30 M (olfactory neuron loss 

and basal cell hyperplasia in nasal olfactory epithelium) 

72 (unconsciousness) Kosmider et al. 1967 

Brenneman et al. 2000 
226

10

30

80808080808080808080

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued) 

Exposure/ LOAEL 

Duration/ 

a 

Key to Species Frequency NOAEL Less Serious Serious Reference (Route) Figure (Strain) System (ppm) (ppm) (ppm) Chemical Form 

40 Rat 

(Fischer- 344) 

90 d 5 d/wk 6 hr/d 

Resp 10 30 (olfactory neuron loss in 

the nasal olfactory epithelium) 

CIIT 1983b 

Cardio 80 Gastro 80 Hemato 80 Musc/skel 80 Hepatic 80 Renal 80 Endocr 80 Dermal 80 Ocular 80 Bd Wt 80 
270

10

30

8080808080808080808030.5

80

034

20

032

50

75

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued) 

Exposure/ LOAEL 

Duration/ 

a 

Key to Species Frequency NOAEL Less Serious Serious Reference (Route) Figure (Strain) System (ppm) (ppm) (ppm) Chemical Form 

41 Rat 

(SpragueDawley) 

42 Rat 

(SpragueDawley) 

43 Rat 

(SpragueDawley) 

90 d 5 d/wk 6 hr/d 

Resp 10 30 (olfactory neuron loss in 

the nasal olfactory epithelium and bronchiolar epithelial hyperplasia) 

CIIT 1983c 

Cardio 80 Gastro 80 Hemato 80 Musc/skel 80 Hepatic 80 Renal 80 Endocr 80 Dermal 80 Ocular 80 Bd Wt 80 M 

d

30.5 F 

80 F (10% decrease in body 

weight) 

gd 1-ppd 21 7 hr/d Metab 20 F (50% increase in circulating glucose levels 

in dams) 

Hayden et al. 1990a 

gd 6-ppd 21 7 hr/d Hepatic 50 F 75 F (increased maternal liver cholesterol levels) Hayden et al. 1990b 
057

100

150

229

10

3080

80808080808080808030.5

80

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued) 

Exposure/ LOAEL 

Duration/ 

a 

Key to Species Frequency NOAEL Less Serious Serious Reference (Route) Figure (Strain) System (ppm) (ppm) (ppm) Chemical Form 

44 Rat 

(SpragueDawley) 

gd 6-20 6 hr/d Bd Wt 100 F 150 F (pregnant rats lost weight) Saillenfait et al. 1989 

45 Mouse 

(B6C3F1) 

90d 5 d/wk 6 hr/d 

Resp 10 30 (olfactory neuron loss in 

the nasal olfactory epithelium) 

CIIT 1983a 

80 (inflammation of nasal 

mucosa) 

Cardio Gastro Hemato Musc/skel Hepatic Renal Endocr Dermal Ocular Bd Wt 

80 

80 

80 80 80 80 80 80 80 

30.5 80 (7-14% decrease in body 

weight) 
236

8.58.58.58.58.58.5

267

80

272

80

274

80

227

80

271

30.580

80

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued) 

Exposure/ 

Duration/ 

a 

Key to Species Frequency (Route) Figure (Strain) System NOAEL (ppm) 

LOAEL 

Less Serious Serious 

(ppm) (ppm) 

Reference Chemical Form 

46 Pig 

(Crossbred) 

17 d 24 hr/d Resp 8.5 Curtis et al. 1975 

Immuno/ Lymphoret 

47 Rat 

(Fischer- 344) 

90 d 5 d/wk 6 hr/d 

Gastro Hepatic Renal Ocular Bd Wt 

8.5 8.5 8.5 8.5 

8.5 

80 CIIT 1983b 

48 Rat 90 d 

(Sprague- 5 d/wk Dawley) 6 hr/d 

80 CIIT 1983c 

49 Mouse 

(B6C3F1) 

90d 5 d/wk 6 hr/d 

Neurological 

50 Rat 

(Fischer- 344) 

90d 5 d/wk 6 hr/d 

80 80 

CIIT 1983a CIIT 1983b 

Rat 90 d (Sprague- 5 d/wk Dawley) 6 hr/d 

51 d 30.5 M 

80 F 

80 M (5% decrease in brain 

weight) 

CIIT 1983c 
025

50

362

125

230

80

305

80

273

80

358

80

275

80

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued) 

a 

Key to Species 

Figure (Strain) 

Exposure/ 

Duration/ 

Frequency 

(Route) System NOAEL (ppm) Less Serious (ppm) 

LOAEL 

Serious 

(ppm) 

Reference Chemical Form 

52 Rat 

(SpragueDawley) 

25 wk 5 d/wk 50 M Gagnaire et al. 1986 

53 Rat 

(SpragueDawley) 

4 hours/day 5 days/week 5-11 weeks 

125 M (impaired learning of new 

tasks on a radial arm maze) 

Partlo et al. 2001 

54 Mouse 

(B6C3F1) 

90d 5 d/wk 6 hr/d 

Reproductive 

55 Rat 

(Fischer- 344) 

90d 5 d/wk 6 hr/d 

80 80 

CIIT 1983a CIIT 1983b 

56 Rat 

(SpragueDawley) 

90 d 5 d/wk 6 hr/d 

80 CIIT 1983c 

57 Rat 

(SpragueDawley) 

6 hr/d 7 d/wk 60-70 d 

80 Dorman et al. 2000 

58 Mouse 

(B6C3F1) 

90d 5 d/wk 6 hr/d 

80 CIIT 1983a 
359

80

073

20

029

50

75

033

75

031

75

056

150

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued) 

a 

Key to Species 

Figure (Strain) 

Developmental 

59 Rat 

(SpragueDawley) 

60 Rat 

(SpragueDawley) 

61 Rat 

(SpragueDawley) 

62 Rat 

(SpragueDawley) 

63 Rat 

(SpragueDawley) 

64 Rat 

(SpragueDawley) 

Exposure/ LOAEL 

Duration/ 

Frequency NOAEL Less Serious Serious Reference (Route) System (ppm) (ppm) (ppm) Chemical Form 

6 hr/d 7 d/wk 60-70 d 

80 Dorman et al. 2000 

gd 5-ppd 21 7 hr/d 20 F (severe alterations in architecture and growth 

characteristics of Purkinje cell dendritic fields which may be indicative of neurotoxicity) 

Hannah and Roth 1991 

gd 5-ppd 21 7 hr/d 50 75 (decreases in brain amino acid levels of 

pups) 

Hannah et al. 1989, 199

gd 1-ppd 21 7 hr/d 75 F Hayden et al. 1990a 

gd 6-ppd 21 7 hr/d 75 F Hayden et al. 1990b 

gd 6-20 6 hr/d 150 F Saillenfait et al. 1989 
058

20

65 

Table 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued) 

Exposure/ LOAEL

Duration/

a

Key to Species Frequency NOAEL Less Serious Serious Reference (Route) Figure (Strain) System (ppm) (ppm) (ppm) Chemical Form Comments 

Rat gd 5-ppd 21 20 F (decreases in Skrajny et al. 1992 7 hr/d (Sprague- norepinephrine in the Dawley) frontal cortex, increase in 

serotonin in the frontal cortex of pups) 

a The number corresponds to entries in Figure 3-1. b Used to derive an acute-duration Minimal Risk Level (MRL) of 0.07 ppm; concentration divided by an uncertainty factor of 27 (3 for use of a minimal LOAEL, 3 for human variability, and 3 for database deficiencies). c Used to derive an intermediate-duration Minimal Risk Level (MRL) of 0.02 ppm; the NOAEL was adjusted for intermittent exposure and multiplied by the regional gas dose ratio (RGDR) for extrathoracic effects to calculate a human equivalent concentration (HEC). The MRL was obtained by dividing the NOAEL(HEC) by an uncertainty factor of 30 (3 for extrapolation from animals to humans with a dosimetric adjustment and 10 for human variability) d Differences in levels of health effects and cancer effects between male and females are not indicated in Figure 3-1. Where such differences exist, only the levels of effect for the most sensitive gender are presented. B = both; Bd Wt = body weight; Cardio = cardiovascular; d = day(s); Endocr = endocrine; F = Female; Gastro = gastrointestinal; gd = gestational day; hemato = hematological; hr = hour(s); LC50 = lethal concentration, 50% kill; LOAEL = lowest-observed-adverse-effect level; M = male; metab = metabolism; min = minute(s); mo = month(s); Musc/skel = musculoskeletal; NOAEL = no-observed-adverse-effect level; NS = not specified; ppd = post-partum day; Resp = respiratory; wk = week(s) 

HYDROGEN SULFIDE

 3. HEALTH EFFECTS

40
Death 

Respiratory Cardiovascular 

Figure 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation
	

Acute (≤14 days)
	

Systemic

ppm 

26r 28r 

17r 19r 22r 

20r 20r 25r 17r 18r 23r 23r 

21r 22r 

18r 

12 21r 24r 

11 13 

16 

30h 

15 

11 13 

10000 

3r 

1000 1r 9m 4r 5r 2r 10h 8r 7r 6r 

100 

10 

1 

0.1 

0.01 

c-Cat 

d-Dog

r-Rat 

p-Pig

q-Cow

 -Humans 

k-Monkey

m-Mouse 

h-Rabbit 

a-Sheep 

f-Ferret 

j-Pigeon

e-Gerbil 

s-Hamster 

g-Guinea Pig 

n-Mink 

o-Other

 Cancer Effect Level-Animals

 LOAEL, More Serious-Animals

 LOAEL, Less Serious-Animals

 NOAEL - Animals

 Cancer Effect Level-Humans

 LOAEL, More Serious-Humans

LOAEL, Less Serious-Humans

NOAEL - Humans
Neurological 

Metabolic Im

Ocular 

muno/Lymphor 

Figure 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (Continue

Acute (≤14 days) 

Systemic
 

ppm 

10000 

1000 

100
	 34r
	 36r 38h 

31r 

36r 

37g
	

10
	

29g 

15
	

11
	

11
	 32
	

1
	

0.1 

0.01 

33r 

35r 27r 

31r 34r 35r 27r 

c-Cat 

d-Dog

r-Rat 

p-Pig

q-Cow

 -Humans 

k-Monkey

m-Mouse 

h-Rabbit 

a-Sheep 

f-Ferret 

j-Pigeon

e-Gerbil 

s-Hamster 

g-Guinea Pig 

n-Mink 

o-Other

 Cancer Effect Level-Animals

 LOAEL, More Serious-Animals

 LOAEL, Less Serious-Animals

 NOAEL - Animal s

 Cancer Effect Level-Humans

 LOAEL, More Serious-Humans

LOAEL, Less Serious-Humans

NOAEL - Humans
Respiratory 

Cardiovascular Gastrointestinal Hematological Musculoskeletal 

Figure 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continued)

Intermediate (15-364 days) 

Systemic 

ppm 

1000 

100 

45m 45m 40r 41r 45m 40r 41r 45m 40r 41r 45m 40r 41r 

45m 39r 40r 41r 

10 45m 39r 40r 41r 46p 46p 

1 

0.1 

0.01 

c-Cat 

d-Dog

r-Rat 

p-Pig

q-Cow

 -Humans 

k-Monkey

m-Mouse 

h-Rabbit 

a-Sheep 

f-Ferret 

j-Pigeon

e-Gerbil 

s-Hamster 

g-Guinea Pig 

n-Mink 

o-Other 

LOAEL, Less Serious-Animals

NOAEL - Animals 

LOAEL, Less Serious-Humans for effects

 Cancer Effect Level-Animals

 LOAEL, More Serious-Animals LOAEL, More Serious-Humans Minimal Risk Level

 Cancer Effect Level-Humans 

NOAEL - Humans

 LD50/LC50

 other than

 Cancer 
Hepatic Renal Endocrine Dermal Ocu

Figure 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continue

Intermediate (15-364 days) 

ppm 	 Systemic 

1000 

100 

45m 40r 41r 43r 45m 40r 41r 45m 40r 41r 45m 40r 41r 45m 40r 

43r 

10 46p 46p 

1 

0.1 

0.01 

c-Cat f-Ferret n-Mink

-Humans Cancer Effect Level-Humans Cancer Effect Level-Animals 

d-Dog k-Monkey j-Pigeon o-Other LOAEL, More Serious-Humans 

LOAEL, More Serious-Animals r-Rat m-Mouse e-Gerbil LOAEL, Less Serious-Animals LOAEL, Less Serious-Humans 

p-Pig h-Rabbit s-Hamster NOAEL - Animals NOAEL - Humans q-Cow a-Sheep g-Guinea Pig 	 
Body Weight Metabolic Immuno/Lymphor Neurological Reproductive 

1000 

Figure 3-1 Levels of Significant Exposure to Hydrogen Sulfide - Inhalation (continue

Intermediate (15-364 days) 

Systemic 

ppm 

44r 

53r 

100 44r 

45m 40r 41r 49m 47r 48r 54m 50r 51r 58m 55r 56r 57r 5

52r 

45m 41r 51r 

42r 6

10 46p 

1 

0.1 

0.01 

c-Cat f-Ferret n-Mink -Humans Cancer Effect Level-Humans Cancer Effect Level-Animals 

d-Dog k-Monkey j-Pigeon o-Other LOAEL, More Serious-Humans 

LOAEL, More Serious-Animals r-Rat m-Mouse e-Gerbil LOAEL, Less Serious-Animals LOAEL, Less Serious-Humans 

p-Pig h-Rabbit s-Hamster NOAEL - Animals NOAEL - Humans q-Cow a-Sheep g-Guinea Pig 	 
HYDROGEN SULFIDE 46 

3. HEALTH EFFECTS 

were noted, but exposure to 5 ppm resulted in a significant increase in maximum oxygen uptake 

compared to controls. At exposures to 2 and 5 ppm, the respiratory exchange ratio was decreased 

significantly compared to controls. The study authors attributed this to a nonsignificant trend toward 

increased oxygen uptake and decreased carbon dioxide output compared to controls (Bhambhani and 

Singh 1991). Another study examined the effects of inhalation of 5 ppm hydrogen sulfide on respiratory 

physiological parameters and found no changes in partial pressure of oxygen, partial pressure of carbon 

dioxide, oxygen uptake (VO2), percentage of oxygen uptake (VO2%), uptake of carbon dioxide (VCO2) 

and VE, or respiratory exchange ratio in male or female volunteers during 30 minutes of submaximal 

exercise (Bhambhani et al. 1994). A third study found that inhalation of 10 ppm of hydrogen sulfide for 

15 minutes at elevated metabolic and ventilation rates did not result in significantly altered pulmonary 

function test results in men and women (Bhambhani et al. 1996a). It should be noted that the subjects 

were unable to smell the hydrogen sulfide and their eyes were not exposed to the gas. 

Pulmonary function tests were performed on persons with asthma exposed to 2 ppm of hydrogen sulfide 

for 30 minutes in a sealed chamber (Jappinen et al. 1990). Although no significant changes were noted in 

airway resistance or specific airway conductance as a group, 2 of 10 subjects showed changes in excess of 

30% in both airway resistance and specific airway conductance, an indication of bronchial obstruction 

(Jappinen et al. 1990). No statistically significant changes were noted in forced vital capacity (FVC), 

forced expiratory volume in 1 second (FEV1), and forced expiratory flow (Jappinen et al. 1990). 

Pulmonary function was unaffected following the same exposure protocol in 26 male pulp mill workers 

who had previously had daily hydrogen sulfide exposures, usually to <10 ppm (Jappinen et al. 1990). No 

significant changes were noted in FVC, FEV1, or bronchial responsiveness to histamine challenge in this 

group of workers, which included subgroups of smokers, workers with previous allergies, and atopic 

individuals. Findings in this study are similar to those observed in Bhambhani et al. (1996a). 

Hessel et al. (1997) examined the pulmonary health effects of hydrogen sulfide exposure in a group of 

Canadian oil and gas workers. Exposure to hydrogen sulfide was assessed by questionnaire as was the 

occurrence of respiratory symptoms; in addition, smoking and occupational histories were conducted. 

Lung health was assessed via spirometric testing and by skin prick testing for six common antigens. The 

workers were divided into three exposure groups: none, gas exposure (sufficient to produce symptoms), 

and knockdown (exposure sufficient to cause unconsciousness). None of the lung function indicators 

(FEV1, FVC, or FEV1/FVC) differed significantly among the three groups. Significantly increased odds 

ratios (ORs) were seen only in those in the knockdown group who showed significant excesses for several 

symptoms, including: shortness of breath (OR=3.55; 95% confidence interval [CI]=1.02–12.4); wheeze 
HYDROGEN SULFIDE 47 

3. HEALTH EFFECTS 

with chest tightness (OR=5.15; 95% CI=1.29–20.6); and attacks of wheeze (OR=5.08; 95% CI=1.28– 

20.6). 

In a cross-sectional study of sewer and water treatment workers, Richardson (1995) evaluated the 

association of hydrogen sulfide exposures to reduced lung function using spirometric testing. Job titles 

were used to categorize sewer workers into high, medium, and low exposure groups; however, there was 

no quantification of hydrogen sulfide levels. Water treatment workers who were not occupationally 

exposed to hydrogen sulfide were chosen as a comparison group. Findings included significant 

differences between spirometric values (FEV1/FVC) of sewer and water treatment workers across a 

number of age strata, irrespective of smoking status, although smoking status reduced the impact 

somewhat. When stratified by presumed exposure to hydrogen sulfide, only those sewer workers with 

presumed high exposure showed a significant difference from water workers, although a dose-related 

trend in lung function at both medium and high exposures was observed. In addition, the prevalence OR 

for obstructive lung disease was 21.0 (95% CI=2.4–237.8) in nonsmoking sewer workers with presumed 

high hydrogen sulfide exposure when compared to nonsmoking water treatment workers. The prevalence 

odds ratio for sewer workers who smoke versus water treatment workers who smoke was 1.7 (95% 

CI=0.2–13.6). 

In a report comparing community responses to low-level exposure to a mixture of air pollutants from pulp 

mills, Jaakkola et al. (1990) reported significant differences in respiratory symptoms between polluted 

and unpolluted communities. The pollutant mixture associated with the pulp mills included particulates, 

sulfur dioxide, and a series of ‘malodorous sulfur compounds.’ Major contributors in the latter mixture 

include hydrogen sulfide, methyl mercaptan, and methyl sulfides. In this study, the responses of 

populations from three communities (a nonpolluted community, a moderately polluted community, and a 

severely polluted community were compared). Initial exposure estimates were derived from dispersion 

modeling; these estimates were subsequently confirmed with measurements taken from monitoring 

stations located in the two polluted communities. These measurements indicated that both the mean and 

the maximum 4-hour concentrations of hydrogen sulfide were higher in the more severely polluted 

community (4 and 56 μg/m3

; 2.9 and 40 ppb) than in the moderately polluted one (2 and 22 μg/m3; 

1.4 and 16 ppb). Particulate measurements made concurrently, and sulfur dioxide measurements made 

subsequently, showed a similar difference in the concentrations of these two pollutants between the two 

polluted communities. A cross-sectional, self-administered questionnaire was used to gather data on the 

occurrence (i.e., often or constantly) of a variety of symptoms and effects during two time periods (the 

past 4 weeks and the previous 12 months). Respiratory end points evaluated included cough, nasal 
HYDROGEN SULFIDE 48 

3. HEALTH EFFECTS 

symptoms, breathlessness or wheezing, numbers of respiratory infections, history of asthma, and chronic 

respiratory diseases. The occurrence of nasal symptoms and cough was found to be significantly greater 

in the subjects living in the two polluted communities when compared to those in the nonpolluted 

community. Breathlessness or wheezing was also increased, although not to the level of significance. All 

three of these end points showed a dose-related increase; that is, the greatest occurrence of symptoms 

occurred in the more highly-polluted community, followed by the less polluted, and then the nonpolluted 

communities. Because of the mixed exposures, however, the role of hydrogen sulfide in these effects is 

unclear. 

A subsequent report by Marttila et al. (1994b) examined the impact of long-term exposure to the same 

mixture of malodorous sulfur compounds on children from these same three communities. The findings 

in children (i.e., nasal symptoms and cough) in the most severely polluted community were similar to 

those reported above and showed increased risks both for the 4-week and the 12-month intervals, 

although none of these risks reached statistical significance. 

Marttila et al. (1995) also examined the relationship between daily exposure to malodorous sulfur 

compounds (measured as total reduced sulfur [TRS]) from pulp production and experience of symptoms 

in a small population living in the vicinity of a pulp mill. The major components of the malodorous 

sulfur compounds are hydrogen sulfide, methyl mercaptan, and methyl sulfides. This work was initiated 

due to the observation that an unusually high short-term exposure to malodorous sulfur compounds 

(maximum 4-hour concentrations of hydrogen sulfide at 135 μg/m3

 [96 ppb]) led to a considerable 

increase in the occurrence of ocular, respiratory, and neuropsychological symptoms (Haahtela et al. 

1992). During the study period, daily mean TRS concentrations varied from 0 to 82 μg/m3

, and monthly 

mean concentrations varied from 3 to 19 μg/m3

. Following a baseline questionnaire, the study was 

conducted with six consecutive questionnaires after three predefined levels of exposure to TRS (daily 

mean <10 μg/m3

, medium exposure 10–30 μg/m3, high exposure >30 μg/m3). The study found a doserelated increase in the probability of both nasal (i.e., stuffy or runny nose) and pharyngeal irritation. For 

nasal symptoms, the probability ratios were 3.13 (95% CI=1.25–7.25) and 8.50 (95% CI=3.19–18.64) for 

medium and high exposure, respectively. For pharyngeal symptoms, the probability ratios were 2.0 (95% 

CI=0.92–4.14) and 5.20 (95% CI=1.95–1.99) for the medium and high exposure levels, respectively. 

Partti-Pellinen et al. (1996) used a cross-sectional, self-administered questionnaire to assess the eye, 

respiratory tract, and central nervous system symptoms experienced by adults in a slightly polluted and a 

reference community. In the polluted community, the mean annual TRS concentrations were 2–3 μg/m3

, 
HYDROGEN SULFIDE 49 

3. HEALTH EFFECTS 

the 24-hour average concentrations varied between 0 and 56 μg/m3, and the maximum 1-hour 

concentration was 155 μg/m3

; there was no TRS detected in the reference community. In the polluted 

community, the sulfur dioxide annual mean concentration was 1 μg/m3

, the 24-hour average 

concentrations varied between 0 and 24 μg/m3

, and the maximum 1-hour concentration was 152 μg/m3. 

In the reference community, the mean sulfur dioxide level was 1 μg/m3

 and the maximum 1-hour 

concentration was 30 μg/m3

. 

Symptoms evaluated over the previous 4 weeks and previous 12 months included eye irritation, nasal 

irritation, cough, breathlessness or wheezing, and headache or migraine. After adjusting for age, sex, 

smoking, history of allergic diseases, education, and marital status, increased odds ratios were seen for all 

of these symptoms at both time periods. However, significant increases in odds ratios were seen only for 

headache or migraine in the previous 4 weeks (OR=1.82; 95% CI=1.06–31.5) and in the past 12 months 

(OR=1.70; 95% CI=1.05–2.73) and cough in the past 12 months (OR=1.64; 95% CI=1.01–2.64). These 

findings led the authors to conclude that the adverse health effects of TRS occur at lower concentrations 

than previously reported. However, these findings are also confounded by daily average levels of TRS as 

high as 56 μg/m3

 and by the presence of sulfur dioxide which, though occurring at the same mean annual 

concentration in the two communities, showed much higher peaks in the polluted community. 

Furthermore, no information was provided on particulate levels, which could also be important to these 

findings. 

This series of studies (Jaakkola et al. 1990; Haahtela et al. 1992; Marttila et al. 1994a, 1994b, 1995; 

Partti-Pellinen et al. 1996) report the results of the South Karelia Air Pollution Study, which began in 

1986 to evaluate the effects of air pollution on human health and the environment. In the early studies of 

this series (Haahtela et al. 1992; Jaakkola et al. 1990; Marttila et al. 1994b), levels of hydrogen sulfide, 

sulfur dioxide, particulates, and methyl mercaptan were individually reported. In the later studies 

(Marttila et al. 1994a, 1995; Partti-Pellinen et al. 1996), a complex mixture of ‘malodorous sulfur 

components’ (that included hydrogen sulfide, methyl mercaptan, and methyl sulfides) was monitored as 

TRS using a method that first removes any sulfur dioxide, then oxidizes the TRS compounds to sulfur 

dioxide, and reports the results as μg/m3

 TRS. It is not possible, from the information provided, to 

determine precisely what proportion of the TRS is actually hydrogen sulfide, although the authors 

indicate that it is about two-thirds (Marttila et al. 1994b). The fact that in virtually all of these studies, 

effects were linked to exposures to mixtures, even though hydrogen sulfide appears to have been the 

dominant sulfur compound, complicates interpretation of these results. It is probably reasonable to 

conclude that these studies demonstrate that low levels of hydrogen sulfide in combination with other 
HYDROGEN SULFIDE 50 

3. HEALTH EFFECTS 

sulfur-containing pollutants, and possibly due to combination with particulates and/or sulfur dioxide, can 

have an adverse effect on respiratory health. However, it is not possible at this time to determine whether 

it is the low annual average values of 1–2 μg/m3

 TRS, or the daily average concentrations (56 μg/m3 TRS) 

that are associated with these findings. 

ATSDR (Campagna et al. 2004) examined the possible relationship between ambient levels of hydrogen 

sulfide and total reduced sulfur and hospital visits among residents of Dakota City and South Sioux City, 

Nebraska. Total reduced sulfur is the combined concentrations of hydrogen sulfide, methyl mercaptan, 

dimethyl sulfide, and dimethyl disulfide; air monitoring data indicate that hydrogen sulfide was the 

primary constituent of the total reduced sulfur. The primary sources of total reduced sulfur were a beef 

slaughter facility and a leather tanning facility. Among children under 18 years of age, positive 

associations were found between hospital visits for all respiratory disease (including asthma) and the high 

hydrogen sulfide level the previous day and the high levels of total reduced sulfur on the previous day. 

Positive associations were found between hospital visits for asthma and the previous day’s high hydrogen 

sulfide level in adults and total reduced sulfur in children. A high total reduced sulfur or hydrogen sulfide 

level was defined as a 30-minute rolling average of ≥30 ppb. 

As discussed in more detail in Section 3.2.1.1, Bates et al. (1997) found a significant increase in mortality 

from diseases of the respiratory system for residents of the Rotorua area of New Zealand for the period of 

1981–1990. Rotorua is in an area of high geothermal activity; sampling from a campaign in 1978 

indicated a median concentration for hydrogen sulfide of about 20 μg/m3

 with 35% of the measurements 

>70 μg/m3

 and 10% of the measurements >400 μg/m3. Problems with the analysis, however, led these 

authors to conclude that there were no clear indications of excess mortality. In a follow-up to this study, 

Bates et al. (2002) used hospital discharge records for 1993–1996 to assess the incidence of respiratory 

disease; unlike the previous study, exposure was classified as high, medium, or low, based on residence at 

the time of discharge. A statistically significant (p<0.001), exposure-related trend for increased incidence 

of respiratory disease was found. The incidence of minor respiratory disease groups was also 

significantly (p<0.01) increased. In general, the incidence of respiratory disease was significantly 

elevated in the high exposure group, but not at lower exposure levels, with the exception of the incidences 

of other diseases of the upper respiratory tract category, which were increased in all three exposure 

groups. The standardized incidence ratios (SIRs) (and 95% confidence limits) for this category were 

1.48 (1.34–1.63), 1.68 (1.39–2.01), and 1.98 (1.58–2.45) in the low, medium, and high exposure groups, 

respectively. Limitations in the design of this study, such as lack of exposure monitoring data, lack of 

data on potential confounding factors (e.g., smoking, differences in socioeconomic status in the different 
HYDROGEN SULFIDE 51 

3. HEALTH EFFECTS 

exposure groups), lack of residence history data, and lack of information on potential exposure at work, 

limit the interpretation of these data. 

In addition to an increase in respiration rate that was noted in Wistar rats exposed to 100–200 ppm 

hydrogen sulfide for 1 hour (Higuchi and Fukamachi 1977), a number of histological and biochemical 

changes have been noted in the respiratory tissues and fluids of animals acutely exposed to hydrogen 

sulfide. Cytotoxicity to both nasal or bronchioalveolar lavage and pulmonary cells was demonstrated in a 

study of male F-344 rats exposed to 0, 10, 200, or 400 ppm hydrogen sulfide for 4 hours and examined at 

1, 20, or 44 hours postexposure (Lopez et al. 1987). Cellularity of nasal lavage fluid was increased at all 

exposure concentrations, because of either exfoliation of degenerated epithelial cells at 1 hour, or 

exudation of polymorphonuclear leukocytes (PMNs) at 20 hours postexposure, which served as an 

indicator of cell damage. Altered pulmonary vascular permeability was indicated by increased protein in 

nasal lavage fluids in animals exposed to airborne concentrations of 400 ppm, but this condition resolved 

by 20 hours postexposure. Increased lactate dehydrogenase activity (at exposure levels of 200 and 

400 ppm) and alkaline phosphatase activity (with exposure to 400 ppm) in bronchoalveolar lavage fluid 

observed in this study were indicative of toxic effects on the pulmonary epithelium. In addition, 

pulmonary alveolar macrophages from animals exposed by inhalation to airborne concentrations of 200 or 

400 ppm hydrogen sulfide had some increase in cytoplasmic vacuolation, but the bronchoalveolar 

epithelium did not show signs of cellular degeneration or ciliocytophthoria (Lopez et al. 1987). 

In similar experiments, Green et al. (1991) exposed male F-344 rats to 200 and 300 ppm hydrogen sulfide 

for 4 hours, and evaluated the impact on lung lavage fluid surface tension, protein concentrations, and 

lactate dehydrogenase activity. These authors found significant increases in protein concentrations and 

lactate dehydrogenase activity at both exposure concentrations, but a significant change in the surface 

tension of lavage fluids only at the high dose. Focal area of perivascular edema and proteinaceous 

material in the alveoli were also seen in the lungs of the exposed animals. 

Histopathological changes have been reported in the nasal cavity of F-344 rats (Lopez et al. 1988b). Male 

rats were exposed to 0, 10, 200, or 400 ppm hydrogen sulfide for 4 hours. Necrosis and exfoliation of the 

respiratory and olfactory mucosal cells were observed 1 hour postexposure at concentrations >200 ppm; 

by 20 hours postexposure, the respiratory epithelium was covered by a layer of deeply basophilic cells 

containing mitotic figures and severe inflammatory response was noted. The necrosis ultimately 

ulcerated the respiratory epithelium, causing exposure of the basement membrane (Lopez et al. 1988b). 

Although some histological changes were observed at 10 and 200 ppm hydrogen sulfide, no dose 
HYDROGEN SULFIDE 52 

3. HEALTH EFFECTS 

response was evident; it appears that a concentration >200 ppm is necessary to induce these lesions 

(Lopez et al. 1988b). 

Similarly, Brenneman et al. (2002) observed bilateral symmetrical mucosal necrosis in the nasal olfactory 

epithelium and respiratory epithelial regeneration in rats exposed to 200 or 400 ppm hydrogen sulfide for 

3 hours; the NOAEL for these effects is 80 ppm. However, the respiratory epithelial was not adversely 

affected in rats similarly exposed 3 hours/day for 5 days (Brenneman et al. 2002). In these rats, necrotic 

olfactory epithelium and hyperplastic basal cells were observed in rats exposed to 80, 200, or 400 ppm, 

but not at 30 ppm. A partial regeneration of the olfactory epithelium was observed 2 weeks after 

exposure termination and a complete regeneration was observed 6 weeks post-exposure. 

Cytochrome c oxidase activity in lung mitochondria of F-344 rats was significantly decreased at 50 ppm 

(15%), 200 ppm (43%), and 400 ppm (68%) hydrogen sulfide compared to controls after a 4-hour 

exposure (Khan et al. 1990). Cytochrome c oxidase activity had returned to normal for animals exposed 

to 200 ppm, but not for those exposed to 400 ppm, by 24 hours postexposure. Succinate oxidase activity 

was reduced at 200 ppm (40%) and 400 ppm (63%), but was not affected at 50 ppm (Khan et al. 1990). A 

5-week exposure to 10 or 100 ppm hydrogen sulfide (8 hours/day, 5 days/week) also resulted in 

significant decreases in cytochrome oxidase activity in lung mitochondria (Khan et al. 1998); exposure to 

1 ppm did not result in significant alterations. 

Significant decreases in numbers of viable pulmonary alveolar macrophages were noted in the lung 

lavage fluid of male rats exposed for 4 hours to 400 ppm hydrogen sulfide (Khan et al. 1991). This study 

also showed complete abolition of zymosan-induced stimulation of respiratory rates of pulmonary 

alveolar macrophages in animals exposed to 200 or 400 ppm. No changes were noted after exposure to 

50 ppm hydrogen sulfide. 

Histological changes were characterized in the lungs of male F-344 rats exposed to 83 or 439 ppm for 

4 hours (Lopez et al. 1988a). At the low dose, mild perivascular edema was found, but at the high dose, 

numerous changes were observed, including severe but transient pulmonary edema and fibrocellular 

alveolitis in proximal alveoli; cytoplasmic blebs in the alveolar endothelium; increased numbers of 

mitotic figures in the bronchiolar epithelium; minor changes in the alveolar epithelium; and necrosis of 

the ciliated bronchiolar cells. Moderate-to-massive pulmonary edema was evident in male F-344 rats 

exposed to 375 or 399 ppm for 4 hours (Prior et al. 1990), and slight pulmonary congestion was found in 

male Wistar rats exposed to 75 ppm hydrogen sulfide for 1 hour (Kohno et al. 1991). 
HYDROGEN SULFIDE 53 

3. HEALTH EFFECTS 

The effects of intermediate-duration exposures to hydrogen sulfide have been examined in rats, mice, and 

pigs. Respiratory effects were not observed in F-344 (CIIT 1983b) or Sprague-Dawley (CIIT 1983c) rats 

exposed to hydrogen sulfide at concentrations up to 80 ppm 6 hours/day, 5 days/week, for 90 days. 

However, a re-examination of the histologic specimens from this study (Dorman et al. 2004) found 

significant increases in the incidence of olfactory neuron loss in Sprague-Dawley and F-344 rats exposed 

to 30 or 80 ppm and in male rats exposed to 80 ppm; the no-effect levels in these strains were 10 and 

30 ppm, respectively. In addition, increases in the incidence of bronchiolar epithelial hypertrophy and 

hyperplasia were observed in the female Sprague-Dawley rats exposed to 30 or 80 ppm hydrogen sulfide 

and in male Sprague-Dawley and F-344 rats exposed to 80 ppm. These findings are similar to those of 

Brenneman et al. (2000) who found significant increases in the incidence and severity of nasal lesions in 

male Sprague-Dawley rats exposed to hydrogen sulfide for 6 hours/day, 7 days/week for 10 weeks. The 

nasal lesions, which were limited to the olfactory mucosa, consisted of multifocal, bilaterally symmetrical 

olfactory neuron loss, and basal cell hyperplasia. The olfactory neuron loss and basal cell hyperplasia 

was found in most animals exposed to 30 or 80 ppm, but was not found in controls or rats exposed to 

10 ppm. At 30 ppm, the severity of the olfactory neuron loss and basal cell hyperplasia was graded as 

mild to moderate. At 80 ppm, the severity of the olfactory neuron loss was moderate to severe and the 

basal cell hyperplasia was scored as mild. 

Inflammation of the nasal mucosa described as minimal to mild rhinitis was observed in B6C3F1 mice 

exposed to hydrogen sulfide at 80 ppm for 6 hours/day, 5 days/week for 90 days (CIIT 1983a); these 

lesions were not observed at 30 ppm. A re-examination of the histological specimens from this study 

confirmed these results (Dorman et al. 2004) and also found significant increases in the incidence of 

olfactory neuron loss in the nasal olfactory epithelium of male and female mice exposed to 30 or 80 ppm, 

but not at 10 ppm. 

Three crossbred pigs of unspecified sex were continuously exposed to 0 or 8.5 ppm hydrogen sulfide in 

inhalation chambers for 17 days (Curtis et al. 1975). No significant changes in body weight gain and no 

histopathological changes in the respiratory tract (including turbinates, trachea, and lungs) were noted. 

This study is limited by the number of animals used and because only one exposure concentration was 

used. 

Cardiovascular Effects. Cardiovascular effects have been noted after acute exposures to high 

concentrations of hydrogen sulfide via inhalation (Arnold et al. 1985). Slight blood pressure increases 
HYDROGEN SULFIDE 54 

3. HEALTH EFFECTS 

were noted in several workers exposed to hydrogen sulfide in a pelt room, however, their electrocardiograms (EKGs) were normal (Audeau et al. 1985). In other instances of hydrogen sulfide poisoning 

that occurred after a short exposure to high concentrations, no changes in blood pressure were noted 

despite other cardiac irregularities (Ravizza et al. 1982). Hemodynamic instability was noted in one of 

two men who survived acute exposure to an unknown concentration of hydrogen sulfide and also 

swallowed large amounts of manure after entering a partially drained liquid manure pit (Osbern and 

Crapo 1981). Sinus tachycardia has been noted in men who completely recovered after exposure to 

hydrogen sulfide (Peters 1981; Ravizza et al. 1982). Supraventricular tachycardia and left bundle block 

were noted in a worker exposed to hydrogen sulfide generated from a sodium sulfide waste solution 

dumped onto acid waste material; the effects were temporary (Stine et al. 1976). Extreme tachycardia and 

hypotension were noted in a woman who attempted to clean a well with muriatic acid and was exposed to 

an unknown concentration of hydrogen sulfide gas; hypertension was noted in a man exposed during this 

same incident (Thoman 1969). 

EKGs taken on two workers about 2.5 hours after an acute exposure to hydrogen sulfide showed cardiac 

arrhythmias (Krekel 1964). The workers were exposed for <5 minutes after a spill of sodium sulfide that 

broke down to release hydrogen sulfide. In one individual, a negative P wave, indicating a substitute 

rhythm, was noted, while in the other individual, a continuous arrhythmia due to atrial flutter was found. 

EKGs for both men had returned to normal within 24 hours. 

No adverse cardiovascular effects were found when healthy male volunteers were exposed to hydrogen 

sulfide concentrations up to 5 ppm for >16 minutes after graded exercise performed to exhaustion 

(Bhambhani and Singh 1991). A study that examined the effects of inhalation of 5 ppm hydrogen sulfide 

on physiological parameters found no changes in heart rate, blood pressure, percent hemoglobin 

saturation, perceived exertion, or other parameters in healthy male and female volunteers during 

30 minutes of submaximal exercise (Bhambhani et al. 1994). A subsequent study examining the effects 

of inhaling 10 ppm hydrogen sulfide during two 30-minute sessions of submaximal exercise found no 

significant changes in cardiovascular responses under these conditions (Bhambhani et al. 1997). 

In a retrospective epidemiologic study using hospital discharge data from 1981 to 1990, Bates et al. 

(1998) evaluated the risk of disease to known target organ systems of hydrogen sulfide toxicity in 

residents of Rotorua, a New Zealand city that uses geothermal energy for industrial and domestic heating 

purposes. A significant increase in incidence was found for diseases of the circulatory system (SIR=1.05; 

p=0.001) among Rotorua residents as compared to all other New Zealand residents. Although previous 
HYDROGEN SULFIDE 55 

3. HEALTH EFFECTS 

monitoring information from Rotorua in 1978 showed a median concentration of hydrogen sulfide of 

20 μg/m3

, with 35% of the measurements over 70 μg/m3 and 10% over 400 μg/m3 (Bates et al. 1997), the 

lack of monitoring information concurrent with these data precludes conclusions with regard to a causal 

relationship between circulatory system disease and hydrogen sulfide exposures. Using hospital 

discharge records for 1993–1996, Bates et al. (2002) attempted to examine exposure-related trends for 

cardiovascular disease among residents of Rotorua. Residents were divided into three exposure 

categories (low, medium, and high) based on surrogate exposure data. A statistically significant 

(p<0.001) trend for exposure-related increases in the incidence of circulatory system disease was 

observed. When the circulatory system disease category was further divided into minor disease 

categories, significant (p<0.01) exposure-related trends for cerebrovascular disease and diseases of 

arteries, arterioles, and capillaries were found. However, no significant increases in SIRs were found for 

the cerebrovascular disease category. For artery, arteriole, and capillary disease category, the SIRs were 

significantly elevated for the medium (SIR=1.58, 95% confidence level of 1.17–2.08) and high 

(SIR=1.66, 95% confidence interval of 1.30–2.09) exposure groups. The lack of exposure data, the 

assumption that hydrogen sulfide exposure only occurred at home, and the lack of control for potential 

confounding factors such as smoking and socioeconomic status limit the interpretation of these data. 

Studies in experimental animals have reported EKG alterations (e.g., cardiac arrhythmia) following acuteduration exposure to 72–75 ppm for 1.5 hours or less (Kohno et al. 1991; Kosmider et al. 1967); however, 

the lack of statistical analysis precludes interpretation of these studies. Alterations in heart rate have also 

been reported. A decrease in heart rate (10–27% of controls) was observed in rats exposed to 75 ppm for 

60 minutes (Kohno et al. 1991). In contrast, another study found an increase in heart rates in rats exposed 

to 100–200 ppm for 1 hour (Higuchi and Fukamachi 1977). The differences may be reflective of the 

different exposure levels. Data on the cardiotoxicity of hydrogen sulfide following longer-term exposure 

is limited to a study by CIIT (1983a, 1983b, 1983c). This study found no treatment-related 

histopathological alterations in the cardiovascular system of F-344 or Sprague-Dawley rats or B6C3F1 

mice exposed via inhalation to time-weighted-average (TWA) concentrations of 10, 30, or 80 ppm 

hydrogen sulfide for 6 hours/day, 5 days/week, for 90 days (CIIT 1983a, 1983b, 1983c). 

Gastrointestinal Effects. Nausea and vomiting have been noted in several cases of human 

inhalational hydrogen sulfide poisoning (Allyn 1931; Audeau et al. 1985; Deng and Chang 1987; Krekel 

1964; Osbern and Crapo 1981; Thoman 1969). 
HYDROGEN SULFIDE 56 

3. HEALTH EFFECTS 

In two evaluations of the acute health effects associated with communities experiencing episodes of high 

emissions, significant increases in the reporting of nausea as a symptom have been reported (Haahtela et 

al. 1992; Marttila et al. 1995). In the first study, increased emissions from a pulp mill resulted in 

increased concentrations of hydrogen sulfide over 2 days. The highest 4-hour concentration of hydrogen 

sulfide was 135 μg/m3

 (96.4 ppb) and the 24-hour averages for the 2 days were 35 and 43 μg/m3 (25 and 

31 ppb). Following the high exposure, and then after a low exposure period (hydrogen sulfide level of 

0.1 to 3.5 μg/m3 [0.07–2.5 ppb] for 4 hours), community responses were evaluated with a questionnaire. 

In this comparison, the concentration of sulfur dioxide was the same. In a study, Marttila et al. (1995) 

compared community responses using six consecutive questionnaires after three predefined levels of 

exposure. The three exposure levels were expressed as μg/m3

 of TRS as a way to summarize the complex 

pollution mixture of hydrogen sulfide, methyl mercaptan, and methylsulfides produced by pulp mills 

using the sulfate pulping method. The three categories of exposure were low (daily mean of TRS 

<10 μg/m3

), (medium 10–30 μg/m3), and high exposure (>30 μg/m3). An increase in reports of nausea 

was significant only with the highest level of exposure. Interpretation of these results is complicated by 

the presence of multiple sulfur compounds as well as other air pollutants. Earlier work indicated that 

hydrogen sulfide represented two-thirds of the TRS (Marttila et al. 1994a). Concurrent measurements of 

sulfur dioxide, total suspended particles, and nitrogen oxides for the periods covered by each of the 

questionnaires, indicated that only sulfur dioxide appeared to co-vary with TRS. 

No treatment-related histopathological changes were detected in the gastrointestinal tract of F-344 or 

Sprague-Dawley rats or B6C3F1 mice exposed via inhalation TWA concentrations of 10, 30, or 80 ppm 

hydrogen sulfide 6 hours/day, 5 days/week, for 90 days (CIIT 1983a, 1983b, 1983c). No gastrointestinal 

effects were reported in crossbred pigs exposed to 8.5 ppm hydrogen sulfide for 24 hours/day for 17 days 

(Curtis et al. 1975). 

Hematological Effects. The cyanosis that has been reported in a number of cases of accidental 

exposure to hydrogen sulfide is believed to result from respiratory distress (Arnold et al. 1985; Burnett et 

al. 1977; Deng and Chang 1987; Peters 1981; Ravizza et al. 1982; Stine et al. 1976; Tvedt et al. 1991a, 

1991b). 

Complete blood counts were normal in four individuals overcome by unknown concentrations of 

hydrogen sulfide gas in a pelt room (Audeau et al. 1985). Percent hemoglobin saturation was unchanged 

by inhalation of either 5 ppm hydrogen sulfide by volunteers during 30-minutes of submaximal exercise 
HYDROGEN SULFIDE 57 

3. HEALTH EFFECTS 

(Bhambhani et al. 1994), or 10 ppm hydrogen sulfide during two 30-minute sessions of submaximal 

exercise (Bhambhani et al. 1997). 

Workers who were sometimes exposed to airborne concentrations of >20 ppm hydrogen sulfide did not 

have any changes in hematological parameters (Ahlborg 1951). Pulp industry workers (n=17) exposed to 

8-hour TWA concentrations of 0.05–5.2 ppm hydrogen sulfide had no signs of clinical anemia (Tenhunen 

et al. 1983). Jappinen and Tenhunen (1990) examined blood sulfide concentration and changes in heme 

metabolism at 2 hours, 1 week, and 1 month post-hydrogen sulfide poisoning in six cases of occupational 

exposure. Decreased delta-aminolaevulinic acid synthase activities and erythrocyte protoporphyrin 

concentrations were noted at the 2-hour and 1-week time periods, but not to the level of significance, and 

there was no change in heme synthase activity. 

No treatment-related changes in hematological parameters were noted in F-344 or Sprague-Dawley rats or 

B6C3F1 mice exposed by inhalation to TWA concentrations of 10, 30, or 80 ppm of hydrogen sulfide 

6 hours/day, 5 days/week, for 90 days (CIIT 1983a, 1983b, 1983c). 

Musculoskeletal Effects. In a series of reports characterizing the responses of healthy volunteers to 

low level, short-term exposures to hydrogen sulfide, Bhambhani and his colleagues (Bhambhani and 

Singh 1991; Bhambhani et al. 1994, 1996a, 1996b, 1997) concluded that exposures to 5 or 10 ppm 

hydrogen sulfide via oral inhalation resulted in increases in blood lactate concentrations and a decrease in 

muscle citrate synthase activity indicative of an inhibition of the aerobic capacity of exercising muscle. 

Men appeared to be more sensitive to this effect, showing a small response at 5 ppm where women did 

not show an effect until the 10 ppm level (Bhambhani et al. 1996b, 1997). 

No treatment-related histopathological changes were detected in the skeletal muscle, bone marrow, or 

bone of F-344 or Sprague-Dawley rats or B6C3F1 mice exposed to TWA concentrations of 10, 30, or 

80 ppm hydrogen sulfide for 6 hours/day, 5 days/week, for 90 days (CIIT 1983a, 1983b, 1983c). 

Hepatic Effects. Increases in unspecified liver enzyme activities were noted in some of 221 persons 

exposed by inhalation to hydrogen sulfide (Burnett et al. 1977). No baseline for these effects was 

available and they were not quantified. 

No changes in serum protein, lactate dehydrogenase (LDH), serum glutamic-oxaloacetic transaminase 

(serum glutamic oxaloacetic transaminase [SGOT]; aspartate aminotransferase), or alkaline phosphatase 
HYDROGEN SULFIDE 58 

3. HEALTH EFFECTS 

activities were noted in Sprague-Dawley rat dams exposed to 20, 50, or 75 ppm of hydrogen sulfide for 

7 hours/day from gestation day 1 through postnatal day 21 (Hayden et al. 1990a). Maternal liver 

cholesterol levels were increased in Sprague-Dawley dams exposed to 75 ppm, but not 50 ppm, for 

7 hours/day from gestation day 6 to postpartum day 21 (Hayden et al. 1990b). 

No treatment-related histopathological changes were detected in the livers of F-344 or Sprague-Dawley 

rats or B6C3F1 mice exposed to TWA concentrations of 10, 30, or 80 ppm of hydrogen sulfide 

6 hours/day, 5 days/week, for 90 days (CIIT 1983a, 1983b, 1983c). No gross or histopathological lesions 

were found in the livers of crossbred pigs exposed to 8.5 ppm of hydrogen sulfide continuously for 

17 days (Curtis et al. 1975). 

Renal Effects. Blood urea nitrogen and serum electrolyte levels were normal in several individuals 

overcome by unknown concentrations of hydrogen sulfide gas in a pelt room (Audeau et al. 1985). One 

of these four patients had protein and blood in the urine initially, which was not detected upon later 

testing. Albumin and some granular casts were noted in the urine in another patient, but these findings 

were transient (Audeau et al. 1985). 

F-344 and Sprague-Dawley rats as well as B6C3F1 mice were exposed to TWA concentrations of 10, 30, 

or 80 ppm of hydrogen sulfide for 6 hours/day, 5 days/week, for 90 days (CIIT 1983a, 1983b, 1983c). No 

treatment-related histopathological changes were detected in the kidneys of these animals and urinalysis 

findings were negative, indicating no renal effects due to hydrogen sulfide exposure. No gross or 

histopathological lesions were found in the kidneys of crossbred pigs exposed to 8.5 ppm of hydrogen 

sulfide continuously for 17 days (Curtis et al. 1975). 

Endocrine Effects. No studies were located regarding endocrine effects in humans after inhalation 

exposure to hydrogen sulfide. 

No treatment-related histopathological changes were detected in the pituitary, adrenal, thyroid, or 

parathyroid glands of F-344 or Sprague-Dawley rats or B6C3F1 mice exposed to TWA concentrations of 

10, 30, or 80 ppm hydrogen sulfide 6 hours/day, 5 days/week, for 90 days (CIIT 1983a, 1983b, 1983c). 

Dermal Effects. Six men lost consciousness after acute hydrogen sulfide exposure; one man with 

probable exposure to 8–16 ppm had peeling facial skin (Tvedt et al. 1991a, 1991b). 
HYDROGEN SULFIDE 59 

3. HEALTH EFFECTS 

No treatment-related histopathological changes were detected in the skin of F-344 or Sprague-Dawley 

rats or B6C3F1 mice exposed to TWA concentrations of 10, 30, or 80 ppm hydrogen sulfide for 

6 hours/day, 5 days/week, for 90 days (CIIT 1983a, 1983b, 1983c). Slate-grey skin discoloration and 

erythema were noted in rabbits exposed to unspecified concentrations of hydrogen sulfide for 2 hours 

(Laug and Draize 1942). 

Ocular Effects. Ocular effects reported after inhalation exposure are believed to have resulted from 

direct eye contact with hydrogen sulfide gas. Hydrogen sulfide gas is an eye irritant. Keratoconjunctivitis (sometimes with subsequent infection), punctate corneal erosion, blepharospasm, lacrimation, 

and photophobia have developed in individuals exposed to brief high-level concentrations of hydrogen 

sulfide gas (Ahlborg 1951; Luck and Kaye 1989). Hemorrhagic keratoconjunctivitis and subconjunctival 

hemorrhage were reported in cases of near-lethal poisoning to unknown concentrations of hydrogen 

sulfide (Deng and Chang 1987; Stine et al. 1976). A retrospective study of 250 Canadian workers who 

submitted workers' compensation claims for hydrogen sulfide exposure found that 18% had developed 

conjunctivitis, which persisted for several days in some cases (Arnold et al. 1985). Stinging of the eyes 

has been reported in acute occupational hydrogen sulfide poisoning (Audeau et al. 1985). None of these 

reports of ocular exposure suggested that permanent eye effects may occur (Ahlborg 1951; Arnold et al. 

1985; Audeau et al. 1985; Deng and Chang 1987; Luck and Kaye 1989; Stine et al. 1976). People 

exposed to hydrogen sulfide, methyl mercaptan, and methyl sulfides while living in a community around 

a paper mill reported eye irritation 12 times more often than people without exposure (Jaakkola et al. 

1990). These effects were observed at mean annual hydrogen sulfide exposures estimated at 6 μg/m3 

(4.3 ppb). However, the ocular symptoms that were reported may have been due to exposure to peak 

concentrations of hydrogen sulfide (daily peaks as high as 100 μg/m3

; 70 ppb) and not annual mean 

concentrations, or may have been due to co-exposure to methyl mercaptan and methyl sulfides. Methyl 

mercaptan is also an eye irritant (NIOSH 2006) and it was also present at an annual mean concentration of 

2–5 μg/m3

 with the highest daily average concentration being 50 μg/m3 (Jaakkola et al. 1990). 

In a retrospective epidemiologic study using hospital discharge data from 1981 to 1990, Bates et al. 

(1998) evaluated the risk of disease to known target organ systems of hydrogen sulfide toxicity in 

residents of Rotorua, a New Zealand city that uses geothermal energy for industrial and domestic heating 

purposes. No information on hydrogen sulfide levels was presented in this report, but the authors indicate 

concerns that exposures to hydrogen sulfide and/or mercury from geothermal sources could have health 

impacts. In their previous work, it was indicated that the most reliable monitoring information for 

hydrogen sulfide in the area came from a monitoring exercise in 1978, which found a median 
HYDROGEN SULFIDE 60 

3. HEALTH EFFECTS 

concentration of hydrogen sulfide of 20 μg/m3, with 35% of the measurements >70 μg/m3 and 10% 

>400 μg/m3

 (Bates et al. 1997). On the basis of hospital discharge data, significant increases in incidence 

were found for diseases of the nervous system and sense organs (SIR=1.11; p<0.001) among Rotorua 

residents as compared to the rest of New Zealand. When incidence rates were examined for minor 

disease groupings within this group of nervous system and sense organ diseases, significantly increased 

risks were seen for other disorders of the eye and adnexa (SIR=1.12; p<0.001). At the level of individual 

diseases, statistically significant incidence ratios were found for cataract (SIR=1.26; p<0.001), disorders 

of the conjunctiva (SIR=2.09; p<0.001), and disorders of the orbit (SIR=1.69; p=0.005). The effect of 

hydrogen sulfide on the eye is of considerable importance because ocular effects occur at concentrations 

that provide no other observable systemic effect (NIOSH 1977a). 

Ocular irritation has also been noted after animals were exposed to hydrogen sulfide. Epiphora was noted 

in F-344 rats exposed to 400 ppm, but not 200 ppm, of hydrogen sulfide for 4 hours (Lopez et al. 1988b). 

Eye irritation was noted in guinea pigs exposed to 20 ppm of hydrogen sulfide 1 hour/day for 20 days 

(Haider et al. 1980). No ocular lesions were found upon microscopic examination of the eyes of 

crossbred pigs exposed to 8.5 ppm of hydrogen sulfide 24 hours/day for 17 days (Curtis et al. 1975). 

No treatment-related histopathological changes were detected in the eyes of F-344 or Sprague-Dawley 

rats or B6C3F1 mice exposed to TWA concentrations of 10, 30, or 80 ppm of hydrogen sulfide for 

6 hours/day, 5 days/week, for 90 days (CIIT 1983a, 1983b, 1983c). 

Body Weight Effects. No studies were located regarding body weight effects in humans after 

inhalation exposure to hydrogen sulfide. 

Pregnant Sprague-Dawley rats exposed to 100 or 150 ppm hydrogen sulfide on gestation days 6– 

20 showed decreased body weight gains that reached significance at the higher dose. Absolute weight 

gain (i.e., minus the gravid uterine weight) was significantly depressed at both of these doses. Exposure 

at 50 ppm hydrogen sulfide had no effect on body weight gain or on absolute weight gain (Saillenfait al. 

1989). No effects on body weight were noted in Sprague-Dawley rats exposed to 50 ppm of hydrogen 

sulfide 5 days/week, for 25 weeks (Gagnaire et al. 1986). No treatment-related body weight changes 

were noted in F-344 rats exposed to TWA airborne concentrations of 10, 30, or 80 ppm of hydrogen 

sulfide 6 hours/day, 5 days/week, for 90 days (CIIT 1983b). However, when Sprague-Dawley rats were 

exposed on the same regimen, females at 80 ppm showed a significant (10%) decrease in body weight at 

the end of the study compared to controls, which was not evident at 30 ppm (CIIT 1983c). At 80 ppm, 
HYDROGEN SULFIDE 61 

3. HEALTH EFFECTS 

the body weight of males was significantly less (8%) than controls during weeks 1–3, but the final body 

weight differences were not significant (CIIT 1983c). Similarly, B6C3F1 mice of both sexes exposed to 

TWA concentrations of 80 ppm hydrogen sulfide 6 hours/day, 5 days/week, for 90 days showed decreases 

in body weight of 7–14% compared to controls; these changes were not observed at 30 ppm (CIIT 1983a). 

No body weight changes were found in crossbred pigs exposed to 8.5 ppm hydrogen sulfide continuously 

for 17 days (Curtis et al. 1975). 

Metabolic Effects. Severe metabolic acidosis developed in a worker exposed to hydrogen sulfide 

generated from a sodium sulfide waste solution dumped onto acid waste material (Stine et al. 1976). 

Blood lactate concentrations were significantly increased (65%) compared to controls during exercise in 

men exposed to 5 ppm hydrogen sulfide via oral inhalation for >16 minutes (Bhambhani and Singh 1991), 

but not at 2 ppm. Additional studies by the same group (Bhambhani et al. 1994, 1996b) exposed both 

men and women to 5 ppm hydrogen sulfide during 30 minutes of exercise and failed to observe 

significant increases in lactate concentrations, but did see a decrease in muscle citrate synthase in men, 

suggesting that aerobic metabolism was being compromised at this level of exposure. 

In a subsequent study, Bhambhani et al. (1997) observed significant increases in blood lactate 

concentrations in male and female volunteers exposed to 10 ppm hydrogen sulfide, although there was not 

a significant change in the activities of muscle lactate dehydrogenase, citrate synthase, or cytochrome 

oxidase. 

In Sprague-Dawley rat dams exposed to 20, 50, or 75 ppm of hydrogen sulfide for 7 hours/day from 

gestation day 1 through postnatal day 21, blood glucose levels were increased about 50% at all exposure 

concentrations (Hayden et al. 1990a). 

3.2.1.3 Immunological and Lymphoreticular Effects 

No studies were located regarding immunological and lymphoreticular effects in humans after inhalation 

exposure to hydrogen sulfide. 

No treatment-related histopathological changes were found in the spleen or lymph nodes of F-344 or 

Sprague-Dawley rats or B6C3F1 mice exposed to TWA concentrations of 10, 30, or 80 ppm of hydrogen 

sulfide 6 hours/day, 5 days/week, for 90 days (CIIT 1983a, 1983b, 1983c). Pulmonary alveolar 

macrophage function was studied using lavage fluid from F-344 rats exposed for 4 hours to 50, 200, or 
HYDROGEN SULFIDE 62 

3. HEALTH EFFECTS 

400 ppm hydrogen sulfide (Khan et al. 1991). Although the number of pulmonary alveolar macrophage 

cells was not influenced by hydrogen sulfide exposure, the number of viable cells was significantly 

decreased at 400 ppm. When the pulmonary alveolar macrophage cells were treated with Zymosan to 

stimulate respiration rates, it was found that there was no stimulation of respiration in cells from animals 

exposed to 200 or 400 ppm; these rates were significantly different from controls and were approximately 

equal to basal cell levels (Khan et al. 1991). 

The highest NOAEL values and all reliable LOAEL values for immunological effects in rats and mice 

exposed in acute- and intermediate-duration studies are recorded in Table 3-1 and plotted in Figure 3-1. 

3.2.1.4 Neurological Effects 

Acute human exposure to hydrogen sulfide can result in nausea, headaches, delirium, disturbed 

equilibrium, poor memory, neurobehavioral changes, olfactory paralysis, loss of consciousness, tremors, 

and convulsions. Fatigue, poor memory, dizziness, and irritability have been observed in workers 

chronically exposed to hydrogen sulfide (Beauchamp et al. 1984); however, it is not known if these 

effects are the result of chronic exposure or due to reoccurring acute exposures. 

Available information on the neurotoxic effects of acute exposures to high levels of hydrogen sulfide in 

humans comes primarily from case reports. In most instances, exposure concentrations were either 

unknown or estimated. In most cases, the exact exposure duration was not known, but estimated 

durations ranged from several minutes to an hour. The most commonly reported nonlethal effect found in 

individuals exposed to high concentrations is unconsciousness followed by apparent recovery, 

colloquially referred to as knockdown (Deng and Chang 1987; Krekel 1964; McDonald and McIntosh 

1951; Milby 1962; Spolyar 1951). Other described neurological effects in the case reports include 

disturbed equilibrium, nausea, headache, poor memory, insomnia, irritability, delirium, severe vertigo, 

unusual sweating, neuropsychological symptoms, convulsions, and tremors (Arnold et al. 1985; Krekel 

1964). While deaths were often noted, there were cases in which individuals survived and had complete 

neurological recovery (Deng and Chang 1987; Krekel 1964; Osbern and Crapo 1981; Ravizza et al. 

1982). In a study of the possible effects of exposure to low concentrations of hydrogen sulfide, 

3/10 asthmatic volunteers complained of headache after being exposed in a sealed chamber to 2 ppm 

hydrogen sulfide for 30 minutes (Jappinen et al. 1990). 
HYDROGEN SULFIDE 63 

3. HEALTH EFFECTS 

A few case reports have described permanent or persistent neurological effects in humans following acute 

inhalation exposure to high concentrations of hydrogen sulfide. One patient developed symptoms of 

frontal headaches, irritability, poor concentration ability and attention span, and deficits of cortical 

function tests, including verbal abstraction, attention, and short-term retention 1 month after accidental 

exposure to unspecified concentrations of hydrogen sulfide (Stine et al. 1976). All effects except 

headaches resolved by 2 months after the accident. A 5–10-year follow-up re-examination of several 

individuals who became unconscious after exposure to unspecified concentrations of hydrogen sulfide 

revealed permanent neurological symptoms (Tvedt et al. 1991a, 1991b) including vision and memory 

impairment; rigid movements; reduced motor function; slight tremor; ataxia; psychosis; abnormal 

learning, retention, and motor function; and slight cerebral atrophy. The probable exposure concentration 

in one of the patients may have exceeded 200 ppm (as measured 2.5 hours after exposure). Divergent 

reports of the risk of permanent neurological damage due to hydrogen sulfide may result from lack of 

follow-up after hospital discharge (Tvedt et al. 1991b). Permanent neurologic damage including effects 

on balance, vibration sense, and impaired verbal and visual recall were observed in one man exposed to a 

very high concentration (14,000 ppm) of hydrogen sulfide (Kilburn 1993). In another case report, a 

worker who suffered ‘knockdown’ and presented in a coma, remained in a coma through standard 

treatment (i.e., sodium nitrite), underwent several treatments with hyperbaric oxygen, and became 

responsive to simple commands by day 5. However, at the time of discharge, an extensive head injury 

assessment found effects on speech, attention span, insight, and ability to communicate, as well as a 

marked impact on visual memory and the ability to acquire, retain, and recall new information. These 

effects had not resolved by 12 and 18 months after exposure (Snyder et al. 1995). In a somewhat similar 

scenario, Schneider et al. (1998) describe a case in which another worker lost consciousness when he 

descended into a 27-foot pit that was part of a sewer construction project. He was overcome by hydrogen 

sulfide fumes (concentration not specified), fell from a ladder from an unspecified height, and was 

subsequently removed in a coma and transported to a local trauma center. At the emergency room (and 

potentially at the site), the patient experienced seizure activity. A body computed tomography (CT) scan 

showed pulmonary edema while a head CT scan was normal. The patient was transferred to a hyperbaric 

medicine unit and started on hyperbaric oxygen treatments (starting approximately 10 hours postepisode). Five days later, he recovered consciousness, and by 7 days, his status had improved enough to 

discontinue hyperbaric oxygen treatments. He was able to feed himself and move with assistance, but had 

impaired language, memory, and attention, and appeared agitated and restless. Over the course of the 

next 4 years, the patient was evaluated on a variety of occasions. He continued to show a constellation of 

deficits, which even 4 years later, included problems with general cognition, motor function, and 
HYDROGEN SULFIDE 64 

3. HEALTH EFFECTS 

cognitive function; some of these symptoms appeared to be alleviated through a combined treatment with 

fairly high doses of Ritalin and Cyclert drugs, which enhance dopaminergic functioning. 

In a case control study of 16 subjects who had been exposed for minutes, hours, or years to hydrogen 

sulfide, Kilburn (1997) found evidence of permanent neurobehavior impairment in exposed individuals 

when compared to 353 controls matched for sex, age, and years of education. A large battery of tests was 

used to evaluate these individuals, including a detailed self-administered questionnaire, complete physical 

and clinical screen neurologic examinations, as well as a series of neurophysiologic and neuropsychologic 

tests. Among those who had chronic low-dose exposure, the most sensitive tests were those evaluating 

balance, simple reaction time, left visual field, and verbal recall. The group exposed to hydrogen sulfide 

for hours showed additional defects, including impacts on a variety of neuropsychological tests, although 

remote memory remained intact. The group that experienced momentary knock-down exposure had an 

even larger suite of deficit cognitive functions, leading the study author to conclude that “...brief high 

doses were devastating, whereas protracted low doses showed effects on the more sensitive tests.” 

A 20-month-old child was exposed for nearly 1 year to >0.6 ppm hydrogen sulfide and other emitted 

chemicals from a coal mine (Gaitonde et al. 1987). Symptoms included ataxia, choreoathetosis, dystonia, 

and inability to stand. A CT scan of the brain showed bilateral areas of low density in the region of both 

basal ganglia and surrounding white matter. Neurophysiological investigations of electroencephalography, visual evoked responses, brain stem evoked responses, and peripheral nerve conduction studies 

were normal. The child's condition improved spontaneously, shortly after hospital admission; after 

10 weeks, ataxia had resolved and the choreoathetoid movements were reduced. A repeat brain scan 

showed complete resolution of abnormalities. The relationship of these complaints to low-level hydrogen 

sulfide exposure is unclear. 

Neurological effects resulting from chronic-duration exposure to hydrogen sulfide in the shale industry 

have been reported (Ahlborg 1951). Symptoms observed in workers exposed to daily concentrations of 

hydrogen sulfide that often exceeded 20 ppm included fatigue, loss of appetite, headache, irritability, poor 

memory, and dizziness. The frequency of fatigue increased with length of employment and the degree of 

hydrogen sulfide exposure. 

In the South Karelia air pollution study, discussed in more detail under respiratory effects, all of the 

reports found increases in the incidence of headaches or migraines in polluted communities when 

compared to nonpolluted communities (Jaakkola et al. 1990; Marttila et al. 1994b, 1995; Partti-Pellinen et 
HYDROGEN SULFIDE 65 

3. HEALTH EFFECTS 

al. 1996); however, only in the most recent study did this finding achieve statistical significance. Using a 

cross-sectional, self-administered questionnaire, this report (Partti-Pellinen et al. 1996) evaluated the 

increased risk of headache or migraine in adults in a slightly polluted and a reference community. In the 

polluted community, the mean annual TRS concentrations were 2–3 μg/m3

, the 24-hour concentrations 

varied between 0 and 56 μg/m3

, and the maximum 1-hour concentration was 155 μg/m3; there was no 

TRS detected in the reference community. In the polluted community, the sulfur dioxide annual mean 

concentration was 1 μg/m3

, the 24-hour concentrations varied between 0 and 24 μg/m3 and the maximum 

1-hour concentration was 152 μg/m3

. In the reference community, the mean sulfur dioxide level was 

1 μg/m3

 and the maximum 1-hour concentration was 30 μg/m3. The residents of the polluted community 

showed a significantly increased risk of headache both during the previous 4-week period (OR=1.83; 95% 

CI=1.06–3.15) and the preceding 12 months (OR=1.70; 95% CI=1.01–2.64), when compared to the 

residents of the reference community, even after adjusting for differences in age, gender, smoking, history 

of allergic diseases, education, and marital status between the two communities. 

In a retrospective epidemiologic study using hospital discharge data from 1981 to 1990, Bates et al. 

(1998) evaluated the risk of disease to known target organ systems of hydrogen sulfide toxicity in 

residents of Rotorua, a New Zealand city that uses geothermal energy for industrial and domestic heating 

purposes. Although no information on hydrogen sulfide levels was presented in this report, the authors’ 

previous work indicated that a monitoring exercise in Rotorua in 1978 found a median concentration of 

hydrogen sulfide of 20 μg/m3

, with 35% of the measurements >70 μg/m3 and 10% >400 μg/m3; additionally, elevated concentrations of mercury had previously been found in the hair of residents (Bates et al. 

1997). Significant increases in incidence were found for diseases of the nervous system and sense organs 

(SIR=1.11; p<0.001) among Rotorua residents as compared to the rest of New Zealand residents. When 

the data were stratified by gender and ethnicity, the increased risks remained significant for all but nonMaori men. When incidence rates were examined for minor disease groupings within nervous system 

diseases, significantly increased risks were seen for other disorders of the central nervous system 

(SIR=1.22; p<0.001) and disorders of the peripheral nervous system (SIR=1.35; p<0.001). At the level of 

individual diseases, statistically significant incidence ratios were found for infant cerebral palsy 

(SIR=1.42; p=0.02), migraine (SIR=1.40; p=0.002), other conditions of the brain (SIR=2.50; p<0.001), 

mononeuritis of the upper limbs and mononeuritis multiplex (SIR=1.47; p<0.001), and mononeuritis of 

the lower limbs (SIR=2.06; p<0.001). A follow-up study of this population found a significant exposurerelated trend (p<0.001) for increasing incidence of diseases of the nervous system and sense organs 

(Bates et al. 2002). In this study, the hospital discharge records were used to obtain disease incidence 

data; additionally, the affected individuals were divided into three exposure groups (low, medium, and 
HYDROGEN SULFIDE 66 

3. HEALTH EFFECTS 

high) based on their current residence. Actual exposure levels were not monitored; a surrogate for 

exposure was used. When the nervous system disease incidence was further divided into subcategories, 

significant trends (p<0.001) were found for other disorders of the central nervous system, disorders of the 

eye and adnexa, and disorders of the ear and mastoid process. The SIRs (95% confidence interval) were 

significantly elevated in all groups for disorders of the eye and adnexa: 1.47 (1.33–1.63), 1.57 (1.30– 

1.89), and 2.27 (1.97–2.61) for the low, medium, and high exposure groups, respectively. In the high 

exposure group, the SIRs were also elevated for other disorders of the central nervous system (2.59, 1.91– 

3.44), disorders of the peripheral nervous system (2.27, 1.97–2.61), and disorders of the ear and mastoid 

process (2.00, 1.65–2.40). The lack of exposure data, the assumption that hydrogen sulfide exposure only 

occurred at home, the assumption that current exposure also represented historical exposure, and the lack 

of control for confounding variables such as smoking and socioeconomic status limit the interpretation of 

these data. 

ATSDR (Inserra et al. 2004) examined residents of Dakota City, Nebraska for neurobehavioral effects 

resulting from chronic exposure to ≥90 ppb hydrogen sulfide. Although the 90 ppb level was used as a 

cut off value, historical monitoring data records showed much higher levels; for example, the outdoor 

hydrogen sulfide level exceeded 1,000 ppb 275 times in the 1995–1999 time period. Hydrogen sulfide 

exposure did not appear to adversely affect performance on most neurobehavioral tests; in fact, the 

hydrogen sulfide exposed groups scored better than the referent group on 21 of the 28 tests, although the 

differences were not statistically significant. The hydrogen sulfide group did score lower on a memory 

test (match to sample score) and a test of grip strength, but the differences were not statistically 

significant. 

Rabbits exposed to 72 ppm of hydrogen sulfide for 1.5 hours lost consciousness (Kosmider et al. 1967). 

Haider et al. (1980) observed behaviors in guinea pigs exposed daily to 20 ppm of hydrogen sulfide for 

11 days that were indicative of fatigue, somnolence, and dizziness; no additional information of overt 

behaviors were provided. Neurochemical analyses revealed decreased cerebral hemisphere and brain 

stem total lipids and phospholipids. Rats exposed to 800 ppm of hydrogen sulfide for 20 minutes lost 

consciousness (Beck et al. 1979). Lethargy was observed in rats following exposure to 400 ppm of 

hydrogen sulfide for 4 hours (Lopez et al. 1988b). 

Male Wistar rats were exposed to average concentrations of 100–200, 200–300, 300–400, or 400– 

500 ppm hydrogen sulfide; at 200–300 ppm, a decreased response rate in a discriminated avoidance task 

was observed (Higuchi and Fukamachi 1977). Except at the highest concentrations tested, the response 
HYDROGEN SULFIDE 67 

3. HEALTH EFFECTS 

rates and percent avoidances recovered rapidly when ventilation with clean air was provided, although 

even at 400–500 ppm, they were almost normal the following day (Higuchi and Fukamachi 1977). When 

these same animals were tested for Sidman-type conditioned avoidance response at response-shock 

intervals of 10 or 30 seconds, an inverse relationship between hydrogen sulfide concentration and 

response rate was noted (Higuchi and Fukamachi 1977); this effect dissipated when exposure stopped. 

Female NMRI mice were exposed to 100 ppm of hydrogen sulfide for 2 hours at 4-day intervals; 

excitement was observed (Savolainen et al. 1980). Exposure also resulted in decreased cerebral 

ribonucleic acid (RNA), decreased orotic acid incorporation into the RNA fraction, and inhibition of 

cytochrome oxidase. An increase in the glial enzyme marker, 2’,3’-cyclic nucleotide-3’-phosphohydrolase, was seen. Neurochemical effects have been reported in other studies. Decreased leucine 

uptake and acid proteinase activity in the brain were observed in mice exposed to 100 ppm hydrogen 

sulfide for 2 hours (Elovaara et al. 1978). Inhibition of brain cytochrome oxidase and a decrease in orotic 

acid uptake were observed in mice exposed to 100 ppm hydrogen sulfide for up to 4 days (Savolainen et 

al. 1980). 

Significant decreases in motor activity (ambulations and total movements) were observed in rats receiving 

nose-only exposure to 80, 200, or 400 ppm hydrogen sulfide 3 hours/day for 5 days (Struve et al. 2001). 

However, a decrease in motor activity was not observed in rats receiving whole-body exposures to 

80 ppm 3 hours/day for 5 days (Struve et al. 2001). The study authors did not discuss these conflicting 

results. In addition, significant impairment of learning and memory, as assessed in a water maze test, was 

observed in rats receiving nose-only exposure to 400 ppm. However, these results should be interpreted 

cautiously because the impaired learning and memory may have been secondary to the decrease in motor 

activity and decreased body temperature also observed in these animals. 

A series of intermediate-duration studies conducted by Partlo et al. (2001) used the radial arm maze to 

assess the effect of hydrogen sulfide on learning and memory in rats exposed to 125 ppm hydrogen 

sulfide 4 hours/day, 5 days/week for 5–11 weeks. In the first study, the rats were trained on the radial 

arm maze prior to hydrogen sulfide exposure; 5 weeks of hydrogen sulfide exposure did not adversely 

affect post-exposure performance on the maze, suggesting that 5 weeks of exposure to hydrogen sulfide 

did not adversely affect memory. In the second study, the rats were exposed to hydrogen sulfide and 

trained on the maze daily for 11 weeks. The results of this study suggest that hydrogen sulfide did not 

interfere with acquisition of the maze task, but did adversely affect performance rate. In the third study, 

the rats from the second study were retrained on a modified radial arm maze without additional exposure 
HYDROGEN SULFIDE 68 

3. HEALTH EFFECTS 

to hydrogen sulfide. These results suggested that the hydrogen sulfide-exposed rats had difficulty relearning a complex task. 

The intermediate-duration effects of hydrogen sulfide on neurological function were examined by the 

measurement of motor and sensory nerve conduction velocities of the tail nerve or morphology of the 

sciatic nerve (Gagnaire et al. 1986). Male Sprague-Dawley rats were exposed to 0 or 50 ppm hydrogen 

sulfide for 5 days/week, for 25 weeks. The study authors did not report the duration of exposure to 

hydrogen sulfide per day. No neurotoxic effects were observed in the rats. 

Neurologic function and neuropathology were evaluated in Sprague-Dawley rats exposed to 0, 10, 30, or 

80.0 ppm hydrogen sulfide for 6 hours/day, 5 days/week, for 90 days (CIIT 1983c). Neurological 

function evaluation included: an assessment of posture; gait; tone of facial muscles; pupillary, palpebral, 

extensor thrust; and crossed-extensor thrust reflexes. Besides routine neuropathologic examinations, 

special studies included an examination of teased fibers from muscular and sural branches of the tibial 

nerve together with specimens from cervical and lumbar spinal cord. Absolute brain weights were 

decreased (5%) in male rats exposed to 80 ppm hydrogen sulfide in this study; however, there were no 

treatment-related effects on neurological function or neuropathology. No signs of neurotoxicity were 

noted in a similar study in which F-344 rats were exposed to 0, 10, 30, or 80 ppm hydrogen sulfide for 

90 days (CIIT 1983b). Likewise, no treatment-related neurological effects were observed in male and 

female B6C3F1 mice exposed to 0, 10.1, 30.5, or 80.0 ppm hydrogen sulfide for 90 days (CIIT 1983a). 

The highest NOAEL values and all reliable LOAEL values for neurological effects in rats, guinea pigs, 

mice, and rabbits from acute- or intermediate-duration studies are recorded in Table 3-1 and plotted in 

Figure 3-1. 

3.2.1.5 Reproductive Effects 

There are limited data on the reproductive toxicity of hydrogen sulfide in humans. Hemminki and Niemi 

(1982) examined the spontaneous abortion rate in relationship to maternal and paternal occupation and 

residential environmental pollution in an industrial community in Finland. Women who were employed 

in rayon textile and paper products jobs had an increased rate of spontaneous abortions (p<0.10), as did 

women whose husbands worked in rayon textile or chemical processing jobs. This study also examined 

the possible relationship between exposure to sulfur dioxide, hydrogen sulfide, and carbon disulfide and 

the occurrence of spontaneous abortions. A non-statistically significant increase in the incidence of 
HYDROGEN SULFIDE 69 

3. HEALTH EFFECTS 

spontaneous abortion was observed in women living in areas with hydrogen sulfide concentrations 

exceeding 2.85 ppm. Interpretation of these results are limited by the lack of control of other potential 

confounding variables, particularly occupational exposure to other chemicals. In a retrospective study of 

spontaneous abortions in a large population of women working in the petrochemical industry in China, 

Xu et al. (1998) reported a significantly increased risk of spontaneous abortion with frequent exposure to 

petrochemicals (OR of 2.7; 95% CI=1.8–3.9). When the risk associated with exposure to specific 

chemicals was examined, exposure to hydrogen sulfide was found to have an OR of 2.3 (95% CI=1.2– 

4.4). 

No treatment-related histopathological changes were found in male or female reproductive organs of 

F-344 or Sprague-Dawley rats or B6C3F1 mice exposed to TWA concentrations of 10, 30, or 80 ppm 

hydrogen sulfide for 6 hours/day, 5 days/week, for 90 days (CIIT 1983a, 1983b, 1983c). No significant 

alterations in gestation length, viability, or litter size were observed in Sprague-Dawley rats exposed to 0, 

20, 50, or 75 ppm hydrogen sulfide for 7 hours/day on gestation days 6–21 (Hayden et al. 1990b). An 

apparent increase in parturition time was observed in the hydrogen sulfide-exposed dams; the mean 

lengths of parturition were 105.0, 148.8, and 117.5 minutes, compared to 85.2, 124, and 82.5 minutes in 

the three control groups; these data were not statistically analyzed. The study authors noted that increased 

parturition time was observed in 6 out of 18 exposed animals and in 1 of 17 controls. Dorman et al. 

(2000) did not find any significant alterations in gestation length in Sprague-Dawley rats exposed to 10, 

30, or 80 ppm hydrogen sulfide for 6 hours/day, 7 days/week for 2 weeks prior to mating with exposed 

males, during the 2 week mating period, and on gestational days 0–19. This study also found no 

significant alterations in fertility (as assessed by mating index, fertility index, postimplantation loss, late 

resorptions, or still births), number of females with live pups, litter size, or number of implants per 

female. No histological alterations in the reproductive organs and accessory sex organs of rats in the 

controls and 80 ppm group were found; a slight, nonstatistically significant increase in the incidence of 

testicular degeneration was observed at 80 ppm. Additionally, no significant alterations in sperm count or 

morphology were observed. 

The highest NOAEL values for reproductive effects in rats and mice from intermediate-duration studies 

are recorded in Table 3-1 and plotted in Figure 3-1. 
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3. HEALTH EFFECTS 

3.2.1.6 Developmental Effects 

No studies were located regarding developmental effects in humans after inhalation exposure to hydrogen 

sulfide. 

No changes in serum protein, LDH, SGOT, or alkaline phosphatase activities were noted in the offspring 

of Sprague-Dawley rats exposed to 20, 50, or 75 ppm hydrogen sulfide for 7 hours/day from gestation 

day 1 through postnatal day 21 (Hayden et al. 1990a). No effects on blood glucose were noted in the 

offspring, although glucose levels were increased by about 50% in dams at all exposure concentrations on 

postnatal day 21 (Hayden et al. 1990a). In a second study, these authors (Hayden et al. 1990b) found a 

dose-related increase in parturition time in animals exposed to 20, 50, or 75 ppm hydrogen sulfide for 

7 hours/day from gestation day 6 until postpartum day 21. The study also showed developmental delays 

in pinna attachment and hair growth, but these effects were not dose related. 

No fetal effects were noted in a dose range-finding developmental study in which pregnant SpragueDawley rats were exposed to 150 ppm hydrogen sulfide on gestation days 6–20, despite body weight loss 

in the dams (Saillenfait et al. 1989). 

No significant alterations in the incidence of structural anomalies were found in the offspring of SpragueDawley rats exposed to 10, 30, or 80 ppm hydrogen sulfide 6 hours/day, 7 days/week on gestational days 

0–19 (Dorman et al. 2000). Continued exposure on postnatal days 5–18 did not result in developmental 

delays (pinnae detachment, surface righting, incisor eruption, negative geotaxis, and eyelid detachment), 

performance on developmental neurobehavioral tests (motor activity, passive avoidance, acoustic startle, 

or functional observation battery), or brain histopathology. 

An examination of Purkinje cells from Sprague-Dawley rat pups exposed to 20 or 50 ppm hydrogen 

sulfide for 7 hours/day from gestation day 5 through postpartum day 21 showed severe alterations in the 

architecture and growth characteristic of the Purkinje cell dendritic fields compared to controls (Hannah 

and Roth 1991). The study did not mention whether any maternal effects were observed; however, the 

authors did indicate that “these findings suggest that developing neurons exposed to low concentrations of 

hydrogen sulfide are at risk of severe deficits.” Two studies by Hannah et al. (1989, 1990) examined the 

effects of prenatal exposure to hydrogen sulfide on amino acid levels in the brain. In the first study, 

pregnant Sprague-Dawley rats were exposed to 75 ppm hydrogen sulfide for 7 hours/day, from postcoitus 

day 5 to postpartum day 21 (Hannah et al. 1989). Aspartate, glutamate, and GABA in the cerebrum and 
HYDROGEN SULFIDE 71 

3. HEALTH EFFECTS 

cerebellum were significantly reduced (about 20%) compared to controls by postpartum day 21. Taurine 

levels of the offspring were initially 25% higher than controls but had returned to control range by 

postpartum day 21; taurine levels were not measured in dams. In the 1990 study, pregnant SpragueDawley rats were exposed to 50 ppm hydrogen sulfide for 7 hours/day, from postcoital day 6 to 

postpartum day 21 (Hannah et al. 1990). In this study, maternal taurine levels were determined on 

parturition and on postpartum day 21. Taurine in maternal plasma was 30% higher than controls; taurine 

levels were not determined in offspring, so relating these levels to high taurine levels found in offspring in 

the 1989 study is speculative. 

Further investigation into the developmental neurological effects of hydrogen sulfide was undertaken by 

Skrajny et al. (1992). Pregnant Sprague-Dawley rats were exposed to 20 or 75 ppm hydrogen sulfide 

7 hours/day from gestation day 5 to postpartum day 21; separate control groups were used for each 

exposure level. Exposure to 20 ppm caused significant increases compared to controls in serotonin levels 

in the frontal cortex on postpartum day 21. Exposure to 75 ppm hydrogen sulfide caused significant 

increases compared to controls in levels of serotonin in the cerebellum and cortex on postpartum days 14 

and 21. Norepinephrine levels were significantly increased compared to controls at 75 ppm in the 

cerebellum and the frontal cortex. At 20 ppm, norepinephrine levels were below control levels by 

days 14 and 21, and in the cerebellum, levels fluctuated but were normal by postpartum day 21 (Skrajny 

et al. 1992). In a subsequent study using the same exposure regimen (i.e., between day 5 postcoital until 

day 21 postnatal), but following the monoamine levels in various regions of the brain up to 60 days 

postnatal, Roth et al. 1995 found that the alterations of monoamine levels observed at day 21 postnatal 

(the last day of exposure) gradually returned to control values by day 45. 

The highest NOAEL and all reliable LOAEL values for developmental effects in each species and 

duration category are recorded in Table 3-1 and plotted in Figure 3-1. 

3.2.1.7 Cancer 

There was no increase in cancer incidence noted in a residential cohort study of individuals living 

downwind from natural gas refineries in Alberta, Canada, from 1970 to 1984 (Schechter et al. 1989). In a 

retrospective epidemiologic study using cancer registry data from 1981 to 1990, Bates et al. (1998) 

evaluated the risk of cancer to known target organ systems of hydrogen sulfide toxicity in residents of 

Rotorua, a New Zealand city that uses geothermal energy for industrial and domestic heating purposes. 

No information on hydrogen sulfide levels was presented in this report, but the authors indicate concerns 
HYDROGEN SULFIDE 72 

3. HEALTH EFFECTS 

that exposures to hydrogen sulfide and/or mercury from geothermal sources could have health impacts. 

In their previous work, it was indicated that the most reliable monitoring information for hydrogen sulfide 

in the area came from a monitoring exercise in 1978 that found a median concentration of hydrogen 

sulfide of 20 μg/m3

, with 35% of the measurements over 70 μg/m3 and 10% over 400 μg/m3 (Bates et al. 

1997). Based on the cancer registry information, these workers found a significantly increased risk of 

nasal cancers (SIR=3.17; p=0.01) among Rotorua residents as compared to the rest of the population of 

New Zealand. However, since this is a rare cancer, this finding is based on only four cancers. Because 

the population of Rotorua has a higher percentage of Maoris than the rest of New Zealand, these 

researchers also examined their data stratified by ethnicity and sex and found a significantly increased 

risk of cancers of the trachea, bronchus, and lung (SIR=1.48; p=0.02) among female Maoris in Rotorua as 

compared to female Maoris in the rest of New Zealand. Differences in smoking history between these 

two populations were not sufficient to explain the observed differences in risk. The authors concluded 

that the lack of adequate exposure information did not permit findings of causal relationships between 

hydrogen sulfide and cancer incidence. The potential co-exposure to mercury also confounds the 

interpretation of these results. 

No studies were located regarding cancer effects in animals after inhalation exposure to hydrogen sulfide. 

3.2.2 Oral Exposure 

3.2.2.1 Death 

No studies were located regarding death in humans or animals after oral exposure to hydrogen sulfide. 

3.2.2.2 Systemic Effects 

No studies were located regarding respiratory, cardiovascular, hematological, musculoskeletal, hepatic, 

renal, endocrine, dermal, ocular, or metabolic effects after oral exposure to hydrogen sulfide. 

Gastrointestinal Effects. No studies were located regarding gastrointestinal effects in humans after 

oral exposure to hydrogen sulfide. 
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3. HEALTH EFFECTS 

Diarrheic digestive disorder was observed in adult pigs fed hydrogen sulfide at a dose level of 

15 mg/kg/day for a few days (Wetterau et al. 1964). The study authors reported that in a repeat study 

using younger pigs that weighed less, no diarrheic disorder was noted. 

Body Weight Effects. No studies were located regarding body weight effects in humans after oral 

exposure to hydrogen sulfide. 

Decreased body weight gain (48.2 kg total weight gain in treated animals versus 62.5 kg total weight gain 

in controls) was observed in pigs fed hydrogen sulfide at a dose level of 6.7 mg/kg/day for 105 days 

(Wetterau et al. 1964). 

No studies were located regarding the following health effects in humans or animals after oral exposure to 

hydrogen sulfide: 

3.2.2.3 Immunological and Lymphoreticular Effects 

3.2.2.4 Neurological Effects 

3.2.2.5 Reproductive Effects 

3.2.2.6 Developmental Effects 

3.2.2.7 Cancer 

3.2.3 Dermal Exposure 

3.2.3.1 Death 

No studies were located regarding death in humans after dermal exposure to hydrogen sulfide. 

A study by Laug and Draize (1942) reported death in two out of three rabbits exposed to unknown 

concentrations of hydrogen sulfide through either clipped, intact, or abraded skin. One rabbit with intact 

skin exposed to hydrogen sulfide for 2 hours survived, while another died in this interval. The rabbit 

exposed to hydrogen sulfide through abraded skin also died (Laug and Draize 1942). When two guinea 

pigs were exposed to unknown concentrations of hydrogen sulfide gas for 60 minutes on a small area of 

their shaved abdomen, neither died (Walton and Witherspoon 1925). However, both guinea pigs that had 

their entire shaved torso (about 50% body area) exposed to an unknown concentration of hydrogen sulfide 
HYDROGEN SULFIDE 74 

3. HEALTH EFFECTS 

died after about 45 minutes (Walton and Witherspoon 1925). No clinical signs of toxicity were seen in a 

dog with shaved abdomen exposed full body (except head) to unknown concentrations of hydrogen 

sulfide in a chamber for 1 hour (Walton and Witherspoon 1925). 

3.2.3.2 Systemic Effects 

No studies were located regarding respiratory, cardiovascular, gastrointestinal, hematological, 

musculoskeletal, hepatic, renal, endocrine, dermal, ocular, or body weight effects in humans or animals 

after dermal exposure to hydrogen sulfide. However, several sources indicate that care must be taken 

with liquefied hydrogen sulfide in order to avoid frostbite (Agency for Toxic Substances and Disease 

Registry 1994; NIOSH 2006). 

3.2.3.3 Immunological and Lymphoreticular Effects 

No studies were located regarding immunological and lymphoreticular effects in humans or animals after 

dermal exposure to hydrogen sulfide. 

3.2.3.4 Neurological Effects 

No studies were located regarding neurological effects in humans after dermal exposure to hydrogen 

sulfide. 

No clinical signs of neurotoxicity were seen in two guinea pigs exposed to an unknown concentration of 

hydrogen sulfide gas for 60 minutes on a small area of their shaved abdomen (Walton and Witherspoon 

1925). A dog exposed to an unknown concentration of hydrogen sulfide for 1 hour showed no clinical 

signs of neurotoxicity (Walton and Witherspoon 1925). 
HYDROGEN SULFIDE 75 

3. HEALTH EFFECTS 

No studies were located regarding the following health effects in humans or animals after dermal 

exposure to hydrogen sulfide: 

3.2.3.5 Reproductive Effects 

3.2.3.6 Developmental Effects 

3.2.3.7 Cancer 

3.3 GENOTOXICITY 

No studies were located regarding genotoxicity in humans after inhalation exposure to hydrogen sulfide. 

No mutagenicity was observed with hydrogen sulfide gas in Ames assays using Salmonella typhimurium 

TA97, TA98, and TA100 strains, either with or without S9 liver fractions, of male Syrian golden 

hamsters or Sprague-Dawley rats that had been induced with 500 mg/kg Aroclor 1254 (EPA 1984). 

However, it should be noted that the concentration of hydrogen sulfide gas was limited by its solubility in 

ethanol, which was the test solvent (EPA 1984). The highest dose that could be obtained was 

1,750 μg/plate. 

3.4 TOXICOKINETICS 

Although hydrogen sulfide is primarily absorbed through the lungs, it can also be absorbed through the 

gastrointestinal tract and intact skin (Laug and Draize 1942; Wetterau et al. 1964). It is metabolized 

through three pathways: oxidation, methylation, and reactions with metalloproteins or disulfidecontaining proteins (Beauchamp et al. 1984). Although the major metabolic pathway for detoxification of 

hydrogen sulfide is oxidation in the liver, the methylation pathway also serves as a detoxification route 

(EPA 1987a; Weisiger and Jakoby 1979). The major oxidation product of sulfide is thiosulfate, which is 

then believed to be converted to sulfate and subsequently excreted in urine (Bartholomew et al. 1980). 

Hydrogen sulfide is widely distributed in the body. Sulfides have been found in the liver, blood, brain, 

lungs, spleen, and kidneys of humans who died after accidental inhalation exposure. Hydrogen sulfide is 

excreted primarily as sulfate (free sulfate or thiosulfate) in the urine. It is also excreted unchanged in 

exhaled air and in feces and flatus. 
HYDROGEN SULFIDE 76 

3. HEALTH EFFECTS 

3.4.1 Absorption 

3.4.1.1 Inhalation Exposure 

Hydrogen sulfide is absorbed rapidly through the lungs (Adelson and Sunshine 1966; Allyn 1931; 

Breysse 1961; Deng and Chang 1987; Hagley and South 1983; Kimura et al. 1994; NIOSH 1989; Osbern 

and Crapo 1981; Parra et al. 1991). Inhalation absorption of lethal concentrations of hydrogen sulfide is 

rapid in humans, and effects can occur within seconds to minutes. Inhalation is the most common route 

of hydrogen sulfide exposure. Hydrogen sulfide dissociates at physiological pH to the hydrogen sulfide 

anion, which is probably the absorbed form (WHO 1987). No quantitative data are available regarding 

the absorption of hydrogen sulfide in humans. 

Animal data, while demonstrating that absorption of hydrogen sulfide via the lungs occurs readily and 

rapidly, are not sufficient to quantitatively determine the proportion of an inhaled dose that is absorbed 

(Beck et al. 1979; Kage et al. 1992; Khan et al. 1990; Lopez et al. 1989; Nagata et al. 1990; Prior et al. 

1988, 1990; Smith and Gosselin 1964; Tansy et al. 1981). No physiologically based pharmacokinetic 

(PBPK) models have been developed to provide estimates of hydrogen sulfide absorption. 

3.4.1.2 Oral Exposure 

Hydrogen sulfide exists as a gas; therefore, oral exposure to hydrogen sulfide will not normally occur. 

No studies were located regarding absorption in humans after oral exposure to hydrogen sulfide. Some 

case reports showing accidental oral ingestion of liquid manure or other substances that might contain 

hydrogen sulfide exist, but in all of these cases, the ingestion was secondary to being "knocked down" by 

inhalation of hydrogen sulfide (Freireich 1946; Imamura et al. 1996; Kimura et al. 1994; Osbern and 

Crapo 1981). 

One animal study suggests that hydrogen sulfide can be absorbed through the gastrointestinal tract. A 

study where pigs were fed diets containing dried greens with levels of hydrogen sulfide of 1.5, 3.1, or 

6.7 mg/kg/day for 105 days indicated that hydrogen sulfide is absorbed following ingestion (Wetterau et 

al. 1964). 
HYDROGEN SULFIDE 77 

3. HEALTH EFFECTS 

3.4.1.3 Dermal Exposure 

No studies were located regarding absorption in humans after dermal hydrogen sulfide exposure. 

Animal data have shown that dermal hydrogen sulfide absorption can occur, although large surface areas 

of skin must be exposed. Trunk fur of rabbits was clipped for exposure to unknown concentrations of 

hydrogen sulfide gas for 1.5–2 hours; evidence for the absorption of hydrogen sulfide included both the 

death of the animals and a positive sulfide reaction of expired air with lead acetate paper (Laug and 

Draize 1942). No evidence of dermal absorption was found in two guinea pigs exposed to unknown 

concentrations of hydrogen sulfide gas for 1 hour on a small area of their shaved abdomens (Walton and 

Witherspoon 1925). Dermal absorption was indicated, however, when the entire torso of guinea pigs was 

exposed to hydrogen sulfide gas and the animals died after about 45 minutes (Walton and Witherspoon 

1925). No clinical signs of toxicity were reported in a dog that received full-body exposure (except head) 

to unknown concentrations of hydrogen sulfide (Walton and Witherspoon 1925). 

3.4.2 Distribution 

3.4.2.1 Inhalation Exposure 

Few human data are available regarding tissue distribution after inhalation exposure to hydrogen sulfide. 

One case study reported sulfide (as bis[pentafluourobenzyl]sulfide) distribution in three of four men who 

drowned after being overcome, presumably, by hydrogen sulfide and falling unconscious into a lake in 

Japan (Kimura et al. 1994). Concentrations of hydrogen sulfide gas were estimated to be 550–650 ppm, 

based upon extrapolation of tissue concentrations from rat studies (Kimura et al. 1994; Nagata et al. 

1990). Initial blood sulfide concentrations determined 2–3 hours postmortem in these individuals were 

0.1, 0.2, and 0.08 μg/g tissue, while at 24 hours after death, the levels were 0.5 μg/g, 0.23 μg/g, and 

undetected, respectively. At 24 hours after death, sulfide concentrations in the brains of these individuals 

were 0.2, 0.4, and 1.06 μg/g, and lung concentrations were 0.68, 0.21, and 0.23 μg/g. Based on a study in 

rats by this same group of researchers (Nagata et al. 1990) that showed little or no increase in sulfide 

concentrations in rat lung and brain 24 hours after death, as well as a lack of sulfide in these tissues in 

control rats, Kimura et al. postulated that the sulfide levels observed in the brain and lungs in the human 

study may be indicators of tissue levels at the time of death (Kimura et al. 1994). Sulfide was detected in 

liver (1.30–1.56 μg/g), spleen (0.32–0.64 μg/g), and kidney (0.47–1.50 μg/g) (Kimura et al. 1994). 

Hydrogen sulfide levels of 0.92 μg/g in blood, 1.06 μg/g in brain, 0.34 μg/g in kidney, and 0.38 μg/g in 
HYDROGEN SULFIDE 78 

3. HEALTH EFFECTS 

liver were detected at autopsy in a man who was overcome by hydrogen sulfide in a tank (Winek et al. 

1968). Hydrogen sulfide concentrations in the tank after the accident were 1,900–6,100 ppm (Winek et 

al. 1968). 

Data from animal studies suggest that the distribution of inhaled hydrogen sulfide is rapid and 

widespread, while storage of hydrogen sulfide in the body is limited by rapid metabolism and excretion. 

Adult male rats exposed to 550 or 650 ppm hydrogen sulfide until death had tissue samples taken at 0, 4, 

24, and 48 hours after death (Nagata et al. 1990). Sulfide concentrations were measured 1, 7, and 30 days 

later. Immediately after death, sulfide concentrations in whole blood were 0.48 μg/g in exposed animals 

and were nondetectable in control animals. Sulfide concentrations rapidly increased with time after death 

in both control and treated animals. Significant increases in sulfide concentrations were found in the lung 

(0.60 μg/g), brain (0.31 μg/g), thigh muscle (0.21 μg/g), and abdominal muscles (0.22 μg/g), as compared 

to controls (tissues collected immediately after death) (Nagata et al. 1990). Liver and kidney samples had 

similar sulfide concentrations in both exposed and control groups when taken immediately after death. 

Certain tissues (blood, liver, and kidneys) exhibited an increase in sulfide concentration with time after 

death, whether hydrogen sulfide exposure occurred or not, while other tissues (lung, brain, and muscle) 

had little or no change in sulfide concentration (Nagata et al. 1990). 

Distribution of hydrogen sulfide in male Wistar rats was examined by Kohno et al. (1991). Animals 

exposed to 75 ppm hydrogen sulfide for 20, 40, or 60 minutes showed essentially the same distribution of 

hydrogen sulfide irrespective of duration: 10 μg/mL blood, 25 μg/g brain, 20 μg/g lung, 37 μg/g heart, 

20 μg/g liver, 25 μg/g spleen, and 30 μg/g kidney. The levels in the brain, lung, heart, liver, spleen, and 

kidney were significantly (p>0.01) higher than blood levels after 20 minutes of exposure. 

Japanese white rabbits exposed to 500–1,000 ppm of hydrogen sulfide (the lethal concentration), for 

60 minutes, had thiosulfate concentrations of 0.08 μmol/mL in blood, 0.095 μmol/g in lung, and 

0.023 μmol/g in brain (Kage et al. 1992). Little or no thiosulfate was found in the liver, kidney, or 

muscle. When rabbits were exposed to 100–200 ppm of hydrogen sulfide for 60 minutes, blood 

thiosulfate levels decreased from 0.061 μmol/mL immediately postexposure to a trace level at 2 hours 

postexposure (Kage et al. 1992). 
HYDROGEN SULFIDE 79 

3. HEALTH EFFECTS 

3.4.2.2 Oral Exposure 

No studies were located regarding tissue distribution in humans or animals after oral exposure to 

hydrogen sulfide. 

3.4.2.3 Dermal Exposure 

No studies were located regarding tissue distribution in humans or animals after dermal exposure to 

hydrogen sulfide. 

3.4.2.4 Other Routes of Exposure 

No studies were located regarding tissue distribution in humans or animals after hydrogen sulfide 

exposure by other routes. 

3.4.3 Metabolism 

Hydrogen sulfide metabolism occurs through three pathways: oxidation, methylation, and reaction with 

metallo- or disulfide-containing protein (Beauchamp et al. 1984; EPA 1987a). Hydrogen sulfide is 

primarily detoxified by oxidation reactions to sulfate (Tabacova 1986). Hydrogen sulfide can also be 

detoxified by methylation (EPA 1987a; Weisiger and Jakoby 1979). The proposed detoxification 

pathways most currently accepted for the metabolism of hydrogen sulfide are shown in Figure 3-2 and 

include oxidation and methylation, as well as the toxic pathways resulting from interactions with 

metalloproteins and disulfide-containing proteins. 

The major metabolic pathway for hydrogen sulfide in the body is the oxidation of sulfide to sulfate, which 

is excreted in the urine (Beauchamp et al. 1984). The major oxidation product of sulfide is thiosulfate, 

which is then converted to sulfate; the primary location for these reactions is in the liver (Bartholomew et 

al. 1980). 

Urinary thiosulfate levels were measured in volunteers exposed to 8, 18, or 30 ppm of hydrogen sulfide 

for 30–45 minutes and compared to levels in unexposed individuals at a pelt processing plant (Kangas and 

Savolainen 1987). Very little urinary thiosulfate was excreted in controls (2.9 μmol/mmol creatinine). 
containing 

Figure 3-2. Metabolic Pathways of Hydrogen Sulfide 

Thiol-S-methylCH3SH 

CH3SCH3 

Thiol-S-methylMethylation 

Metalloproteins

 (Fe, Cu) 

 Reaction 

consequences 

Detoxification 

Toxicity 

H2S 

S-Adenosyl­

 methionine 

Disulfde1. Methemoglobin, 

ferritin 

2. Cytochrom oxidase 

3. Catalase, peroxidase 

Succinic dehydrogenase 

Interactions with metalloproteins 

and disulfide-containing proteins 

proteins 

HS

 Heme 

compounds O2 

H2O + S

 Polysulfide 

intermediates 

Sulfide 

oxidase 

O2 

S2O3 

= 

(Thiosulfate) 

GSH 

HS-

+SO3 

=+GSSG 

NAPD+ 

NADPH 

GSH reductase 

Sulfite 

oxidase O2 

SO4 

= 

Oxidation 

 transferase 

 transferase 

HYDROGEN SULFIDE 80 

3. HEALTH EFFECTS 

­

Source: Adapted from Beauchamp et al. 1984 
HYDROGEN SULFIDE 81 

3. HEALTH EFFECTS 

The highest urinary thiosulfate levels among exposed individuals occurred 15 hours after exposure and 

decreased to control levels by 17 hours postexposure (Kangas and Savolainen 1987). Most absorbed 

hydrogen sulfide was already oxidized by 15 hours postexposure (Kangas and Savolainen 1987). This 

study was limited by the lack of summary data on exposed individuals and inadequate data regarding the 

numbers of subjects. Using perfused rat liver, Bartholomew et al. (1980) found that there was a rapid 

oxidation of 35S-sulfide to sulfate. Furthermore, there was a decrease in thiosulfate released from the liver 

when nonlabelled thiosulfate was added to the perfusion system, suggesting that thiosulfate may act as an 

intermediate in the oxidation to sulfate (Bartholomew et al. 1980). 

Japanese white rabbits exposed to 500–1,000 ppm hydrogen sulfide (the lethal concentration, for 14– 

30 minutes) had thiosulfate concentrations of 0.08 μM/mL in blood, 0.095 μM/g in lung, and 0.023 μM/g 

in brain (Kage et al. 1992). Although sulfide was not detected in blood or urine samples of rabbits 

exposed to a concentration of 100–200 ppm hydrogen sulfide for 60 minutes, thiosulfate levels were 

highest (1.2 μM/mL) 1–2 hours after exposure and could still be detected in urine 24 hours after exposure 

(Kage et al. 1992). Thiosulfate levels in blood peaked (0.061 μM/mL) immediately after exposure and 

were undetectable after 4 hours (Kage et al. 1992). 

Evidence for the methylation of hydrogen sulfide comes primarily from in vitro studies of SpragueDawley rats' intestinal mucosa (Weisiger et al. 1980). Thiol S-methyltransferase catalyzed the 

methylation of hydrogen sulfide to methanethiol (CH3SH). Methanethiol can act as a substrate for 

another methylation also catalyzed by thiol S-methyltransferase, yielding dimethylsulfide (CH3SCH3). 

The activity of thiol S-methyltransferase was widely distributed, with the greatest in cecal and colonic 

mucosa, liver, lung, and kidney, and was also found in other parts of the intestine and stomach, spleen, 

heart, and skeletal muscle. No enzyme activity was found in the feces. Although it has been postulated 

that methylation is a method of detoxification of hydrogen sulfide, a constituent of human flatus produced 

in the intestine, the extent to which the toxicity of exogenous hydrogen sulfide is attenuated by 

methylation is not known. 

The interaction of hydrogen sulfide with metalloproteins was postulated because the mechanism of 

toxicity for hydrogen sulfide is the inhibition of cytochrome oxidase and thus, inhibition of the electron 

transport system. It appears that hydrogen sulfide interacts with other metalloproteins and may represent 

a detoxification pathway in some instances (Beauchamp et al. 1984). Reduction of disulfide bridges by 

hydrogen sulfide was suggested by Smith and Abbanat (1966), who found that mice were protected from 

lethal concentrations of hydrogen sulfide by the administration of oxidized glutathione. This protection 
HYDROGEN SULFIDE 82 

3. HEALTH EFFECTS 

was not afforded by the administration of reduced glutathione. The study authors believed that the 

disulfide linkage of the oxidized glutathione interacted with the hydrosulfide, which prevented the 

reaction of sulfide with other sites (Smith and Abbanat 1966). This is attributed to the polarizability of 

the disulfide bond. The nucleophilic sulfhydryl group of hydrogen sulfide reacts with the δ+

 of the 

disulfide bond, thus converting it to a less toxic product. 

No studies were located regarding metabolism in humans or animals after oral, dermal, or other routes of 

exposure to hydrogen sulfide. 

3.4.4 Elimination and Excretion 

3.4.4.1 Inhalation Exposure 

The major metabolic pathway for hydrogen sulfide in the body is oxidation of sulfide to sulfate, with the 

sulfate being excreted in the urine (Beauchamp et al. 1984). Thiosulfate excretion was measured in 

volunteers exposed to 8, 18, or 30 ppm of hydrogen sulfide for 30–45 minutes and compared to that of 

unexposed individuals at a pelt processing plant (Kangas and Savolainen 1987). The study did not report 

the summary results of all exposed individuals; however, data from one individual exposed to 18 ppm 

hydrogen sulfide for 30 minutes found urinary thiosulfate concentrations of approximately 2, 4, 7, 30, and 

5 μM/mM creatinine at 1, 2, 5, 15, and 17 hours postexposure, respectively. The highest urinary 

thiosulfate levels among exposed individuals occurred 15 hours after exposure and dropped to control 

levels by 17 hours postexposure. 

Kage et al. (1992) evaluated sulfide and thiosulfate levels in the blood and urine of Japanese white rabbits 

exposed to 100–200 ppm for 60 minutes and concluded that thiosulfate was a better marker for exposure 

since it could be detected immediately in the blood, but also was detectable in the urine 24 hours after 

exposure. In the blood, thiosulfate levels decreased from 0.061 μM/mL immediately following exposure 

to an undetectable amount after 4 hours (Kage et al. 1992). In urine samples from these same animals, 

thiosulfate levels were highest (1.2 μM/mL) 1–2 hours after exposure, but were still detectable after 

24 hours of exposure at slightly higher level than that of control (Kage et al. 1992). 

3.4.4.2 Oral Exposure 

No studies were located regarding excretion in humans or animals after oral exposure to hydrogen sulfide. 
HYDROGEN SULFIDE 83 

3. HEALTH EFFECTS 

3.4.4.3 Dermal Exposure 

No studies were located regarding excretion in humans after dermal exposure to hydrogen sulfide. 

Excretion of hydrogen sulfide was documented after dermal exposure in rabbits. Trunk fur of rabbits was 

clipped and left intact or abraded for exposure to hydrogen sulfide gas (unknown concentrations) for 1.5– 

2 hours; the animals then breathed clean air (Laug and Draize 1942). Evidence for the excretion of 

hydrogen sulfide by the rabbits was a sulfide reaction of the expired air with lead acetate paper (Laug and 

Draize 1942). Sulfides in the expired air were noted in one rabbit with intact skin after 7 minutes of 

exposure. This study was limited by the lack of measurement of exposure concentrations and the small 

number of animals used. 

3.4.5 Physiologically Based Pharmacokinetic (PBPK)/Pharmacodynamic (PD) Models 

Physiologically based pharmacokinetic (PBPK) models use mathematical descriptions of the uptake and 

disposition of chemical substances to quantitatively describe the relationships among critical biological 

processes (Krishnan et al. 1994). PBPK models are also called biologically based tissue dosimetry 

models. PBPK models are increasingly used in risk assessments, primarily to predict the concentration of 

potentially toxic moieties of a chemical that will be delivered to any given target tissue following various 

combinations of route, dose level, and test species (Clewell and Andersen 1985). Physiologically based 

pharmacodynamic (PBPD) models use mathematical descriptions of the dose-response function to 

quantitatively describe the relationship between target tissue dose and toxic end points. 

PBPK/PD models refine our understanding of complex quantitative dose behaviors by helping to 

delineate and characterize the relationships between: (1) the external/exposure concentration and target 

tissue dose of the toxic moiety, and (2) the target tissue dose and observed responses (Andersen and 

Krishnan 1994; Andersen et al. 1987). These models are biologically and mechanistically based and can 

be used to extrapolate the pharmacokinetic behavior of chemical substances from high to low dose, from 

route to route, between species, and between subpopulations within a species. The biological basis of 

PBPK models results in more meaningful extrapolations than those generated with the more conventional 

use of uncertainty factors. 
HYDROGEN SULFIDE 84 

3. HEALTH EFFECTS 

The PBPK model for a chemical substance is developed in four interconnected steps: (1) model 

representation, (2) model parameterization, (3) model simulation, and (4) model validation (Krishnan and 

Andersen 1994). In the early 1990s, validated PBPK models were developed for a number of 

toxicologically important chemical substances, both volatile and nonvolatile (Krishnan and Andersen 

1994; Leung 1993). PBPK models for a particular substance require estimates of the chemical substancespecific physicochemical parameters, and species-specific physiological and biological parameters. The 

numerical estimates of these model parameters are incorporated within a set of differential and algebraic 

equations that describe the pharmacokinetic processes. Solving these differential and algebraic equations 

provides the predictions of tissue dose. Computers then provide process simulations based on these 

solutions. 

The structure and mathematical expressions used in PBPK models significantly simplify the true 

complexities of biological systems. If the uptake and disposition of the chemical substance(s) are 

adequately described, however, this simplification is desirable because data are often unavailable for 

many biological processes. A simplified scheme reduces the magnitude of cumulative uncertainty. The 

adequacy of the model is, therefore, of great importance, and model validation is essential to the use of 

PBPK models in risk assessment. 

PBPK models improve the pharmacokinetic extrapolations used in risk assessments that identify the 

maximal (i.e., the safe) levels for human exposure to chemical substances (Andersen and Krishnan 1994). 

PBPK models provide a scientifically sound means to predict the target tissue dose of chemicals in 

humans who are exposed to environmental levels (for example, levels that might occur at hazardous waste 

sites) based on the results of studies where doses were higher or were administered in different species. 

Figure 3-3 shows a conceptualized representation of a PBPK model. 

No PBPK models have been developed for hydrogen sulfide. 

3.5 MECHANISMS OF ACTION 

3.5.1 Pharmacokinetic Mechanisms 

Hydrogen sulfide is primarily absorbed through the lungs. It can also be absorbed through the 

gastrointestinal tract and the skin. Hydrogen sulfide is widely distributed in the body after inhalation 

exposure. Based on analyses of tissues from humans who died after accidental exposure, sulfides have 

 


 


 

HYDROGEN SULFIDE 85 

3. HEALTH EFFECTS 

Figure 3-3. Conceptual Representation of a Physiologically Based 

Pharmacokinetic (PBPK) Model for a 

Hypothetical Chemical Substance 

Lungs 

Liver 

Fat 

Slowly 

perfused 

tissues 

Richly 

perfused 

tissues 

Kidney 

Skin 

V 

E 

N 

O 

U 

S 

B 

L 

O 

O 

D 

A 

R 

T 

E 

R 

I 

A 

L 

B 

L 

O 

O 

D 

Vmax Km 

Ingestion 

GI 

Tract 

Feces 

Urine

Inhaled chemical Exhaled chemical 

 Chemicals in air 

contacting skin 

Source: Adapted from Krishnan et al. 1994 

Note: This is a conceptual representation of a physiologically based pharmacokinetic (PBPK) model for a 

hypothetical chemical substance. The chemical substance is shown to be absorbed via the skin, by inhalation, or by 

ingestion, metabolized in the liver, and excreted in the urine or by exhalation. 
HYDROGEN SULFIDE 86 

3. HEALTH EFFECTS 

been detected in the liver, blood, brain, lungs, spleen, and kidneys. Hydrogen sulfide is metabolized by 

oxidation, methylation, and reaction with metalloproteins or disulfide-containing proteins. The major 

metabolic pathway for detoxification of hydrogen sulfide is oxidation of the sulfide to sulfate in the liver. 

Hydrogen sulfide is excreted primarily as sulfate in the urine. 

3.5.2 Mechanisms of Toxicity 

Exposure to hydrogen sulfide at concentrations of 500 ppm and greater causes an initial increase in the 

rate of respiration as a result of the stimulation of the carotid bodies, chemosensors associated with 

ventilatory control (Ammann 1986). Under normal conditions, these chemosensors stimulate ventilation 

of the lung during extreme cases in which a significant decrease in the partial pressure of oxygen in the 

arterial blood traveling to the head occurs (Ammann 1986). This action results in an increase in the 

number of impulses originating from the chemosensors to the respiratory center in the brain. The rate and 

depth of ventilation increases to the point of hyperpnea (rapid, deep breathing). 

Direct inhibition of cellular enzymes has been postulated as one of many underlying mechanisms of 

toxicity of hydrogen sulfide (Beauchamp et al. 1984; Deng 1992). In particular, cytochrome oxidase, an 

enzyme involved in cellular oxidative processes and energy production, has been implicated. Inhibition 

of cytochrome oxidase is believed to disrupt the electron transport chain and to significantly impair 

oxidative metabolism, leading to anaerobic metabolism, severely decreased ATP production with 

curtailed cellular energy generation, and the generation of lactic acid. Nervous and cardiac tissues, which 

have the highest oxygen demand, are especially sensitive to the disruption of oxidative metabolism 

(Ammann 1986). In the central nervous system, this effect may result in death from respiratory arrest. 

Inhibition of cytochrome oxidase by hydrogen sulfide is similar to that of cyanide (Smith and Gosselin 

1979). Although the suggestion has been frequently made that the effects of hydrogen sulfide on nervous 

tissue are, as with cyanide, simply due to inhibition of oxidative metabolism, recent authors suggest that 

this is not the case. Reiffenstein et al. (1992) examined this issue and concluded that while treatment with 

hydrogen sulfide and anoxic conditions arrive at the same end point, there are pharmacological 

dissimilarities. Baldelli et al. (1993) investigated the mechanism of toxicity associated with hydrogen 

sulfide exposure (achieved by intravenous injection of sodium sulfide) and concluded that it resulted not 

from a direct toxicity on central nervous system neurons (i.e., a ‘cerebral necrosis’ due to poisoning of 

mitochondria respiration), but rather, from an indirect effect associated with a profound hypotension most 

likely due to cardiotoxicity. These authors emphasized the importance of immediate cardiopulmonary 
HYDROGEN SULFIDE 87 

3. HEALTH EFFECTS 

resuscitation as a way to prevent the delayed toxicity associated with hydrogen sulfide “knock-down” 

exposures. 

An electrophysiological study of the effects of hydrogen sulfide on membrane and synaptic properties of 

dorsal raphe serotonergic cells in an in vitro rat brain-stem slice preparation has elucidated a possible 

mechanism of neurotoxicity of hydrogen sulfide (Kombian et al. 1993). These neurons are considered to 

play an important role in central nervous system control of respiratory rhythm. Hydrogen sulfide has 

been shown to produce two reversible, concentration-dependent effects on the resting membrane 

properties of the dorsal raphe neurons. Some neurons (14%) responded to hydrogen sulfide with an 

outward current accompanied by an increase in conductance, while 39% of the neurons responded with a 

rapid-onset depolarization corresponding to a weakly voltage-dependent inward current showing little or 

no change in conductance. In addition, 30% of the neurons displayed both types of responses. Finally, 

18% of the neurons were unresponsive to hydrogen sulfide. The outward current induced by hydrogen 

sulfide was demonstrated to be caused by an elevated conductance to potassium, whereas the hydrogen 

sulfide-induced inward current is carried by calcium ions. However, the mechanism of calcium ion entry 

is not clear. 

Hydrogen sulfide was shown to inhibit, in a concentration-dependent fashion, all components of the 

complex evoked synaptic responses of the dorsal raphe serotonergic neurons (Kombian et al. 1993). This 

effect was rapid and reversible, and involved both pre- and postsynaptic mechanisms. Similar effects of 

hydrogen sulfide on brain hippocampal CA1 neurons have been reported. The electrophysiological 

effects of hydrogen sulfide are comparable to those elicited by anoxia. The neuronal action of hydrogen 

sulfide may involve an interaction with free thiols and disulfide bonds present in most membrane 

proteins. Collectively, the electrophysiology data suggest a possible role of the effects of hydrogen 

sulfide on synaptic and membrane properties of the dorsal raphe serotonergic neurons of the brain stem in 

the cessation of respiratory drive following acute hydrogen sulfide exposure. 

Inhibition of monoamine oxidase has been proposed as a possible mechanism underlying the hydrogen 

sulfide–mediated disruption of neurotransmission in brain stem nuclei controlling respiration (Warenycia 

et al. 1989a). Administration of sodium hydrosulfide, an alkali salt of hydrogen sulfide, has been shown 

to increase brain catecholamine and serotonin levels in rats. It has also been suggested that persulfide 

formation resulting from sulfide interaction with tissue cystine and cystinyl peptides may underlie some 

aspects of hydrogen sulfide neurotoxicity, including inhibition of monoamine oxidase (Warenycia et al. 

1990). 
HYDROGEN SULFIDE 88 

3. HEALTH EFFECTS 

3.5.3 Animal-to-Human Extrapolations 

The toxicokinetic disposition of hydrogen sulfide in humans is not understood. However, available 

toxicity and toxicokinetic data indicate that hydrogen sulfide can be readily absorbed through the lung 

and, to a lesser and clinically irrelevant extent, through the gastrointestinal tract and skin. Although the 

metabolism of hydrogen sulfide has been characterized in animals, there are limited data to suggest that 

the metabolism of hydrogen sulfide may be in part similar in humans. For instance, human data indicate 

that hydrogen sulfide is oxidized to sulfate and thiosulfate and excreted in the urine. Neurotoxicity 

induced by hydrogen sulfide has been observed in experimental animals and humans. 

3.6 TOXICITIES MEDIATED THROUGH THE NEUROENDOCRINE AXIS 

Recently, attention has focused on the potential hazardous effects of certain chemicals on the endocrine 

system because of the ability of these chemicals to mimic or block endogenous hormones. Chemicals 

with this type of activity are most commonly referred to as endocrine disruptors. However, appropriate 

terminology to describe such effects remains controversial. The terminology endocrine disruptors, 

initially used by Thomas and Colborn (1992), was also used in 1996 when Congress mandated the EPA to 

develop a screening program for “...certain substances [which] may have an effect produced by a 

naturally occurring estrogen, or other such endocrine effect[s]...”. To meet this mandate, EPA convened a 

panel called the Endocrine Disruptors Screening and Testing Advisory Committee (EDSTAC), and in 

1998, the EDSTAC completed its deliberations and made recommendations to EPA concerning endocrine 

disruptors. In 1999, the National Academy of Sciences released a report that referred to these same types 

of chemicals as hormonally active agents. The terminology endocrine modulators has also been used to 

convey the fact that effects caused by such chemicals may not necessarily be adverse. Many scientists 

agree that chemicals with the ability to disrupt or modulate the endocrine system are a potential threat to 

the health of humans, aquatic animals, and wildlife. However, others think that endocrine-active 

chemicals do not pose a significant health risk, particularly in view of the fact that hormone mimics exist 

in the natural environment. Examples of natural hormone mimics are the isoflavinoid phytoestrogens 

(Adlercreutz 1995; Livingston 1978; Mayr et al. 1992). These chemicals are derived from plants and are 

similar in structure and action to endogenous estrogen. Although the public health significance and 

descriptive terminology of substances capable of affecting the endocrine system remains controversial, 

scientists agree that these chemicals may affect the synthesis, secretion, transport, binding, action, or 
HYDROGEN SULFIDE 89 

3. HEALTH EFFECTS 

elimination of natural hormones in the body responsible for maintaining homeostasis, reproduction, 

development, and/or behavior (EPA 1997). Stated differently, such compounds may cause toxicities that 

are mediated through the neuroendocrine axis. As a result, these chemicals may play a role in altering, 

for example, metabolic, sexual, immune, and neurobehavioral function. Such chemicals are also thought 

to be involved in inducing breast, testicular, and prostate cancers, as well as endometriosis (Berger 1994; 

Giwercman et al. 1993; Hoel et al. 1992). 

No studies were identified on the potential for hydrogen sulfide to disrupt the function of the neuronendocrine axis. 

3.7 CHILDREN’S SUSCEPTIBILITY 

This section discusses potential health effects from exposures during the period from conception to 

maturity at 18 years of age in humans, when all biological systems will have fully developed. Potential 

effects on offspring resulting from exposures of parental germ cells are considered, as well as any indirect 

effects on the fetus and neonate resulting from maternal exposure during gestation and lactation. 

Relevant animal and in vitro models are also discussed. 

Children are not small adults. They differ from adults in their exposures and may differ in their 

susceptibility to hazardous chemicals. Children’s unique physiology and behavior can influence the 

extent of their exposure. Exposures of children are discussed in Section 6.6, Exposures of Children. 

Children sometimes differ from adults in their susceptibility to hazardous chemicals, but whether there is 

a difference depends on the chemical (Guzelian et al. 1992; NRC 1993). Children may be more or less 

susceptible than adults to health effects, and the relationship may change with developmental age 

(Guzelian et al. 1992; NRC 1993). Vulnerability often depends on developmental stage. There are 

critical periods of structural and functional development during both prenatal and postnatal life, and a 

particular structure or function will be most sensitive to disruption during its critical period(s). Damage 

may not be evident until a later stage of development. There are often differences in pharmacokinetics 

and metabolism between children and adults. For example, absorption may be different in neonates 

because of the immaturity of their gastrointestinal tract and their larger skin surface area in proportion to 

body weight (Morselli et al. 1980; NRC 1993); the gastrointestinal absorption of lead is greatest in infants 

and young children (Ziegler et al. 1978). Distribution of xenobiotics may be different; for example, 

infants have a larger proportion of their bodies as extracellular water, and their brains and livers are 
HYDROGEN SULFIDE 90 

3. HEALTH EFFECTS 

proportionately larger (Altman and Dittmer 1974; Fomon 1966; Fomon et al. 1982; Owen and Brozek 

1966; Widdowson and Dickerson 1964). The infant also has an immature blood-brain barrier (Adinolfi 

1985; Johanson 1980) and probably an immature blood-testis barrier (Setchell and Waites 1975). Many 

xenobiotic metabolizing enzymes have distinctive developmental patterns. At various stages of growth 

and development, levels of particular enzymes may be higher or lower than those of adults, and 

sometimes unique enzymes may exist at particular developmental stages (Komori et al. 1990; Leeder and 

Kearns 1997; NRC 1993; Vieira et al. 1996). Whether differences in xenobiotic metabolism make the 

child more or less susceptible also depends on whether the relevant enzymes are involved in activation of 

the parent compound to its toxic form or in detoxification. There may also be differences in excretion, 

particularly in newborns who all have a low glomerular filtration rate and have not developed efficient 

tubular secretion and resorption capacities (Altman and Dittmer 1974; NRC 1993; West et al. 1948). 

Children and adults may differ in their capacity to repair damage from chemical insults. Children also 

have a longer remaining lifetime in which to express damage from chemicals; this potential is particularly 

relevant to cancer. 

Certain characteristics of the developing human may increase exposure or susceptibility, whereas others 

may decrease susceptibility to the same chemical. For example, although infants breathe more air per 

kilogram of body weight than adults breathe, this difference might be somewhat counterbalanced by their 

alveoli being less developed, which results in a disproportionately smaller surface area for alveolar 

absorption (NRC 1993). 

Although there is a fair amount of data on the toxicity of hydrogen sulfide in humans, there is very little 

information to judge the impacts of exposure to hydrogen sulfide in infants and children. In adults, 

exposure to high concentrations of hydrogen sulfide can result in unconsciousness followed by an 

apparent complete recovery. At lower exposure levels, exposure to hydrogen sulfide can result in less 

severe neurological (e.g., incoordination, poor memory, olfactory impairment) and respiratory symptoms. 

Animal data suggest that the respiratory tract, particularly the nasal olfactory epithelium, may be the most 

sensitive target following hydrogen sulfide exposure. It is likely that similar toxicological effects will be 

seen in children. 

Available human data suggest that maternal or paternal exposure may increase the risk of spontaneous 

abortions (Hemminki and Niemi 1982; Xu et al. 1998). However, co-exposure to other chemicals 

precludes establishing a causal relationship from these data. Animal studies did not find structural 

anomalies, developmental delays, or alterations in performance on developmental neurobehavioral tests 
HYDROGEN SULFIDE 91 

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or brain histology in the offspring of animals exposed to 80 ppm or lower hydrogen sulfide during 

gestation (Dorman et al. 2000; Hayden et al. 1990a; Saillenfait et al. 1989). In contrast, alterations in 

Purkinje cells (Hannah et al. 1990), brain amino acid levels (Hannah et al. 1989), and neurotransmitter 

levels (Skrajny et al. 1992) have been observed in rat offspring exposed to low levels (20–75 ppm) of 

hydrogen sulfide during gestation. However, the toxicological significance of these alterations in the 

absence of alterations in neurobehavioral performance is not known. 

3.8 BIOMARKERS OF EXPOSURE AND EFFECT 

Biomarkers are broadly defined as indicators signaling events in biologic systems or samples. They have 

been classified as markers of exposure, markers of effect, and markers of susceptibility (NAS/NRC 

1989). 

Due to a nascent understanding of the use and interpretation of biomarkers, implementation of biomarkers 

as tools of exposure in the general population is very limited. A biomarker of exposure is a xenobiotic 

substance or its metabolite(s) or the product of an interaction between a xenobiotic agent and some target 

molecule(s) or cell(s) that is measured within a compartment of an organism (NAS/NRC 1989). The 

preferred biomarkers of exposure are generally the substance itself, substance-specific metabolites in 

readily obtainable body fluid(s), or excreta. However, several factors can confound the use and 

interpretation of biomarkers of exposure. The body burden of a substance may be the result of exposures 

from more than one source. The substance being measured may be a metabolite of another xenobiotic 

substance (e.g., high urinary levels of phenol can result from exposure to several different aromatic 

compounds). Depending on the properties of the substance (e.g., biologic half-life) and environmental 

conditions (e.g., duration and route of exposure), the substance and all of its metabolites may have left the 

body by the time samples can be taken. It may be difficult to identify individuals exposed to hazardous 

substances that are commonly found in body tissues and fluids (e.g., essential mineral nutrients such as 

copper, zinc, and selenium). Biomarkers of exposure to hydrogen sulfide are discussed in Section 3.8.1. 

Biomarkers of effect are defined as any measurable biochemical, physiologic, or other alteration within an 

organism that, depending on magnitude, can be recognized as an established or potential health 

impairment or disease (NAS/NRC 1989). This definition encompasses biochemical or cellular signals of 

tissue dysfunction (e.g., increased liver enzyme activity or pathologic changes in female genital epithelial 

cells), as well as physiologic signs of dysfunction such as increased blood pressure or decreased lung 

capacity. Note that these markers are not often substance specific. They also may not be directly 
HYDROGEN SULFIDE 92 

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adverse, but can indicate potential health impairment (e.g., deoxyribonucleic acid adducts). Biomarkers 

of effects caused by hydrogen sulfide are discussed in Section 3.8.2. 

A biomarker of susceptibility is an indicator of an inherent or acquired limitation of an organism's ability 

to respond to the challenge of exposure to a specific xenobiotic substance. It can be an intrinsic genetic or 

other characteristic or a preexisting disease that results in an increase in absorbed dose, a decrease in the 

biologically effective dose, or a target tissue response. If biomarkers of susceptibility exist, they are 

discussed in Section 3.10, Populations That Are Unusually Susceptible. 

3.8.1 Biomarkers Used to Identify or Quantify Exposure to Hydrogen Sulfide 

The most frequently used biomarker of hydrogen sulfide exposure is urinary thiosullfate levels (Milby 

and Baselt 1999). Thiosulfate is an oxidation product of hydrogen sulfide metabolism and is not specific 

to hydrogen sulfide metabolism. Ingestion of food or water with a high sulfur content can also increase 

urinary thiosulfate concentrations (Milby and Baselt 1999). An increase in urinary thiosulfate levels were 

observed in individuals exposed to 8, 18, or 30 ppm hydrogen sulfide for 30–45 minutes (Kangas and 

Savolainen 1987). The urinary thiosulfate levels peaked approximately 15 hours after exposure. In a 

subject exposed to 18 ppm for 30 minutes, the peak urinary thiosulfate concentration at 15 hours was 

30 μmol/mmol creatinine; 17 hours after exposure, the urinary thiosulfate levels were similar to nonexposed individuals (mean concentration of 2.9 μmol/mmol creatinine). A quantitative relationship 

between hydrogen sulfide exposure levels and urinary thiosulfate levels has not been established. 

Measurement of blood sulfide levels has also been proposed as a biomarker of exposure (Jappinen and 

Tenhunen 1990). This has limited clinical value because the blood samples must be collected within 

2 hours of exposure (Jappinen and Tenhunen 1990). As with urinary thiosulate levels, a relationship 

between airborne hydrogen sulfide levels and blood sulfide levels has not been established. 

Jappinen and Tenhunen (1990) also investigated the use of alterations in blood heme metabolism as a 

possible biomarker of hydrogen sulfide exposure. The activities of the enzymes of heme synthesis, i.e., 

delta-aminolaevulinic acid synthase (ALA-S) and heme synthase, were examined in 21 cases of acute 

hydrogen sulfide toxicity in Finnish pulp mill and oil refinery workers exposed to 20–200 ppm hydrogen 

sulfide for periods ranging from approximately 1 minute up to 3.5 hours. Several subjects lost 

consciousness for up to 3 minutes. Activities of delta-aminolaevulinic acid synthase and heme synthase 

were decreased after exposure to hydrogen sulfide. However, the changes in heme metabolism are not 
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specific for hydrogen sulfide, and other sulfur-containing compounds, such as methyl mercaptan, can 

produce similar effects. 

3.8.2 Biomarkers Used to Characterize Effects Caused by Hydrogen Sulfide 

Hydrogen sulfide-specific biomarkers of effect have not been identified. Potential biomarkers for 

neurological effects of hydrogen sulfide include indices of cortical, hippocampal, brain stem, basal 

ganglia, and diencephalon dysfunction. An oil-field worker who became unconscious following exposure 

to hydrogen sulfide had a diminished vibration sense, delayed visual reaction times, abnormal balance 

with eyes closed, slow blink reflex latency, impaired verbal and visual recall, and decreased cognitive 

performance (Kilburn 1993). Cortical function tests revealed deficits in verbal abstraction, attention, and 

short-term retention in a hydrogen sulfide-poisoned patient (Stine et al. 1976). A 5-year neuropsychological re-examination of patients who lost consciousness after hydrogen sulfide exposure revealed 

neurological impairment (Tvedt et al. 1991b); memory and motor function were most affected. Such 

neurological effects are not specific for hydrogen sulfide and could indicate exposure to other neurotoxic 

substances. 

3.9 INTERACTIONS WITH OTHER CHEMICALS 

In a group of Belgian viscose rayon workers exposed to 0.14 or 6.4 ppm of hydrogen sulfide and at least 

26 mg/m3

 of carbon disulfide, the incidence of eye irritation was significantly higher in all hydrogen 

sulfide-exposed workers than in unexposed controls (Vanhoorne et al. 1995). Control for confounders 

such as cigarette smoke was not performed (Vanhoorne et al. 1995). Simultaneous exposure of SpragueDawley rats to 500 ppm of carbon disulfide and 50 ppm of hydrogen sulfide 5 days/week, for 25 weeks, 

had no interactive effect on sensory tail nerve conduction velocities (SNCV) or motor tail nerve 

conduction velocities (MNCV) (Gagnaire et al. 1986). Additionally, the amount of 2-thio-thiazolidine-4-carboxylic acid, a urinary metabolite of carbon disulfide excreted in urine after exposure to 

carbon disulfide, was unaffected by hydrogen sulfide exposure (Gagnaire et al. 1986). In a series of 

reproductive and developmental studies in which albino rats were exposed to hydrogen sulfide and carbon 

disulfide, both pre- and postimplantational lethality as well as developmental anomalies of the genitourinary and skeletal systems were reported (Barilyak et al. 1975). However, in some cases, these effects 

occurred in conjunction with maternal toxicity. It is not clear whether the reported concentration 
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(10 mg/m3) to which the animals were exposed includes both hydrogen sulfide and carbon disulfide or 

represents individual concentrations of each chemical. 

There appears to be some evidence that ethanol can increase the effects of hydrogen sulfide. In six cases, 

less hydrogen sulfide was needed for toxic effects to be observed when workers had consumed alcohol 

16–24 hours earlier (Poda 1966). 

Much of the occupational data on hydrogen sulfide comes from studies of pulp and paper mill workers 

who were exposed to other compounds in addition to hydrogen sulfide. An increase in chronic or 

recurrent headache was noted in Finnish pulp workers who were exposed simultaneously to hydrogen 

sulfide, methyl mercaptans, and sulfur dioxide (Kangas et al. 1984). Peak concentrations of the 

chemicals, up to 20 ppm hydrogen sulfide, were believed to be responsible for the occurrence of the 

symptoms, rather than the lower mean concentrations. A respiratory survey of almost 2,000 Canadian 

pulp and paper mill workers did not show any increases in the prevalence of respiratory symptoms or 

pulmonary function abnormalities among exposed workers (Chan-Yeung et al. 1980). Mean exposure 

concentrations of toxicants measured in this study were 0.05 ppm hydrogen sulfide, 0.3 ppm sulfur 

dioxide, 8.3 ppm carbon monoxide, 0.8 ppm total particulates, and <0.05 ppm chlorine. 

No changes in body weight or microscopic changes in respiratory tract, eye, or visceral organs were noted 

in crossbred pigs inhaling 2 ppm of hydrogen sulfide and 50 ppm of ammonia continuously for 19 days 

when compared to controls (Curtis et al. 1975). The toxicity of hydrogen sulfide after dermal exposure 

was found to be enhanced by dermal exposure to ammonia (Laug and Draize 1942). 

Male Wistar rats were administered 330 or 660 mg/kg of ethanol intraperitoneally 30 minutes before 

being exposed to 800 ppm of hydrogen sulfide for a maximum of 20 minutes, which was a potentially 

fatal hydrogen sulfide exposure (Beck et al. 1979). Mean times to unconsciousness in animals that were 

exposed to hydrogen sulfide with ethanol pretreatment at either of these dose levels were approximately 

35% less than times to unconsciousness without ethanol pretreatment (Beck et al. 1979). The clinical 

relevance of these findings, which used potentially fatal doses of both ethanol and hydrogen sulfide, is 

unclear. 
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3.10 POPULATIONS THAT ARE UNUSUALLY SUSCEPTIBLE 

A susceptible population will exhibit a different or enhanced response to hydrogen sulfide than will most 

persons exposed to the same level of hydrogen sulfide in the environment. Reasons may include genetic 

makeup, age, health and nutritional status, and exposure to other toxic substances (e.g., cigarette smoke). 

These parameters result in reduced detoxification or excretion of hydrogen sulfide, or compromised 

function of organs affected by hydrogen sulfide. Populations who are at greater risk due to their 

unusually high exposure to hydrogen sulfide are discussed in Section 6.7, Populations with Potentially 

High Exposures. 

Some asthmatics exposed to 2 ppm hydrogen sulfide for 30 minutes had changes in pulmonary function 

tests indicative of bronchial obstruction, although the exposed group as a whole did not show a 

statistically significant change in these parameters (Jappinen et al. 1990). Asthmatics have also been 

found to have a worsening of their condition upon exposure to odors (Shim and Williams 1986). 

Although this has not been tested with exposure to hydrogen sulfide, it might be reasonably anticipated 

due to the malodorous quality of hydrogen sulfide gas. These findings suggest that some asthmatics may 

be more sensitive to hydrogen sulfide than the general population. 

Evidence from a number of studies suggests that hydrogen sulfide, endogenously produced by bacteria in 

the digestive tract, may play a role in the etiology of ulcerative colitis (Babidge et al. 1998; Pitcher and 

Cummings 1996; Roediger et al. 1997). It is unclear whether patients are affected due to the excess 

production of hydrogen sulfide or the inability to detoxify it as effectively as controls. Irrespective of 

mechanism, it seems likely that individuals already suffering from hydrogen sulfide-associated toxicity 

will be at higher risk from further hydrogen sulfide exposures. Ulcerative colitis is usually found in 

adults, so children are less susceptible. 

3.11 METHODS FOR REDUCING TOXIC EFFECTS 

This section will describe clinical practice and research concerning methods for reducing toxic effects of 

exposure to hydrogen sulfide. However, because some of the treatments discussed may be experimental 

and unproven, this section should not be used as a guide for treatment of exposures to hydrogen sulfide. 

When specific exposures have occurred, poison control centers and medical toxicologists should be 
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consulted for medical advice. The following texts provide specific information about treatment following 

exposures to hydrogen sulfide: 

Agency for Toxic Substances and Disease Registry. 1994. Hydrogen sulfide. Managing hazardous 

materials incidents. Volume III. Medical management guidelines for acute chemical exposures. Atlanta, 

GA: Agency for Toxic Substances and Disease Registry. 

Ellenhorn MJ. 1997. Hydrogen sulfide. In: Ellenhorn's medical toxicology: Diagnosis and treatment of 

human poisoning. 2nd edition. Baltimore, MD: Williams and Wilkins, 1489-1493. 

Hall AH. 1996. Systemic asphyxiants. In: Rippe JM, Irwin RS, Fink MP, et al. eds. Intensive care 

medicine. 3rd edition. Boston, MA: Little, Brown, and Company, 1706-1718. 

There is no widely accepted antidote for hydrogen sulfide poisoning. Treatment consists of supportive 

measures such as evaluating and supporting airway, breathing, and circulation (Agency for Toxic 

Substances and Disease Registry 1994). A number of case reports of individuals exposed to high 

concentrations of hydrogen sulfide resulting in unconsciousness suggest that administration of sodium 

nitrite and/or amyl nitrite may be an effective antidote for hydrogen sulfide poisoning (Hall 1996; Hall 

and Rumack 1997; Hoidal et al. 1986; Stine et al. 1976). The nitrite induces the formation of 

methemoglobin, which has a higher affinity for hydrogen sulfide than does cytochrome oxidase. 

Hyperbaric oxygen therapy is controversial, but it may be effective for patients not treated successfully by 

other measures (Agency for Toxic Substances and Disease Registry 1994). 

There are no pediatric-specific methods for reducing toxic effects. 

3.11.1 Reducing Peak Absorption Following Exposure 

There are no specific methods available to reduce the absorption of hydrogen sulfide following exposure. 

Supportive treatment includes artificial respiration if respiration is depressed; administration of oxygen; 

and standard medical treatment for eye irritation, pulmonary edema, seizures, and hypotension (Sorokin 

1993). 
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3.11.2 Reducing Body Burden 

There are no known methods for reducing the body burden of hydrogen sulfide, although adopting a diet 

low in sulfur-containing, exogenously acquired foods, e.g., milk and cheese, has been shown to reduce the 

endogenous production of hydrogen sulfide (Roediger et al. 1997). 

The major metabolic pathway of hydrogen sulfide is the oxidation of the sulfide to sulfate in the liver 

(Beauchamp et al. 1984). Methylation also serves as a detoxification route. Hydrogen sulfide is excreted 

primarily as sulfate (either as free sulfate or as thiosulfate) in the urine. 

3.11.3 Interfering with the Mechanism of Action for Toxic Effects 

Hydrogen sulfide inhibits mitochondrial cytochrome oxidase, resulting in disruption of the electron 

transport chain and impairing oxidative metabolism. Nervous and cardiac tissues, which have the highest 

oxygen demand (e.g., brain and heart), are especially sensitive to disruption of oxidative metabolism 

(Ammann 1986; Hall 1996). 

Nitrites such as amyl and sodium nitrites have been used in the treatment of hydrogen sulfide poisoning, 

and the mechanism of therapeutic action may involve the prevention or reversal of cytochrome oxidase 

inhibition (Ellenhorn 1997; Hall 1996; Hoidal et al. 1986; Osbern and Crapo 1981; Reiffenstein et al. 

1992). It has been postulated that nitrites induce methemoglobin, which inactivates sulfide, thereby 

preventing cytochrome oxidase inhibition and reactivating aerobic respiration (Ellenhorn 1997; Hall 

1996). There is antidotal evidence to suggest that this is an effective treatment in cases of exposure to 

high concentrations of hydrogen sulfide (Hall 1996; Hall and Rumack 1997; Hoidal et al. 1986; Stine et 

al. 1976). 

Oxygen treatment may be used after hydrogen sulfide poisoning, although its use is somewhat 

controversial (Ellenhorn 1997; Ravizza et al. 1982). Smith et al. (1976) found that oxygen was not useful 

as an antidote to hydrogen sulfide poisoning in mice. High intracellular oxygen pressure may result in 

nonenzymatic oxidation of cytochrome oxidase, and oxygen may release sulfide from cytochrome 

oxidase binding by a concentration effect (Ravizza et al. 1982). Hyperbaric oxygen therapy has been 

suggested for cases not responding to supportive care and nitrite treatment, but its clinical efficacy has not 

yet been determined (Ellenhorn 1997; Hall 1996). 
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In one case report (Schneider et al. 1998) where an individual suffered long-term (4 years later) 

neuropsychological sequelae from a “knock-down” exposure to hydrogen sulfide, treatment with two 

drugs, Ritalin and Cyclert, partially alleviated some of the observed deficits in cognitive function and 

general cognition; these drugs enhance dopaminergic functioning. However, more examples of the 

efficacy of this treatment are required. 

3.12 ADEQUACY OF THE DATABASE 

Section 104(I)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of hydrogen sulfide is available. Where adequate information 

is not available, ATSDR, in conjunction with the National Toxicology Program (NTP), is required to 

assure the initiation of a program of research designed to determine the health effects (and techniques for 

developing methods to determine such health effects) of hydrogen sulfide. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would 

reduce the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 

3.12.1 Existing Information on Health Effects of Hydrogen Sulfide 

The existing data on health effects of inhalation, oral, and dermal exposure of humans and animals to 

hydrogen sulfide are summarized in Figure 3-4. The purpose of this figure is to illustrate the existing 

information concerning the health effects of hydrogen sulfide. Each dot in the figure indicates that one or 

more studies provide information associated with that particular effect. The dot does not necessarily 

imply anything about the quality of the study or studies, nor should missing information in this figure be 

interpreted as a “data need”. A data need, as defined in ATSDR’s Decision Guide for Identifying 

Substance-Specific Data Needs Related to Toxicological Profiles (Agency for Toxic Substances and 

Disease Registry 1989), is substance-specific information necessary to conduct comprehensive public 

health assessments. Generally, ATSDR defines a data gap more broadly as any substance-specific 

information missing from the scientific literature. 
Figure 3-4. Existing Information on Health Effects of Hydrogen Sulfide 

Death

Acute 

Intermediate 

Chronic 

Immunologic/Lymphoretic 

Neurologic 

Reproductive 

Developmental 

Genotoxic 

Cancer 

Systemic 

Inhalation 

Oral 

Dermal 

Human 

Death

Acute 

Intermediate 

Chronic 

Immunol gic/Lymphor 

eu o 

ep o 

ev l 

en

t 

an e

o 

etic 

N

r logic 

R

r ductive 

D

e opmental 

G

o oxic 

C

c

r 

Systemic 

Inhalation 

Oral 

Dermal 

Animal 

Existing Studies 

HYDROGEN SULFIDE 99 

3. HEALTH EFFECTS 
HYDROGEN SULFIDE 100 

3. HEALTH EFFECTS 

3.12.2 Identification of Data Needs 

Acute-Duration Exposure. There are numerous case reports of human fatalities (Adelson and 

Sunshine 1966; Allyn 1931; Breysse 1961; Campanya et al. 1989; Deng and Chang 1987; Freireich 1946; 

Hagley and South; Morse et al. 1981; Osbern and Crapo 1981; Parra et al. 1991) or survivors who 

developed immediate as well as delayed neurological effects (Deng and Chang 1987; Kilburn 1993, 1997; 

Krekel 1964; McDonald and McIntosh 1951; Milby 1962; Schneider et al. 1998; Spolyar 1951) following 

acute-duration hydrogen sulfide inhalation exposure. Estimates of exposure concentrations were not 

often reported in these studies. Cardiac arrhythmia has also been reported in workers exposed to 

hydrogen sulfide (Krekel 1964). Experimental exposure studies in which subjects were exposed to 

hydrogen sulfide for 15–30 minutes did not identify any respiratory or cardiovascular effects in healthy 

subjects at 5 or 10 ppm (Bhambhani and Singh 1991; Bhambhani et al. 1994, 1996a). Pulmonary 

function tests were normal in workers exposed to up to 10 ppm hydrogen sulfide (Jappinen et al. 1990). 

Evidence of bronchial obstruction was observed in 2 of 10 asthmatics exposed to 2 ppm of hydrogen 

sulfide, although the group as a whole had no significant change in these parameters (Jappinen et al. 

1990). Additionally, studies are needed to assess whether asthmatic subjects are a sensitive 

subpopulation. Because hydrogen sulfide gas is an eye irritant (Ahlborg 1951; Luck and Kaye 1989), 

such studies should also monitor ocular effects. Additional studies of the delayed consequences of acute 

exposures are also needed. 

Acute-duration inhalation studies of hydrogen sulfide in animals have reported death (Beck et al. 1979; 

Khan et al. 1990; Lopez et al. 1989; Nagata et al. 1990; Prior et al. 1988, 1990; Smith and Gosselin 1964; 

Tansy et al. 1981), respiratory (Brenneman et al. 2002; Green et al. 1991; Khan et al. 1990; Kohno et al. 

1991; Lopez et al. 1987, 1988a, 1988b; Prior et al. 1990), cardiovascular (Higuchi and Fukamachi 1977; 

Kohno et al. 1991; Kosmider et al. 1967), immunological/lymphoreticular (Khan et al. 1991), and 

neurological effects (Beck et al. 1979; Haider et al. 1980; Higuchi and Fukamachi 1977; Kosmider et al. 

1967; Lopez et al. 1988b; Struve et al. 2001). Additional acute-duration inhalation animal studies would 

be useful to further define any direct cardiovascular effects of hydrogen sulfide as opposed to those due to 

hypoxia. The available data on the acute toxicity of inhaled hydrogen sulfide were sufficient for 

derivation of an acute-duration inhalation MRL. 

Data are not sufficient for the development of an acute-duration oral MRL. The only oral study of 

hydrogen sulfide is a study in which a diarrheic digestive disorder was observed in pigs fed hydrogen 

sulfide at 15 mg/kg/day for "a few days" (Wetterau et al. 1964). Acute dermal exposure of animals has 
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3. HEALTH EFFECTS 

resulted in death (Laug and Draize 1942). In addition to a lack of route-specific toxicity data, insufficient 

pharmacokinetic data are available to support the identification of target organs across routes of exposure. 

However, although oral and dermal data regarding the effects of hydrogen sulfide are very limited, human 

exposure would be expected to be principally by inhalation. 

Intermediate-Duration Exposure. Intermediate-duration studies in humans are fairly limited and 

virtually all are complicated by exposures to other chemicals as well as rarely being accompanied with 

adequate exposure assessment. Additional epidemiologic studies, particularly prospective or casecontrol, of populations exposed environmentally to various levels of hydrogen sulfide (where other 

pollutants are monitored and ideally, do not vary) are needed. 

A series of 90-day inhalation studies in rats (CIIT 1983b, 1983c) reported significantly decreased body 

weights in Sprague-Dawley female rats at 80 ppm, but not in male Sprague-Dawley (CIIT 1983c) nor in 

either sex of F-344 rats (CIIT 1983b). Although CIIT (1983b, 1983c) did not report increases in the 

occurrence histological lesions, a re-examination of the histological slides from this study (Dorman et al. 

2004) found increases in the incidence of nasal (olfactory neuron loss) and lung (bronchiolar epithelial 

hypertrophy and hyperplasia) lesions at 30 ppm and higher. In a companion study with B6C3F1 mice, a 

significant increase in the incidence of inflammation of the nasal mucosa was observed at a dose level of 

80 ppm but not at 30.5 ppm. Brenneman et al. (2000) identified a NOAEL and LOAEL for nasal effects 

(loss of olfactory neurons) in Sprague-Dawley rats exposed to 10 and 30 ppm, respectively, for 10 weeks. 

This study was used as the basis of an intermediate-duration inhalation MRL for hydrogen sulfide. 

No histopathological effects were found in respiratory tract tissues or organs when pigs were exposed to 

8.5 ppm hydrogen sulfide continuously for 17 days (Curtis et al. 1975). Additional effects reported in rats 

following inhalation exposure to hydrogen sulfide include increased glucose in lactating rats (Hayden et 

al. 1990a), increased liver cholesterol in female rats exposed during gestation and lactation (Hayden et al. 

1990b), and weight loss in pregnant rats (Saillenfait et al. 1989). 

The only oral study of hydrogen sulfide is a study in pigs in which decreased body weights were observed 

in pigs fed hydrogen sulfide in the diet at 6.7 mg/kg/day for 105 days (Wetterau et al. 1964). No effects 

were observed at a dose of 3.1 mg/kg/day. However, because this study lacks details and there are no 

supporting data, no intermediate-duration MRL was derived. Additional intermediate-duration oral 

studies of hydrogen sulfide are needed to provide support for this study. 
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No intermediate-duration dermal studies of hydrogen sulfide were identified. As significant human 

dermal exposure to hydrogen sulfide is unlikely, dermal exposure studies should not be a high priority. 

However, no pharmacokinetic data are available that might support the identification of target organs 

across routes of exposures in the absence of route-specific toxicity data. 

Chronic-Duration Exposure and Cancer. A study of workers exposed to hydrogen sulfide at 

concentrations that often exceeded 20 ppm reported slight irritation of the mucous membranes, fatigue, 

loss of appetite, headache, irritability, poor memory, and dizziness (Ahlborg 1951). Pulp industry 

workers exposed to 8-hour TWA concentrations of 0.05–5.2 ppm hydrogen sulfide had no signs of 

clinical anemia but did show decreases in ALA-S, Heme-S, and ALA dehydratase activities, as well as 

erythrocyte protoporphyrin (Tenhunen et al. 1983). This study was confounded by workers’ exposure to 

other compounds such as methyl mercaptan and dimethylsulfide, inadequately described controls, and an 

absence of statistical analysis. A study of persons living near a paper mill who were exposed to hydrogen 

sulfide showed increased eye irritation and some respiratory effects compared to nonexposed individuals; 

however, they were also exposed to methyl mercaptan and sulfur dioxide (Jappinen et al. 1990). There 

was no increase in cancer incidence noted in a residential cohort study of persons living downwind from 

natural gas refineries (Schechter et al. 1989), but an increased risk of nasal cancers was found in a 

population residing in a location of high geothermal activity (Bates et al. 1998). 

Additional chronic-duration studies of hydrogen sulfide, including studies of the carcinogenic potential of 

hydrogen sulfide in humans and animals by any route of exposure, have not been performed. Follow-up 

epidemiological studies of populations environmentally exposed to hydrogen sulfide due to proximity of 

pulp mills, sour gas plants, or geothermal energy sources are needed, but only if they are accompanied by 

adequate exposure measurements. As limited genotoxicity studies suggest that hydrogen sulfide is 

unlikely to be a carcinogen, lifetime carcinogenicity studies in animals should not be a high priority. In 

the absence of route-specific toxicity data and route-specific pharmacokinetic data, it is not possible to 

identify target organs across routes of exposure. 

Genotoxicity. No mutagenicity was observed in Ames assays using Salmonella typhimurium strains 

TA97, TA98, and TA100, either with or without S9 liver fractions from male Syrian golden hamsters or 

Sprague-Dawley rats (EPA 1984). Specific concentrations of hydrogen sulfide gas were limited because 

of its solubility in ethanol, which was the test solvent. The highest dose that could be obtained was 

1,750 μg/plate. Other studies using hydrogen sulfide in the gaseous state would be useful for testing 

higher doses. 
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Reproductive Toxicity. The findings in two studies (Hemminki and Niemi 1982; Xu et al. 1998) 

that exposures to hydrogen sulfide are associated with an increased risk of spontaneous abortion warrants 

further investigation. A well-designed case-control study is needed in which exposure is well 

characterized in order to ascertain whether this is indeed an effect of concern or merely an anomaly. 

Additional epidemiologic studies of other reproductive effects would also be useful. No treatment-related 

histopathological changes were found in the male or female reproductive organs of rats (CIIT 1983b, 

1983c) or mice (CIIT 1983a) exposed to hydrogen sulfide for 6 hours/day, 5 days/week, for 90 days or in 

rats exposed to 80 ppm hydrogen sulfide 6 hours/day, 7 days/week for 60–70 days (Dorman et al. 2000). 

The Dorman et al. (2000) study also found no exposure-related alterations in fertility, late resorptions or 

stillbirths, litter size, or length of gestation. A multilitter or multigeneration study in several animal 

species after exposure to hydrogen sulfide by inhalation is needed to further evaluate the reproductive 

potential of hydrogen sulfide. 

Developmental Toxicity. No studies were located regarding developmental effects in humans 

following hydrogen sulfide exposure. 

Developmental effects were not observed in rats exposed to hydrogen sulfide by inhalation at 

concentrations that resulted in maternal body weight loss (Saillenfait et al. 1989), increased maternal 

blood glucose levels (Hayden et al. 1990a), or increased cholesterol content of the maternal liver (Hayden 

et al. 1990b). Purkinje cell path length in offspring of exposed rats was increased compared to controls 

(Hannah and Roth 1991). Changes in amino acid levels (Hannah et al. 1989, 1990) and serotonin and 

epinephrine levels (Skrajny et al. 1992) in the brain were found in the offspring of rats exposed by 

inhalation to hydrogen sulfide during gestation. No alterations in performance on neurobehavioral tests 

were observed in the offspring of rats exposed to up to 80 ppm 6 hours/day, 7 days/week during gestation 

and lactation (the pups were also exposed on postnatal days 5–18) (Dorman et al. 2000). Studies 

regarding the developmental toxicity of hydrogen sulfide following oral or dermal exposure were not 

located. 

Immunotoxicity. Immunological effects infrequently observed after human hydrogen sulfide 

exposure appear to result from infection due to the aspiration or ingestion of manure or vomit (Osbern 

and Crapo 1981). No treatment-related histopathological changes were found in the spleen or lymph 

nodes of rats (CIIT 1983b, 1983c) or mice (CIIT 1983a) exposed to hydrogen sulfide for 6 hours/day, 

5 days/week, for 90 days. Although the number of pulmonary alveolar macrophage cells was not 
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influenced by hydrogen sulfide exposure, the number of viable cells was significantly decreased with 

exposure to 400 ppm (Khan et al. 1991). When pulmonary alveolar macrophage cells were treated with 

Zymosan to stimulate respiration rates, there was no stimulation of respiration in cells from animals 

exposed to 200 or 400 ppm of hydrogen sulfide for 4 hours (Khan et al. 1991). Immunological effects 

have not been studied in humans or animals following oral or dermal exposure to hydrogen sulfide. 

Additional studies of immune function in animals exposed to hydrogen sulfide by inhalation are needed. 

A bacterial and/or viral challenge study would be especially useful to determine whether exposure to 

hydrogen sulfide increases susceptibility to infection. 

Neurotoxicity. The nervous system is a target organ for hydrogen sulfide. Effects of acute inhalation 

exposure in humans include nausea, headaches, delirium, disturbed equilibrium, poor memory, loss of 

consciousness, tremors, and convulsions (Arnold et al. 1985; Deng and Chang 1987; Krekel 1964; 

McDonald and McIntosh 1951; Milby 1962; Spolyar 1951). Acute effects observed in animals include 

fatigue, somnolence (Haider et al. 1980), and loss of consciousness (Kosmider et al. 1967). Limited data 

from chronically exposed workers indicate that loss of appetite, fatigue, poor memory, dizziness, and 

irritability may result (Ahlborg 1951; Krekel 1964). Studies in rats have shown decreases in performance 

of discriminated avoidance tasks after exposure to hydrogen sulfide (Higuchi and Fukamachi 1977). The 

potential neurotoxicity of hydrogen sulfide following oral or dermal exposures has not been characterized. 

The transplacental neurological effects of hydrogen sulfide exposure are unknown. There is no reason to 

suspect that the neurotoxic effects observed after hydrogen sulfide exposure are species-specific, and 

insufficient data are available to determine whether effects are route-specific. Well-designed studies 

investigating neurotoxic effects in animals following oral or dermal exposure and chronic neurotoxic 

effects after inhalation exposure are needed to determine the effects that might be seen in exposed 

humans. Additionally, there is antidotal evidence that some individuals experience permanent or 

persistent neurological symptoms, such as memory loss, after acute exposures to high concentrations of 

hydrogen sulfide. Studies are needed to confirm these reports and determine if acute exposure to 

hydrogen sulfide can result in permanent neurological damage. 

Epidemiological and Human Dosimetry Studies. Published reviews have addressed the duration 

of exposure and concentrations of hydrogen sulfide resulting in death and serious effects in humans 

(Beauchamp et al. 1984; EPA 1978; NIOSH 1977a; WHO 1981). The limited chronic-duration 

epidemiological studies (Ahlborg 1951; Jappinen et al. 1990; Schechter et al. 1989; Tenhunen et al. 1983) 

have identified approximate exposure concentrations, but exposure assessment was not sufficient to 
HYDROGEN SULFIDE 105 

3. HEALTH EFFECTS 

divide the study population into more than one exposure group. Epidemiology studies examining the 

potential effects of chronic inhalation exposure to various hydrogen sulfide concentrations are needed. 

There are known populations that have unusually high exposure to hydrogen sulfide. 

Biomarkers of Exposure and Effect. 

Exposure. Both blood sulfide concentrations (Jappinen and Tenhunen 1990) and urinary thiosulfate 

concentrations (Kage et al. 1992; Kangas and Savolainen 1987) have been proposed as indicators of 

hydrogen sulfide exposure. Obtaining background levels of blood sulfide in a population should not be 

problematic, although blood samples to determine sulfide concentrations must be obtained within 2 hours 

of exposure to hydrogen sulfide. Similarly, urinary thiosulfate levels can be obtained for the background 

population. Further study is needed to correlate airborne exposure concentrations with blood sulfide and 

thiosulfate levels. Additional alterations in heme synthesis enzymes (delta-aminolaevulinic acid synthase 

and heme synthase) have been proposed as possible biomarkers of exposure (Jappinen and Tenhunen 

1990). These effects are not specific for hydrogen sulfide, and further study is needed to correlate these 

effects with blood sulfide and urinary thiosulfate levels. 

Effect. No hydrogen-sulfide-specific biomarkers of effect have been identified. Neurological indices are 

also used as biomarkers of effect for hydrogen sulfide (Gaitonde et al. 1987; Kilburn 1993; Stine et al. 

1976; Tvedt et al. 1991b). It is unlikely that a hydrogen-sulfide-specific biomarker of effect will be 

identified based on nonspecific effects that have been observed in humans and animals exposed to 

hydrogen sulfide and the mechanistic similarity between cyanide and hydrogen sulfide. Additional data 

are needed to identify a collection of symptoms that could reasonably characterize hydrogen sulfide 

exposure. 

Absorption, Distribution, Metabolism, and Excretion. Hydrogen sulfide is absorbed through 

the lungs and can be absorbed in minor quantities through the gastrointestinal tract and intact skin (Kohno 

et al. 1991; Laug and Draize 1942; Wetterau et al. 1964). Hydrogen sulfide is also produced 

endogenously in many tissues (e.g., liver, kidney, and heart) as a break-down product of cysteine 

metabolism. Thus, hydrogen sulfide is widely distributed in the body. Sulfides have been found in the 

heart, liver, blood, brain, lungs, spleen, and kidneys of humans who died after accidental inhalation 

exposure (Kohno et al. 1991). However, there are no studies that have tracked the quantitative absorption 

or endogenous production of hydrogen sulfide nor quantified the differences in its distribution in the 
HYDROGEN SULFIDE 106 

3. HEALTH EFFECTS 

various tissues to follow absorption of an external dose. No data are available on distribution after oral or 

dermal exposure to hydrogen sulfide. 

Hydrogen sulfide is metabolized through three pathways: oxidation, methylation, and reactions with 

metalloproteins or disulfide-containing proteins (Beauchamp et al. 1984). Although the major metabolic 

pathway for detoxification is oxidation of the sulfide to sulfate in the liver, methylation also serves to 

detoxify hydrogen sulfide (EPA 1987a; Weisiger and Jakoby 1979). The major oxidation product of 

hydrogen sulfide is thiosulfate, which is then converted to sulfate and excreted in the urine (Bartholomew 

et al. 1980; Kage et al. 1992; Kangas and Savolainen 1987). The primary location for the oxidation 

reaction is the liver (Bartholomew et al. 1980). 

The qualitative data on the absorption, distribution, metabolism, and excretion of hydrogen sulfide in 

humans and animals are well known; quantitative data are generally lacking. Additional studies in 

animals that provide quantitative toxicokinetic data are needed. 

Comparative Toxicokinetics. PBPK models have not been developed to compare the toxicokinetics 

of hydrogen sulfide in humans and animals. Studies providing quantitative data necessary to develop 

PBPK models would be useful. 

Methods for Reducing Toxic Effects. Other than removing the subject from exposure, there is no 

specific method to reduce the absorption of hydrogen sulfide. There are no known methods for reducing 

the body burden of hydrogen sulfide, although reducing the intake of sulfhydryl-containing amino acids 

has been shown to reduce endogenous production. Amyl and sodium nitrites have been used as antidotes 

for hydrogen sulfide. Oxygen treatment, which may result in nonenzymatic oxidation of cytochrome 

oxidase, may also be used in the treatment of hydrogen sulfide poisoning (Hall 1996; Ravizza et al. 1982). 

There is a need to develop an antidote for hydrogen sulfide poisoning, especially since it has a high 

knock-down potency. Additional research into the safe use of oxygen as an antidote for hydrogen sulfide 

poisoning is needed. Studies examining methods to enhance the oxidation or methylation of hydrogen 

sulfide to increase the elimination might also be useful. Further studies of the efficacy of drugs such as 

Retalin and Cyclert to treat the long-term neuropsychological effects of a knock-down exposure are 

needed. 
HYDROGEN SULFIDE 107 

3. HEALTH EFFECTS 

Children’s Susceptibility. Data needs relating to both prenatal and childhood exposures, and 

developmental effects expressed either prenatally or during childhood, are discussed in detail in the 

Developmental Toxicity subsection above. 

There is only limited information available by which to assess the potential toxicity of hydrogen sulfide to 

children and infants. Several case reports suggest that adolescents respond much like adults to high dose 

acute exposures (Allyn 1931; Hagley and South 1983; Morse et al. 1981), but there is no information with 

which to determine whether the long-term consequences of such exposures differ for adolescents versus 

adults, nor is there any information on the effects of hydrogen sulfide exposures in children and very little 

information on infants. Several developmental toxicity studies indicated that the exposure of pregnant 

rats and their pups to hydrogen sulfide resulted in structural and biochemical changes in the brain 

(Hannah and Roth 1991; Hannah et al. 1989, 1991). Subsequent work showed that many of the 

biochemical changes were transient; however, no studies were found that evaluated the behavioral 

consequences of these changes. Thus, a variety of studies are needed in order to determine whether 

children and infants are at risk from neurological deficits following hydrogen sulfide exposures in utero 

or during childhood and adolescence; information from such studies would also be useful in order to 

determine whether children are more sensitive to hydrogen sulfide exposure. 

Child health data needs relating to exposure are discussed in Section 6.8.1, Identification of Data Needs: 

Exposures of Children. 

3.12.3 Ongoing Studies 

A limited number of ongoing studies, designed to investigate mechanisms of hydrogen sulfide production 

in the digestive tract and potential health concerns, were identified in the Federal Research in Progress 

database (FEDRIP 2004). These studies are summarized below. 

Dr. L. Chu, from the University of Texas Health Science Center, has designed studies to elucidate 

enzymatic mechanisms involved in hydrogen sulfide production by the oral bacterium, Treponema 

denticola, and to characterize the effects the hydrogen sulfide-induced effects on host inflammatory/ 

immune functions. 

Dr. M. Levitt, from the Department of Veterans Affairs Medical Center in Minneapolis, Minnesota, has 

designed experiments in rats to investigate toxicity following the intestinal infusion of sodium sulfide. 
HYDROGEN SULFIDE 108 

3. HEALTH EFFECTS 

Dr. Levitt has also designed experiments to investigate the metabolic fate of hydrogen sulfide and other 

sulfur-containing compounds in the rat. 

Dr. Fiedler and associates are investigating the neurological toxicity of hydrogen sulfide following lowlevel exposure. 
HYDROGEN SULFIDE 109 

4. CHEMICAL AND PHYSICAL INFORMATION 

4.1 CHEMICAL IDENTITY 

Information regarding the chemical identity of hydrogen sulfide is located in Table 4-1. This information 

includes synonyms, chemical formula and structure, and identification numbers. 

4.2 PHYSICAL AND CHEMICAL PROPERTIES 

Information regarding the physical and chemical properties of hydrogen sulfide is located in Table 4-2. 

Hydrogen sulfide (H2S) is a heavier-than-air, colorless gas with a sweetish taste and characteristic odor of 

rotten eggs (HSDB 2006). The odor threshold for hydrogen sulfide is variable and various ranges have 

been reported. Ruth (1986) reviewed odor thresholds of several hundred chemicals, including hydrogen 

sulfide, from the industrial hygiene literature and other compilations of odor threshold data; an odor 

threshold range of 0.0005–0.010 ppm was reported. Guidotti (1994) reported an odor threshold range of 

0.01–0.3 ppm. Since high concentrations of hydrogen sulfide (150 ppm) can paralyze the olfactory nerve, 

odor may not be a reliable indicator of the presence of this gas (HSDB 2006). 
HYDROGEN SULFIDE 110 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-1. Chemical Identity of Hydrogen Sulfidea 

Characteristic Information 

Chemical name Hydrogen sulfide 

Synonyms/trade names Hydrosulfuric acid; hydrogen sulphide, sewer gas, stink damp; sulfur 

hydride; sulfurated hydrogen; dihydrogen monosulfide; dihydrogen 

sulfide, sulfuretted hydrogen, hepatic acid, sour gas 

Chemical formula H2S 

Chemical structure S 

H H 

Identification numbers: 

 CAS registry 7783-06-4 

 NIOSH/RTECS MX1225000b 

EPA hazardous waste U135 

DOT/UN/NA/IMCO shipping UN1053; IMO 2.1 

HSDB 576 

EINECS 231-977-3 

NCI No data 

a

All information obtained from HSDB 2006 ,ChemID 2006, and ChemFinder 2006, except where noted. b

NIOSH 2006 

CAS = Chemical Abstract Services; DOT/UN/NA/IMCO = Department of Transportation/United Nations/North 

America/International Maritime Dangerous Goods Code; EINECS = European Inventory of Existing Commercial 

Substances; EPA = Environmental Protection Agency; HSDB = Hazardous Substance Data Bank; NCI = National 

Cancer Institute; NIOSH = National Institute for Occupational Safety and Health; RTECS = Registry of Toxic Effects 

of Chemical Substances 
H2S(aq) H+(aq) + S2- H (aq) (2) +(aq) + HS-

(aq) (1); HS-(aq) 

7.04b − +


 


 

HYDROGEN SULFIDE 111 

4. CHEMICAL AND PHYSICAL INFORMATION 

Table 4-2. Physical and Chemical Identity of Hydrogen Sulfidea 

Property Information 

Molecular weight 

Color 

Taste 

Physical state 

Melting point 

Boiling point 

Density in Air 

Density at 0 °C, 760 mmHg 

Odor 

Odor threshold: 

 Water 

Air 

Solubility: 

Water 

Other solvent(s) 

Partition coefficients: 

 Log Kow

 Log Koc 

Vapor pressure at 25 °C 

Acid dissociation: 

pKa (1) 

pKa (2) 

Henry’s law constant: 

at 20 °C 

at 30 °C 

at 40 °C 

Autoignition temperature 

Conversion factors 

Explosive limits 

34.08 

Colorless 

Sweetish taste 

Gas (under normal ambient condition) 

-85.49 °C 

-60.33 °C 

1.19 (air=1.00)b 

1.5392 g/L 

Rotten eggs 

0.000029 ppmc 

0.0005–0.3 ppmd,e 

5.3 g/L at 10 oC; 4.1 g/L at 20 oC; 3.2 g/L at 30 oCb 

Soluble in glycerol, gasoline, kerosene, carbon disulfide, crude oil 

 Not applicable 

 Not applicable 

15,600 mm Hg 

[HS (aq)][H (aq)] Ka1 = [H 2 S(aq)] 

11.96b 

[S 2− (aq)][H + (aq)] Ka2 = − [HS (aq)] 

468 atm/mole fractionf 

600 atm/mole fractionf 

729 atm/mole fractionf 

500 °F (260 oC) 

1 ppm = 1.40 mg/m3 g 

Upper, 45.5%; lower, 4.3% (by volume in air) 

a

All information obtained from HSDB 2006, except where noted. 

b

O'Neil et al. 2001 

c

Amoore and Hautala 1983 

d

Ruth 1986 

e

Guidotti 1994 

f

Daubert and Danner 1989 

g

Al-Haddad et al. 1989 
HYDROGEN SULFIDE 112 

4. CHEMICAL AND PHYSICAL INFORMATION 

This page is intentionally blank. 
HYDROGEN SULFIDE 113 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

5.1 PRODUCTION 

The Toxics Release Inventory (TRI) database contains no information on facilities that manufacture or 

process hydrogen sulfide because this chemical is not required to be reported under Section 313 of the 

Emergency Planning and Community Right-to-Know Act (Title III of the Superfund Amendments and 

Reauthorization Act of 1986) (EPA 1997). 

Hydrogen sulfide is made commercially available by two typical approaches, recovery from gas mixtures 

and chemical means. Natural gas and gases associated with crude oil contain varying amounts of 

hydrogen sulfide from trace amounts to 70–80% (Pouliquen et al. 1989). Recovery of hydrogen sulfide 

from petroleum, natural gas, or manufactured gas operations is the main non-natural source of hydrogen 

sulfide. These recovery processes can be categorized into several methods, including chemical and 

physical absorption, dry oxidation to form sulfur or oxides (Clause process), and liquid oxidation to form 

oxides (Ferrox process) (Beauchamp et al. 1984). 

Hydrogen sulfide production by chemical reaction can involve reacting sulfur either with hydrogen gas 

(H2) or with a hydrocarbon (Pouliquen et al. 1989). It can also be produced by the hydrogen reduction or 

acid decomposition of a sulfide (Pouliquen et al. 1989). Another method of hydrogen sulfide production, 

which accounts for >90% of the sulfur in crude oil, is hydrodesulfurization, in which gas-oil and coke 

distillate fractions are passed through a fixed-bed catalyst in the presence of hydrogen. Approximately 

80–90% of the sulfur-containing compounds, mostly acyclic and cyclic sulfides, are converted into 

hydrogen sulfide by this process (Beauchamp et al. 1984; Weil and Sandler 1997). 

5.2 IMPORT/EXPORT 

No data on import or export volumes for hydrogen sulfide are available. 
HYDROGEN SULFIDE 114 

5. PRODUCTION, IMPORT/EXPORT, USE, AND DISPOSAL 

5.3 USE 

Hydrogen sulfide has a variety of industrial uses. Its major use is in the production of elemental sulfur 

and sulfuric acid. Sulfur recovered from the treatment of sour gas in 1986 accounted for 14 million tons, 

or 25% of the total world sulfur production. In 1995, the production of sulfuric acid was estimated to 

consume 1.1x105

 metric tons of hydrogen sulfide. More recent data on the consumption of hydrogen 

sulfide were not found. Hydrogen sulfide is used to prepare inorganic sulfides, such as sodium sulfide 

and sodium hydrosulfide, which are used in the manufacture of dyes, rubber chemicals, pesticides, 

polymers, plastic additives, leather, and pharmaceuticals. Hydrogen sulfide is also used in the 

manufacture of metal sulfides and thioorganic compounds and is an intermediate for sulfuric acid and 

elemental sulfur production. Hydrogen sulfide is used in the purification of nickel and manganese, in 

catalyst activation and poisoning, and in the treatment of metallic surfaces. It is used in metallurgy, in the 

production of heavy water for the nuclear industry, and as an analytical reagent. It is an additive in 

extreme pressure lubricants and cutting oils. Hydrogen sulfide is also used as an agricultural disinfectant. 

It is not registered as a pesticide in the United States (Beauchamp et al. 1984; Bingham et al. 2001; HSDB 

2006; Sittig 2002; Weil and Sandler 1997). 

5.4 DISPOSAL 

Hydrogen sulfide is designated as a hazardous substance under Section 311(b) of the Clean Water Act 

(EPA 2004c). Disposal of wastes containing hydrogen sulfide is controlled by a number of federal 

regulations (see Chapter 8). 

The EPA-assigned hazardous waste number for hydrogen sulfide is U135 (EPA 2004e). Generators of 

waste exceeding 100 pounds/month containing hydrogen sulfide must conform to the EPA regulations for 

the storage, transportation, treatment, and disposal of waste (EPA 2004c). Additional information 

concerning the accidental release of hydrogen sulfide and its reporting requirements is found in Chapter 8. 
HYDROGEN SULFIDE 115 

6. POTENTIAL FOR HUMAN EXPOSURE 

6.1 OVERVIEW 

Hydrogen sulfide has been identified in at least 35 of the 1,689 hazardous waste sites that have been 

proposed for inclusion on the EPA National Priorities List (NPL) (HazDat 2006). However, the number 

of sites evaluated for hydrogen sulfide is not known. The frequency of these sites can be seen in 

Figure 6-1. Of these sites, all are located within the coterminous United States. 

Hydrogen sulfide is one of the principal components in the natural sulfur cycle. Bacteria, fungi, and 

actinomycetes (a fungus-like bacteria) release hydrogen sulfide during the decomposition of sulfur 

containing proteins and by the direct reduction of sulfate (SO4

2-). Hydrogen sulfide is also consumed by 

bacteria found in soil and water that oxidize hydrogen sulfide to elemental sulfur. Photosynthetic bacteria 

can oxidize hydrogen sulfide to sulfur and sulfate in the presence of light and the absence of oxygen (EPA 

1993; WHO 1981). Hydrogen sulfide is commonly emitted from volcanoes, stagnant or polluted waters, 

and manure or coal pits with low oxygen content. These natural sources account for about 90% of the 

total hydrogen sulfide in the atmosphere (EPA 1993). Hydrogen sulfide may also enter the environment 

through accidental release, from leakage during manufacture or use, or as a result of industrial waste 

disposal. Because hydrogen sulfide is a natural component of petroleum, sulfur, and natural gas deposits, 

it may also be released into the environment during the extraction, transport, and refining of these 

resources. Landfills are another source of ambient hydrogen sulfide in the air (HazDat 2006; Lehman 

1996). Sulfides, including hydrogen sulfide, constitute up to 1% by volume of typical landfill gases 

(Agency for Toxic Substances and Disease Registry 2001). The Fresh Kills Landfill on Staten Island, 

New York has been estimated to release approximately 16 tons of hydrogen sulfide to the air annually 

(Agency for Toxic Substances and Disease Registry 2000). Hydrogen sulfide is frequently found in 

industrial settings where it is either used as a reactant or is produced as a by-product of manufacturing or 

industrial processes. Examples of these processes are tanneries, waste water treatment facilities, manure 

and sewage facilities, rayon manufacturing plants, sulfur producers, coke oven plants, kraft paper mills, 

iron smelters, food processing plants, tar and asphalt manufacturing plants, and natural gas and 

petrochemicals plants (Fuller and Suruda 2000). 

Degradation of hydrogen sulfide in the atmosphere can occur through oxidation by oxygen (O2) and 

ozone (O3) to give sulfur dioxide (SO2), and ultimately, sulfate compounds. Sulfur dioxide and sulfates 

HYDROGEN SULFIDE 117 

6. POTENTIAL FOR HUMAN EXPOSURE 

are eventually removed from the atmosphere through absorption by plants and soils or through 

precipitation (Hill 1973). Hydrogen sulfide in air can also react with photochemically generated hydroxyl 

radicals. The effective life-times for hydrogen sulfide based on summer daytime and yearly average 

hydroxyl radical concentrations have been estimated to be 0.23 and 2.3 days, respectively, based a 

measured rate constant of 4.8x10-12 cm3

/molecule second (Cox 1975). Life-times in air ranging from 

approximately 1 day in the summer to 42 days in the winter have been estimated for hydrogen sulfide 

(Bottenheim and Strausz 1980). Hydrogen sulfide is not expected to be decomposed by direct absorption 

of ultraviolet radiation, and the reaction with ozone is not expected to be a significant environmental fate 

(Cox 1975). 

Hydrogen sulfide oxidation by O2 may readily occur in surface waters (Millero et al. 1987, 1989). 

Hydrogen sulfide is readily soluble in water. In aqueous solution, hydrogen sulfide is a weak acid, 

exhibiting two acid dissociation constants. The first dissociation yields bisulfide ion (HS–

), and the 

second yields sulfide ion (S2–), with pKa values for each of these dissociations of 7.04 and 11.96, 

respectively (O'Neil et al. 2001). At a pH of 7.0, the ratio of the concentration of aqueous hydrogen 

sulfide to bisulfate ion is approximately 1-to-1. As the pH increases above 7.0, the ratio of the 

concentration of bisulfide ion to aqueous hydrogen sulfide increases. Only above pH 12 will the 

concentration of sulfide ion become significant (>50%). Hydrogen sulfide has been shown to sorb to 

various soils (Cihacek and Bremner 1993; Smith et al. 1973). Several species of soil, aquatic, and marine 

microorganisms oxidize hydrogen sulfide to elemental sulfur, and its half-time in these environments 

usually ranges from 1 hour to several hours (Jørgensen 1982). Because it is a gas under ambient 

conditions, bioconcentration and food chain biomagnification are unlikely (HSDB 2006). 

Exposure of the general population to hydrogen sulfide most likely occurs through inhalation of ambient 

air. As hydrogen sulfide is part of the natural environment, the general population will have some 

exposure to hydrogen sulfide. Hydrogen sulfide is also produced in the human large intestine and by the 

natural bacteria found in the human mouth (Richardson et al. 2000; Rosenberg et al. 1991). Populations 

living in areas of geothermal activity, or near waste sites or industries such as petroleum refineries, 

natural gas plants, petrochemical plants, coke oven plants, kraft paper mills, food processing plants, 

landfills, manure treatment facilities, waste water treatment facilities, and tanneries are more likely to be 

exposed to higher levels of hydrogen sulfide. Facilities where hydrogen sulfide is produced, used, or 

generated include petroleum refineries, natural gas plants, petrochemical plants, coke oven plants, kraft 

paper mills, viscose rayon manufacturing plants, sulfur production plants, iron smelters, food processing 

plants, manure treatment facilities, landfills, textile plants, waste water treatment facilities, and tanneries 
HYDROGEN SULFIDE 118 

6. POTENTIAL FOR HUMAN EXPOSURE 

(Chénard et al. 2003; Devai and DeLaune 1999; Lehman 1996; Rimatori et al. 1996; Svendsen 2001); 

workers in these industries may be occupationally exposed to hydrogen sulfide. 

6.2 RELEASES TO THE ENVIRONMENT 

Hydrogen sulfide is not listed in the Toxics Release Inventory (TRI) as of September, 2005. 

Hydrogen sulfide has been identified in a variety of environmental media (air, surface water, 

groundwater, soil, and sediment) collected at 35 of the 1,689 NPL hazardous waste sites (HazDat 2006). 

6.2.1 Air 

There is no information on releases of hydrogen sulfide to the atmosphere from manufacturing and 

processing facilities because these releases are not required to be reported (EPA 2005). 

Hydrogen sulfide was identified in air collected at 23 of the 35 current or former NPL hazardous waste 

sites where it was detected in some environmental media (HazDat 2006). 

Hydrogen sulfide is produced naturally and as a result of human activity. Natural sources, such as 

swamps, bogs, and volcanoes, account for about 90% of the total amount of hydrogen sulfide in the 

atmosphere (EPA 1993). Annually, 100–324 million tons of hydrogen sulfide are released from natural 

sources with half from volcanoes, flooded ground, or hydrogeologically sources, and the other half from 

the oceans (Pouliquen et al. 1989). Massive release of hydrogen sulfide to the ocean surface and 

atmosphere could occur during intervals of ocean anoxia (Kump et al. 2005). Nearshore hydrogen sulfide 

eruptions occur in the Atlantic Ocean along the central coast of Nambia and have been observed to affect 

areas of ocean surface of >20,000 km2

 (Weeks et al. 2004). Many petroleum deposits and natural gas 

wells also contain hydrogen sulfide ("sour-gas wells") and become sources of atmospheric hydrogen 

sulfide release when developed (Layton and Cederwall 1986; Leahey and Schroeder 1986). Hydrogen 

sulfide is emitted by some plant species as a byproduct of sulfite metabolism (Takemoto et al. 1986; 

Wilson et al. 1978). Emission rates of various biogenic sulfur gases, including hydrogen sulfide, from the 

exposed soils of five wetland plant communities in Florida were measured during April, May, and 

October 1985 and January 1986. Emission rates for hydrogen sulfide varied from 0.1–1.0 to 8.3–152 μg 

sulfur/m2

/hour from a spike grass site in the Everglades National Park in January 1986 and a sawgrass site 
HYDROGEN SULFIDE 119 

6. POTENTIAL FOR HUMAN EXPOSURE 

at Merritt Island National Wildlife Refuge in April 1985, respectively (Cooper et al. 1987). Hydrogen 

sulfide was identified in the volatile emissions of leaf litter of poplar trees (Populus balsamifera) 

(Isidorov and Jdanova 2002). Estimates of the terrestrial emission rates of hydrogen sulfide range from 

58 to 110 million tons of sulfur/year and estimates of the emission rates from oceans range from 30 to 

170 million tons of sulfur/year (Hill 1973). 

Facilities where hydrogen sulfide is produced, used, or generated include petroleum refineries, natural gas 

plants, petrochemical plants, coke oven plants, kraft paper mills, viscose rayon manufacturing plants, 

sulfur production plants, iron smelters, food processing plants, manure treatment facilities, landfills, 

textile plants, waste water treatment facilities, and tanneries (ACGIH 1991; Beck et al. 1981; Chénard et 

al. 2003; Devai and DeLaune 1999; Grant and Schuman 1993; Lehman 1996; Rimatori et al. 1996; Sittig 

2002; Svendsen 2001). Hydrogen sulfide is also used as an agricultural disinfectant, in the production of 

heavy water, and as an additive in lubricants and cutting oils (ACGIH 1991; Bingham et al. 2001; HSDB 

2006; Sittig 2002; Weil and Sandler 1997). Hydrogen sulfide may also be encountered in various 

industrial processes, such as the manufacture of dyes and pigments, felt, artificial silk, farming, brewing, 

glue making, and rubber vulcanization, and in lithography and photoengraving (Beck et al. 1981; Grant 

and Schuman 1993; Sittig 2002). Accidental release or improper disposal of materials resulting from 

these processes may result in hydrogen sulfide emissions. Ambient hydrogen sulfide concentrations in 

the air near landfills indicate that they are a source as well (HazDat 2006). Sulfides, including hydrogen 

sulfide, constitute up to 1% by volume of typical landfill gases (Agency for Toxic Substances and Disease 

Registry 2001). The Fresh Kills Landfill on Staten Island, New York has been estimated to release 

approximately 16 tons of hydrogen sulfide to the air annually (Agency for Toxic Substances and Disease 

Registry 2000). Facilities that treat manure may also release to hydrogen sulfide to the air. Hydrogen 

sulfide emissions were measured from two anaerobic lagoons used for treating swine waste; the overall 

mean hydrogen sulfide release was 5.7 μg/m2

/second (Lim et al. 2003). 

6.2.2 Water 

There is no information on releases of hydrogen sulfide to the water from manufacturing and processing 

facilities because these releases are not required to be reported (EPA 2005). 

Hydrogen sulfide has been identified in groundwater and surface water at 3 and 1 site, respectively, of the 

35 NPL hazardous waste sites where it was detected in some environmental media (HazDat 2006). 
HYDROGEN SULFIDE 120 

6. POTENTIAL FOR HUMAN EXPOSURE 

Releases of hydrogen sulfide to water occur both naturally and as a result of human activity. Hydrogen 

sulfide released from aquatic plants, or as a result of anaerobic chemical processes in swamps and bogs, 

may dissolve in the water column or bind to clay or organic matter. Massive release of hydrogen sulfide 

to the ocean surface could occur during intervals of ocean anoxia (Kump et al. 2005). 

Facilities where hydrogen sulfide is produced, used, or generated include petroleum refineries, natural gas 

plants, petrochemical plants, coke oven plants, kraft paper mills, viscose rayon manufacturing plants, 

sulfur production plants, iron smelters, food processing plants, manure treatment facilities, landfills, 

textile plants, waste water treatment facilities, and tanneries (ACGIH 1991; Beck et al. 1981; Chénard et 

al. 2003; Devai and DeLaune 1999; Grant and Schuman 1993; Lehman 1996; Rimatori et al. 1996; Sittig 

2002; Svendsen 2001). Hydrogen sulfide is also used as an agricultural disinfectant, in the production of 

heavy water, and as an additive in lubricants and cutting oils (ACGIH 1991; Bingham et al. 2001; HSDB 

2006; Sittig 2002; Weil and Sandler 1997). Hydrogen sulfide may also be encountered in various 

industrial processes, such as the manufacture of dyes and pigments, felt, artificial silk, farming, brewing, 

glue making, and rubber vulcanization, and in lithography and photoengraving (Beck et al. 1981; Grant 

and Schuman 1993; Sittig 2002). Discharge liquids from these and other activities can release hydrogen 

sulfide to receiving waters (EPA 1993). 

6.2.3 Soil 

There is no information on releases of hydrogen sulfide to the soil from manufacturing and processing 

facilities because these releases are not required to be reported (EPA 2005). 

Hydrogen sulfide has been identified in soil at 13 sites and in sediment at 4 sites among the 35 NPL 

hazardous waste sites, where it was detected in some environmental media (HazDat 2006). 

Hydrogen sulfide may enter the soil through deposition from the atmosphere, migration of mobilized pore 

water, or from leaks and spills associated with manufacture, transport, or storage. Hydrogen sulfide is 

readily soluble in water and would exist as bisulfide or sulfide ions. Hydrogen sulfide can also form 

insoluble sulfide salts with various metals (i.e., copper, zinc, nickel, and iron) that may be present in soils 

(Pouliquen et al. 1989). 
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6. POTENTIAL FOR HUMAN EXPOSURE 

6.3 ENVIRONMENTAL FATE 

6.3.1 Transport and Partitioning 

Since hydrogen sulfide exists as a gas at atmospheric pressure, partitioning to the air is likely to occur 

after environmental releases. However, the compound is also soluble in oil and water, and therefore, may 

partition as well to surface water, groundwater, or moist soil. In addition, sorption of hydrogen sulfide 

from air onto soil (Cihacek and Bremner 1993) and plant foliage (De Kok et al. 1983, 1988, 1991) occurs. 

Hydrogen sulfide's solubility in pure water varies with temperature from 5.3 g/L at 10 °C to 3.2 g/L at 

30 °C. (O'Neil et al. 2001). Once hydrogen sulfide is dissolved in water, it will dissociate into bisulfide 

ion (HS-

) and sulfide ion (S2-); the ratio of the concentrations of these various ions will depend on the pH 

of the solution. Hydrogen sulfide can also form insoluble sulfide salts with various metals (i.e., copper, 

zinc, nickel, and iron) that may be present in soils or environmental waters (Pouliquen et al. 1989). 

Hydrogen sulfide evaporates easily from water, and the rate of evaporation depends on factors such as 

temperature, humidity, pKa, pH, and the concentration of certain metal ions. Hydrogen sulfide will cross 

the air-water interface with kinetics similar to other unreactive gases, such as oxygen (O2), nitrogen (N2), 

and carbon dioxide (CO2), at pHs ≤6. At higher pHs, such as seawater, which has a pH of 8 or greater, 

hydrogen sulfide escape is enhanced due to an ionic species gradient in the water close to the surface 

(Balls and Liss 1983). The Henry's law constant was determined under a variety of conditions for 

hydrogen sulfide dissolved in sewage or distilled water and was found to increase linearly with 

temperature, indicating an increasing tendency to partition to the gas phase (Al-Haddad et al. 1989; also 

see Table 4-2). Other factors found to affect the Henry's law constant in sewage were pH, pK, flow rate, 

and initial hydrogen sulfide concentration. Complexation of bisulfide and sulfide ions to trace metal ions 

(i.e., Zn2+, Co2+, and Ni2+) found in seawater will also have an effect on the transport of hydrogen sulfide 

across the air-water interface (Elliott and Rowland 1990). 

Clay or organic matter may sorb hydrogen sulfide. Smith et al. (1973) determined the sorption of 

hydrogen sulfide to six air-dried and moist soils in a laboratory study. The capacities of soil samples to 

sorb hydrogen sulfide ranged from 15.4 to 65.2 mg/g soil for the air-dried soils, and from 11.0 to 

62.5 mg/g soil for the moist soils (50% water-holding capacity). Capacities and rates of sorption were not 

significantly affected by sterilization of the soil sample, indicating that soil microorganisms are not likely 

to be involved in the sorption process. The authors noted that these values, however, would not provide 

reliable estimates of the amounts of hydrogen sulfide that could be sorbed by soils under natural 

conditions, where the environmental fate of the sorbed hydrogen sulfide would have to be considered. 
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6. POTENTIAL FOR HUMAN EXPOSURE 

Under natural conditions, it is likely that some of the hydrogen sulfide would be oxidized to sulfate, 

which may be removed by leaching or taken up by plants. This, in turn, may make gas sorption sites 

available for additional sorption (Smith et al. 1973). Cihacek and Bremner (1993) showed that soils can 

sorb considerable amounts of hydrogen sulfide from the air, retaining it as elemental sulfur. Several 

species of soil, aquatic, and marine microorganisms oxidize hydrogen sulfide to elemental sulfur, and its 

half-time in these environments usually ranges from 1 hour to several hours (Jørgensen 1982). Food 

chain bioconcentration and biomagnification are unlikely (HSDB 2006). 

6.3.2 Transformation and Degradation 

6.3.2.1 Air 

In the atmosphere, hydrogen sulfide may be oxidized by oxygen (O2) and ozone (O3) to give sulfur 

dioxide (SO2), and ultimately sulfate compounds. Sulfur dioxide and sulfates are eventually removed 

from the atmosphere through absorption by plants, deposition on and sorption by soils, or through 

precipitation (Hill 1973). A residence time of approximately 1.7 days at an ozone concentration of 

0.05 mg/m3

 has been calculated for hydrogen sulfide (WHO 1981). The effective life-times for hydrogen 

sulfide based on summer daytime and yearly average hydroxyl radical concentrations have been estimated 

to be 0.23 and 2.3 days, respectively, based a measured rate constant of 4.8x10-12 cm3

/molecule second 

(Cox 1975). Life-times in air ranging from approximately 1 day in the summer to 42 days in the winter 

have been estimated for hydrogen sulfide (Bottenheim and Strausz 1980). Hydrogen sulfide is not 

expected to be decomposed by direct absorption of ultraviolet radiation and the reaction with ozone is not 

expected to be a significant environmental fate (Cox 1975). 

6.3.2.2 Water 

In aqueous solution, hydrogen sulfide is a weak acid, exhibiting two acid dissociation constants. The first 

dissociation yields bisulfide ion (HS–

), and the second yields sulfide ion (S2–), with pKa values for each of 

these dissociations of 7.04 and 11.96, respectively (O'Neil et al. 2001). At a pH of 7.0, the ratio of the 

concentration of aqueous hydrogen sulfide to bisulfate ion is approximately 1-to-1. As the pH increases 

above 7.0, the ratio of the concentration of bisulfide ion to aqueous hydrogen sulfide increases. At a pH 

of 8, the ratio of the concentration of bisulfide ion to the concentration of aqueous hydrogen sulfide is 

approximately 10-to-1. The relative concentration of sulfide ion does not begin to increase until a pH of 

11 is exceeded; only above pH 12 will the concentration of sulfide ion become significant (>50%). 
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6. POTENTIAL FOR HUMAN EXPOSURE 

Hydrogen sulfide oxidation by O2 readily occurs in surface waters. At 25 °C and pH 8, half-times of 

50 and 26 hours were reported for hydrogen sulfide in water and seawater, respectively. Above pH 8, 

however, the rate of oxidation was independent of pH (Millero et al. 1987). Using a hydrogen peroxide 

concentration of 1x10-7 M as found in surface seawater, the half-time for sulfide oxidation by peroxide in 

seawater would be 2,800 hours. Only at hydrogen peroxide concentrations >10-5 M, such as found in 

rainwaters, would the oxidation of hydrogen sulfide by hydrogen peroxide become competitive with the 

oxidation by oxygen (Millero et al. 1989). Hydrogen sulfide in waste water may be controlled by 

addition of oxidizing chemicals, which react to form less toxic byproducts (Tomar and Abdullah 1994). 

In warm, damp environments (such as manholes and gravity sewers), hydrogen sulfide may be oxidized 

by autotrophic bacteria to sulfuric acid (Boon 1992). Chemical oxidation of hydrogen sulfide dissolved 

in sewage water produces sulfur at pH 6–7, while sulfur, polysulfides, thiosulfates, and ultimately sulfate 

are formed at pHs of 7–9 (Boon 1992). 

6.3.2.3 Sediment and Soil 

Hydrogen sulfide is one of the principal components in the natural sulfur cycle. Bacteria, fungi, and 

actinomycetes (a fungus-like bacteria) release hydrogen sulfide during the decomposition of sulfur 

containing proteins and by the direct reduction of sulfate (SO4

2-). Hydrogen sulfide is also consumed by 

bacteria found in soil and water that oxidize hydrogen sulfide to elemental sulfur. Photosynthetic bacteria 

can oxidize hydrogen sulfide to sulfur and sulfate in the presence of light and the absence of oxygen (EPA 

1993; WHO 1981). A number of microorganisms have been found to degrade hydrogen sulfide to 

elemental sulfur or sulfate. Among these are a heterotrophic bacterium of the genus Xanthomonas 

isolated from dimethyl disulfide-acclimated peat (Cho et al. 1992), heterotrophic fungi (Phae and Shoda 

1991), and a marine isopod (Vismann 1991). Soils may sorb considerable amounts of hydrogen sulfide 

from the air, retaining most of it in the form of elemental sulfur. Manganese compound found in these 

soils appeared to catalyze the oxidation of hydrogen sulfide to elemental sulfur (Cihacek and Bremner 

1993). 

6.4 LEVELS MONITORED OR ESTIMATED IN THE ENVIRONMENT 

Reliable evaluation of the potential for human exposure to hydrogen sulfide depends in part on the 

reliability of supporting analytical data from environmental samples and biological specimens. 
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6. POTENTIAL FOR HUMAN EXPOSURE 

Concentrations of hydrogen sulfide in unpolluted atmospheres and in pristine surface waters are often so 

low as to be near the limits of current analytical methods. In reviewing data on hydrogen sulfide levels 

monitored or estimated in the environment, it should also be noted that the amount of chemical identified 

analytically is not necessarily equivalent to the amount that is bioavailable. The analytical methods 

available for monitoring hydrogen sulfide in a variety of environmental media are detailed in Chapter 7. 

6.4.1 Air 

The concentration of hydrogen sulfide in air can be represented using various concentration units. All air 

monitoring data reported herein are reported in or have been converted into ppm or ppb for ease of 

comparison. The conversion factors are: 1 ppm=1.40 mg/m3

 and 1 ppb=1.40 μg/m3. 

Hydrogen sulfide ambient air concentrations from natural sources have been estimated to be between 

0.11 and 0.33 ppb (EPA 1993). In an unpolluted area of Colorado, concentrations between 0.02 and 

0.07 ppb were measured (Hill 1973). Near ground level, samples taken around a sulfurous New Zealand 

lake charged by an active underground geothermal vent had average hydrogen sulfide levels in the range 

of 0.125–3.9 ppm, which produced no visible adverse effects on indigenous bird or plant populations 

(Siegel et al. 1986). Hydrogen sulfide concentrations in air in remote marine environments are reported 

to be highly variable, ranging from 0.001 to 0.1 ppb (Elliott and Rowland 1990). Concentrations of 

hydrogen sulfide in urban areas are generally <1 ppb (Svendsen 2001). Hydrogen sulfide concentrations 

>90 ppb were measured during several intermittent periods in the Conimicut Point neighborhood in 

Warwick, Rhode Island that resulted from rotting seaweed and shellfish, after a "die-off" of aquatic plants 

and animals that occurred in August 2003 in parts of the eastern Narragansett Bay. The concentration of 

hydrogen sulfide in the residential areas varied over time, depending on the tides, winds, and weather 

(Fulton et al. 2003). 

Indoor air was monitored in five residential homes in the Dakota City/South Sioux City area in Nebraska 

from April 2 to May 15, 1997. Hydrogen sulfide was routinely found in the indoor air of these homes. In 

general, hydrogen sulfide was found to not exceed 90 ppb, which was the upper detection limit for the 

measuring device used in this monitoring study; however, at one home, hydrogen sulfide was found to 

exceed the upper detection limit for periods of 20 minutes to >3 hours on 10 of the 30 days of sampling 

(Agency for Toxic Substances and Disease Registry 1997). 
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6. POTENTIAL FOR HUMAN EXPOSURE 

Durand and Scott (2005) monitored nine properties in the Rotorua geothermal field area in New Zealand 

for various geothermal gases, including hydrogen sulfide. These buildings or the site had a history of 

geothermal gases penetrating the inside of the building. All buildings in this study were found to have 

chronic contamination of the indoor air by hydrogen sulfide, with the entry of the gas through cracks in 

floors and subsurface ducts as the most common means of entry. The highest levels of hydrogen sulfide 

were reported to be emitted from a vent in a concrete floor of a residential property at 435 ppm. In 

another location, two interior hydrogen sulfide vents were found, with one vent containing hydrogen 

sulfide at >200 ppm and the other at 2.9–4.1 ppm (Durand and Scott 2005). 

In early 1999, ATSDR and EPA conducted a 12-month hydrogen sulfide monitoring program in Dakota 

City. Sixteen hydrogen sulfide monitors were stationed in selected locations around the Dakota City area. 

White et al. (1999) noted that the frequency and concentration of hydrogen sulfide levels in Dakota City 

were higher than in a typical urban setting. During 6 months in 1999, peak hydrogen sulfide 

concentrations >90 ppb (the upper detection limit) were recorded at four monitoring locations, and three 

of these locations had multiple peak concentrations exceeding 90 ppb. Multiple peak levels in the range 

of 30–50 ppb were recorded for other residential areas. For three monitoring locations that were distant 

from a known source of hydrogen sulfide, peak levels of 9 and 19 ppb were recorded while most 

measurements were below the detection limit of 2 ppb (White et al. 1999). 

An air monitoring study at a waste water treatment plant in Australia found time-averaged hydrogen 

sulfide levels of 1–2 ppm near the primary clarifiers and inlet structure, and levels <1 ppm at various 

other locations in the 10-hectare plant site (Koe 1985). Hydrogen sulfide was not detected by airsampling instruments located around the perimeter of a landfill in Ohio after a major landslide occurred in 

March 1996 (Ingram et al. 1997). In a study to determine the quantity and composition of reduced sulfur 

gases, including hydrogen sulfide, being released to the atmosphere at waste water treatment plants in 

Baton Rouge, Louisiana at various steps of the treatment process, hydrogen sulfide was found to be the 

dominant sulfur compound emitted. The concentrations of hydrogen sulfide were typically <7.5 ppm 

sulfur, with concentrations ranging from 0.013 ppm sulfur at the central treatment plant final effluent box 

up to 340 ppm sulfur at the central treatment plant digester dome of the floating roof (Devai and DeLaune 

1999). The hydrogen sulfide concentration in the atmosphere of a Norwegian sewage purification plant 

was generally below 2 ppm; however, a peak concentration of 100 ppm was detected (Søstrand et al. 

2000). As part of the 1997 Fresh Kills Air Monitoring Program, >140,000 observations of ambient air 

were collected over a 2-month period at 16 locations on Staten Island, New York. Hydrogen sulfide was 
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6. POTENTIAL FOR HUMAN EXPOSURE 

measured at detectable levels in only about half of the samples, with measured levels ranging from 2 ppb 

(the detection limit) to 33 ppb (Agency for Toxic Substances and Disease Registry 2000). 

Hydrogen sulfide concentrations in air can vary widely during manure management activities. Levels of 

hydrogen sulfide in air in pig barns during normal operations are generally <5 ppm; however, 

concentrations can rapidly rise up to 800 ppm inside manure transfer pits or lift stations when the manure 

is agitated, and the hydrogen sulfide can back up into pig rooms through open pits or piping. 

Concentrations of hydrogen sulfide have been shown to increase from very low levels to 1,300 ppm in 

deep-pit buildings when manure is agitated (Chénard et al. 2003). 

The concentrations of sulfur compounds, including hydrogen sulfide, were measured in the air at four 

paper pulp mills using the kraft (sulfate) process. In this process, steam, high temperature, high pressure, 

and a solution containing sodium hydroxide and sodium sulfide is used to digest wood chips. Various 

sulfur gases are produced during this process. Hydrogen sulfide concentrations ranged from not detected 

(<0.2 ppm) to 35 ppm at various emission sources in the continuous digester, batch digester, and pulp 

washing areas. In general, hydrogen sulfide was not detected in ambient air sampled at these plants 

(Goyer 1990). A survey of occupational exposure in nonproduction departments of pulp, paper, and 

paper product mills from 147 mills in 11 countries found that hydrogen sulfide was below the detection 

limit in 45% of the 20 measurements taken at 6 mills. A mean concentration of 2.9 ppm was reported, 

with a maximum value of 53 ppm and a lowest detected value of 0.04 ppm (Teschke et al. 1999). The 

concentrations of various pollutants were measured in the air of five textile factories, which included 

three weaving and dyeing factories and two clothing factories; hydrogen sulfide concentrations ranged 

from <0.007 to 1.32 ppm (Rimatori et al. 1996). 

Ten air samples were collected for hydrogen sulfide at the World Trade Center disaster site in New York 

City between September 18 and October 4, 2001. Concentrations ranged from not detected (3 of the 

10 samples) to 3.0 ppm (Wallingford and Snyder 2001). 

Hydrogen sulfide levels in air on some NPL sites ranged from 0.00101 to 808 ppm at the Hartford 

Landfill in 1994 and at the Seattle Municipal Landfill in Washington in 1985, respectively (HazDat 

2006). Data on ambient air concentrations at all NPL sites were not available, however. Concentrations 

of hydrogen sulfide in soil gas from samples taken at some NPL sites ranged from 0.29 to 47,000 ppm, 

reported at Holly Hill Resource Facility in Connecticut in 1999 and at the Industri-plex site in 

Massachusetts in 1990, respectively (HazDat 2006). Data on soil gas concentrations at all NPL sites were 
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6. POTENTIAL FOR HUMAN EXPOSURE 

not available. It should be noted that concentrations in soil gas are likely to be higher than would be 

found in the breathing zone of an individual. 

6.4.2 Water 

Hydrogen sulfide readily evaporates from surface waters and is not likely to persist in highly oxygenated 

waters; levels in these environments are expected to be low. Groundwater samples from an area receiving 

acid-mine drainage in Colorado averaged 0.9 ppm of hydrogen sulfide, while samples from a power plant 

site averaged 0.03 ppm (Patterson and Runnells 1992). 

Accurate measurements of hydrogen sulfide water levels are usually complicated by the presence of other 

sulfide compounds. At pHs ≥7, hydrogen sulfide is significantly dissociated, and the exact source of 

sulfide would not necessarily be known. A method of determining sulfide concentration in unspecified 

waste water by first transforming it to hydrogen sulfide and then measuring the atomic absorption of the 

product yielded results ranging from 3.1 to 5.1 ppm of sulfide sulfur (Parvinen and Lajunen 1994). Total 

sulfide levels in samples from the Mississippi River were about 0.92 ppm, while levels in pond and well 

water in St. Paul, Minnesota were 1.6 and 1.9 ppm, respectively (Slooff et al. 1991). 

Nearshore hydrogen sulfide eruptions occur in the Atlantic Ocean along the central coast of Nambia. 

Dissolved hydrogen sulfide concentrations were found to range from <0.02 to 3.39 ppm in water sampled 

at various depths during eruption events that occurred during 2001–2002 (Weeks et al. 2004). 

6.4.3 Sediment and Soil 

Hydrogen sulfide levels as high as 11.7 ppm in soil water were measured in Louisiana rice fields (Hollis 

1985). The hydrogen sulfide in these samples was presumably bound to colloidal clay or organic matter, 

as these levels were higher than typical solubility would predict and were not accompanied by the 

characteristic hydrogen sulfide odor. Sediment pore water from the Grand Calumet River in an 

industrialized area of Indiana contained 0.2–1.5 ppb of hydrogen sulfide (Hoke et al. 1993). In general, 

undisturbed anoxic sediment pore water may contain up to 100 ppb hydrogen sulfide, while disturbed 

sediments typically contain pore water concentrations of 1–30 ppb (Dillon et al. 1993). 
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6. POTENTIAL FOR HUMAN EXPOSURE 

6.4.4 Other Environmental Media 

Hydrogen sulfide is commonly found in coal, petroleum, and natural gas deposits and may be mobilized 

by human manipulation of these resources. Coal gasification, a process whereby coal is subjected to heat 

and steam treatment to produce a convenient energy source, results in a gas product consisting of up to 

1% hydrogen sulfide (Barik et al. 1987). Hydrogen sulfide was identified as a component in the vapor 

phase of cigarette smoke (Dong et al. 2000), and was found in the emissions of gasoline vehicles (Collier 

et al. 2002). 

Hydrogen sulfide formation has been demonstrated in pediatric intravenous amino acid solutions used to 

treat infants with high protein requirements (Decsi and Koletzko 1993). Levels up to 1.96 ppm were 

found, presumably formed by sulfide liberation from cysteine derivatives during heat sterilization. 

Similar chemical reactions may explain the presence of hydrogen sulfide in dental plaque (Tonzetich and 

Carpenter 1971). Meat products may be contaminated with hydrogen sulfide-producing bacteria, 

resulting in off-odors and spoilage (McMeekin and Patterson 1975). 

Hydrogen sulfide is produced in the large intestine of mammals by metabolism of sulfhydryl proteins by 

anaerobic bacteria, and may compose up to 10% of intestinal gases (Beauchamp et al. 1984; EPA 1978). 

Hydrogen sulfide was found in the gas produced by feces of infants, and levels were found to vary based 

on the types of diets the infants were fed and the age of the infants. Fecal gas production for infants aged 

1–3 months was 372–833, 73–371, and 1,904–2,540 nmol/g (12.7–28.3, 2.5–12.6, and 65.8–86.4 μg/g) 

dry weight for infants fed breast milk, milk-based formula, and soy based formula, respectively (Jiang et 

al. 2001). Fecal sulfide concentrations in 15 adult volunteers ranged from 110 to 720 nmol/g (3.74– 

24.5 μg/g) wet weight. Fecal sulfide concentrations were found to increase significantly from 160 to 

750 nmol/g (5.4–26 μg/g), when subjects were fed diets containing increasing amounts of meat. Sulfide 

concentrations in whole blood samples from 6 healthy adults were found to range from 10 to 100 μmol/L 

(0.3–3 μg/mL). When increasing amounts of protein from meat were added to the diet of these subjects, 

blood sulfide concentrations did not change significantly (Richardson et al. 2000). Hydrogen sulfide is 

also produced in the human mouth by microbial putrefaction (Rosenberg et al. 1991). Mean sulfide levels 

in human brainstems controls were reported as 0.69 and 0.59 μg/g for males (n=36) and females (n=9), 

respectively. Sulfide concentrations of 0.91 and 1.04 μg/g were reported in brainstems from 2 suspected 

hydrogen sulfide inhalation fatalities (Goodwin et al. 1989). Concentrations of sulfide in the blood, brain, 

lung, and femoral muscle of a victim of a fatal hydrogen sulfide poisoning were 0.45 μg/mL, 2.72 μg/g, 

0.42 μg/g, and 0.16 μg/g, respectively. The victim was kept at 0 °C until autopsy, 20 hours after death; 
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6. POTENTIAL FOR HUMAN EXPOSURE 

these conditions were expected to significantly suppress sulfide production due to putrefaction (Kage et 

al. 1998). Blood sulfide levels at 4 μg/mL were found in an individual who died while working at a 

treatment, storage, and disposal facility for hazardous waste materials. Sulfide levels were also analyzed 

in tissue samples and confirmed that the blood sulfide concentrations could not be attributed to cellular 

decay. Through an investigation by the OSHA, it was determined that high concentrations of hydrogen 

sulfide were apparently generated during the waste acid neutralization process (Smith and Cummins 

2004). 

6.5 GENERAL POPULATION AND OCCUPATIONAL EXPOSURE 

Primary exposure of the general population to hydrogen sulfide most likely occurs through inhalation of 

ambient air. As hydrogen sulfide is part of the natural environment, the general population will have 

some exposure to hydrogen sulfide. Hydrogen sulfide is produced in the human large intestine by the 

bacterial reduction of inorganic sulfate and sulfite, and by fermentation of sulfur-containing amino acids, 

cysteine, and methionine (Richardson et al. 2000), and can compose up to 10% of intestinal gases (EPA 

1978). Hydrogen sulfide is produced by the natural bacteria found in the human mouth, and is a 

component of bad breath (halitosis) (Rosenberg et al. 1991). 

Hydrogen sulfide may occur naturally in well water, and can be formed in hot water heaters, giving 

household hot tap water an unpleasant odor. Formation of hydrogen sulfide can occur by the reduction of 

sulfates in the water by sulfur bacteria, which can thrive in the warm environment of the hot water heater, 

or by reaction with the magnesium anode in the hot water heater tank (MDH 2004). Populations living in 

areas of geothermal activity, near waste sites or industries such as petroleum refineries, natural gas plants, 

petrochemical plants, coke oven plants, kraft paper mills, food processing plants, landfills, manure 

treatment facilities, waste water treatment facilities, and tanneries may be more likely to be exposed to 

higher levels hydrogen sulfide. Geothermal gases, including hydrogen sulfide, were found to be entering 

buildings in Rotorua, New Zealand directly from the ground through floors, walls and subsurface pipes; 

indoor vents emitting up to approximately 200 ppm were reported (Durand and Scott 2005). The general 

population may also be exposed to hydrogen sulfide by accidental release ("blowout") from natural gas 

wells during drilling operations near residential areas (Layton and Cederwall 1986; Leahey and Schroeder 

1986). Exposures to hydrogen sulfide have occurred through the mixing of acid and basic drain cleaners, 

and through the use of acid drain cleaner to remove sludge-clogged drains, but these incidents are thought 

to be rare (Oderda 1975). 
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6. POTENTIAL FOR HUMAN EXPOSURE 

Residents of the Conimicut Point neighborhood in Warwick, Rhode Island were exposed to hydrogen 

sulfide from rotting seaweed and shellfish, after a "die-off" of aquatic plants and animals that occurred on 

August 20, 2003 in parts of the eastern Narragansett Bay. The concentration of hydrogen sulfide in the 

residential areas varied over time, depending on the tides, winds, and weather. During the week of 

September 15, 2003, the Rhode Island Department of Environmental Management measured several 

intermittent periods when hydrogen sulfide concentrations were >90 ppb (Fulton et al. 2003). Emissions 

from the Fresh Kills Landfill on Staten Island, New York, which contain hydrogen sulfide, are blown by 

prevailing wind into nearby neighborhoods (Agency for Toxic Substances and Disease Registry 2000). 

Workers may be occupationally exposed to hydrogen sulfide from fermenting manure (Chénard et al. 

2003; Morse et al. 1981), and stagnant wells (McDonald and McIntosh 1951), as well as in areas of 

waste-water treatment facilities (NIOSH 1980b, 1984, 1985a, 1985d, 1990), extruded rubber plants 

(NIOSH 1985b), landfills (Lehman 1996), textile industries (Rimatori et al. 1996), and petroleum 

refineries (NIOSH 1982a, 1982b). Facilities where hydrogen sulfide can be generated include petroleum 

refineries, natural gas plants, petrochemical plants, coke oven plants, kraft paper mills, viscose rayon 

manufacturing plants, sulfur production facilities, iron smelters, food processing plants, and tanneries 

(Svendsen 2001). Major occupational exposures to hydrogen sulfide have resulted from its presence as a 

byproduct of chemical reactions that may take place in viscose rayon and leather tanning processes 

(ACGIH 1991). Hydrogen sulfide is also used as an agricultural disinfectant and as an additive in 

lubricants and cutting oils (Bingham et al. 2001; HSDB 2006; Sittig 2002). Hydrogen sulfide may also be 

encountered in various industrial processes, such as the manufacture of dyes and pigments, felt, rayon and 

artificial silk, in brewing, glue making, and rubber vulcanization, and in lithography and photoengraving 

(Beck et al. 1981; Grant and Schuman 1993; Sittig 2002). Hydrogen sulfide levels were measured using 

personal monitors worn by farm workers in Norway during 1992–1996 while performing various tasks, 

such as handling of harvest, tending to animals, and handling of manure. Hydrogen sulfide was only 

detectable in 7 out of 23 measurements with a range of peak values of 0.2–6 ppm (Eduard et al. 2001). 

Toxic exposure data for 1995, compiled from 67 poison control centers, indicated that there were 

1,407 hydrogen sulfide exposures during that year, 3 of which were intentional exposures (Litovitz et al. 

1996). None of these individuals died, and the vast majority of these exposures resulted in outcomes that 

were either minor or nonexistent. Approximately 34% of the exposed individuals were treated in a health 

care facility (Litovitz et al. 1996). 
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6. POTENTIAL FOR HUMAN EXPOSURE 

6.6 EXPOSURES OF CHILDREN 

This section focuses on exposures from conception to maturity at 18 years in humans. Differences from 

adults in susceptibility to hazardous substances are discussed in Section 3.7, Children’s Susceptibility. 

Children are not small adults. A child’s exposure may differ from an adult’s exposure in many ways. 

Children drink more fluids, eat more food, breathe more air per kilogram of body weight, and have a 

larger skin surface in proportion to their body volume. A child’s diet often differs from that of adults. 

The developing human’s source of nutrition changes with age: from placental nourishment to breast milk 

or formula to the diet of older children who eat more of certain types of foods than adults. A child’s 

behavior and lifestyle also influence exposure. Children crawl on the floor, put things in their mouths, 

sometimes eat inappropriate things (such as dirt or paint chips), and spend more time outdoors. Children 

also are closer to the ground, and they do not use the judgment of adults to avoid hazards (NRC 1993). 

Hydrogen sulfide is found naturally in crude petroleum, natural gas, volcanic gases, hot springs, and often 

as the result of bacterial breakdown of organic matter. Children are more likely to be exposed to 

hydrogen sulfide near animal waste sites such as the sediments of fish aquaculture, livestock barns, or 

manure areas. Inhalation is the most likely route of exposure, and there are no known exposure pathways 

that are unique to children, although hydrogen sulfide is heavier than air so that children might be 

exposed to higher concentrations than adults. Children living in areas of geothermal activity, near waste 

sites or industries such as petroleum refineries, natural gas plants, petrochemical plants, coke oven plants, 

kraft paper mills, food processing plants, and tanneries are more likely to be exposed to higher levels of 

hydrogen sulfide. Geothermal gases, including hydrogen sulfide, were found to be entering buildings in 

Rotorua, New Zealand directly from the ground through floors, walls, and subsurface pipes; indoor vents 

emitting up to approximately 200 ppm were reported. This concentration is high enough to present an 

acute respiratory hazard to persons close to the vent, such as children playing on the floor (Durand and 

Scott 2005). In a clinical case involving a 20-month-old child whose parents lived beside a coal mine 

where a burning tip had been emitting hydrogen sulfide for nearly 1 year, the patient had symptoms of 

ataxia and an abnormal CT scan of the brain (Gaitonde et al. 1987). Monitoring data showed that the 

hydrogen sulfide levels in the air were approximately 0.6 ppm, but may have been higher before data 

were collected. 

Hydrogen sulfide is also produced by bacteria in the mouth and gastrointestinal tract. Hydrogen sulfide 

formation has been demonstrated in pediatric intravenous amino acid solutions used to treat infants with 
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6. POTENTIAL FOR HUMAN EXPOSURE 

high protein requirements (Decsi and Koletzko 1993). Levels up to 1.96 ppm were found, presumably 

formed by sulfide liberation from cysteine derivatives during heat sterilization. 

There are no known studies in which hydrogen sulfide levels were measured in the blood or other tissues 

of children. Hydrogen sulfide was found in the gas produced by feces of infants, and levels were found to 

vary based on the types of diets the infants were fed and the age of the infants. Fecal gas production for 

infants aged 1–3 months were 372–833, 73–371, and 1,904–2,540 nmol/g (12.7–28.3, 2.5–12.6, and 

65.8–86.4 μg/g) dry weight for infants fed breast milk, milk based formula, and soy based formula, 

respectively (Jiang et al. 2001). 

It is not clear whether hydrogen sulfide can be transferred from mother to fetus. There is limited evidence 

that women occupationally exposed to hydrogen sulfide have a higher rate of spontaneous abortions. 

Women employed in rayon textile and paper products jobs in Finland were found to have an increased 

rate of spontaneous abortions when the mean annual level of hydrogen sulfide exceeded 3 ppb 

(Hemminki and Niemi 1982). An increase in spontaneous abortions was also found in women working in 

petrochemical plants in China as compared to women working in non-chemical plants (Xu et al. 1998). 

6.7 POPULATIONS WITH POTENTIALLY HIGH EXPOSURES 

Workers employed at facilities that manufacture or use hydrogen sulfide in the production process are 

especially prone to exposure. Such industries include the manufacture of rayon textiles, lubricants, pulp 

and paper, and sulfuric acid and inorganic sulfides. Workers in facilities where hydrogen sulfide is 

produced as a byproduct, such as farms with manure storage pits, petroleum or natural gas drilling 

operations, landfills, and waste water treatment plants, may also be exposed to high levels of hydrogen 

sulfide. 

6.8 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of hydrogen sulfide is available. Where adequate information 

is not available, ATSDR, in conjunction with NTP, is required to assure the initiation of a program of 
HYDROGEN SULFIDE 133 

6. POTENTIAL FOR HUMAN EXPOSURE 

research designed to determine the health effects (and techniques for developing methods to determine 

such health effects) of hydrogen sulfide. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would 

reduce the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 

6.8.1 Identification of Data Needs 

Physical and Chemical Properties. Information is available on the physical and chemical 

properties of hydrogen sulfide (Al-Haddad et al. 1989; Amoore and Hautala 1983; Daubert and Danner 

1989; HSDB 2006; NIOSH 2006; O'Neil et al. 2001). However, additional information on those 

properties that determine the specific fate, transport, and rates of transformation of hydrogen sulfide as 

part of the larger sulfur cycle would be useful in discerning the environmental fate and behavior of this 

compound. 

Production, Import/Export, Use, Release, and Disposal. Adequate information on the 

production and use of hydrogen sulfide was found; no information on the import/export of hydrogen 

sulfide was located. Since hydrogen sulfide is not required to be reported under the TRI, the production 

and emissions from U.S. industrial facilities is not reported to the EPA. Information of production, 

emissions, and disposal would be useful in identifying important processes leading to human exposure. 

Environmental Fate. Hydrogen sulfide is known to easily evaporate into the air (EPA 1993; Layton 

and Cederwall 1986; Leahey and Schroeder 1986), although its solubility in water may also cause it to 

persist in unperturbed, anoxic sediments. Additional information on the transport, transformation, and 

persistence of the compound in soils and groundwater, particularly at hazardous waste sites, would be 

useful in identifying the most important routes of human exposure to hydrogen sulfide. 

Bioavailability from Environmental Media. Additional information on absorption following 

dermal contact with, or ingestion of, contaminated soil and water would also be helpful in determining the 

importance of this route of exposure for populations of concern. 
HYDROGEN SULFIDE 134 

6. POTENTIAL FOR HUMAN EXPOSURE 

Food Chain Bioaccumulation. Sufficient information is available to demonstrate that hydrogen 

sulfide is not likely to bioaccumulate or biomagnify in the food chain. 

Exposure Levels in Environmental Media. Reliable monitoring data for the levels of hydrogen 

sulfide in media at hazardous waste sites are needed so that the information obtained on levels of 

hydrogen sulfide in the environment can be used in combination with the known body burden of 

hydrogen sulfide to assess the potential risk of adverse health effects in populations living in the vicinity 

of hazardous waste sites. 

Monitoring of hydrogen sulfide levels in ambient air is currently sporadic; additional, more systematic 

sampling is needed, particularly in areas that may have a significant source of hydrogen sulfide. Methods 

for accurately measuring dissolved sulfides in water are also available (APHA 1998). As hydrogen 

sulfide is a weak acid, concentrations of aqueous hydrogen sulfide will depend on the pH of the solution. 

The concentration of un-ionized hydrogen sulfide can be calculated from the concentration of dissolved 

sulfide components, the pH of the solution, and the acidity constants for hydrogen sulfide (APHA 1998). 

Reliable monitoring data for the levels of hydrogen sulfide in contaminated media at hazardous waste 

sites are needed so that the information obtained on levels of hydrogen sulfide in the environment can be 

used in combination with the known body burdens of hydrogen sulfide to assess the potential risk of 

adverse health effects in populations living in the vicinity of hazardous waste sites. More data on the 

levels of hydrogen sulfide at the point of emission (on-site) versus levels at the point of exposure (offsite) would be useful. 

Exposure Levels in Humans. Occupational studies often do not report exposure levels. Additional 

information is needed on the exposure levels among populations living in the vicinity of hazardous waste 

sites and other potential sources of hydrogen sulfide, such as hot springs and waste water treatment plants. 

This information is necessary for assessing the need to conduct health studies on these populations. 

Exposures of Children. The only information that provided an assessment of exposure of children 

and adolescents to hydrogen sulfide was that developed during the South Karelia Air Pollution Study in 

southeastern Finland where there are a cluster of pulp mills using the sulfate method (Marttila et al. 

1994b); however, determining the magnitude of these exposures was complicated by the study's analysis 

of only gross sulfur concentrations rather than measuring the concentrations of individual sulfur­
HYDROGEN SULFIDE 135 

6. POTENTIAL FOR HUMAN EXPOSURE 

containing compounds and particulates. Additional exposure information is needed from communities 

where only hydrogen sulfide exceeds background levels. 

Child health data needs relating to susceptibility are discussed in Section 3.12.2, Identification of Data 

Needs: Children’s Susceptibility. 

Exposure Registries. No exposure registries for hydrogen sulfide were located. This substance is 

not currently one of the compounds for which a sub-registry has been established in the National 

Exposure Registry. The substance will be considered in the future when chemical selection is made for 

sub-registries to be established. The information that is amassed in the National Exposure Registry 

facilitates the epidemiological research needed to assess adverse health outcomes that may be related to 

exposure to this substance. 

6.8.2 Ongoing Studies 

No ongoing studies pertaining to the environmental fate of hydrogen sulfide were identified in a search of 

the Federal Research in Progress database (FEDRIP 2005). 
HYDROGEN SULFIDE 136 

6. POTENTIAL FOR HUMAN EXPOSURE 

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HYDROGEN SULFIDE 137 

7. ANALYTICAL METHODS 

The purpose of this chapter is to describe the analytical methods that are available for detecting, 

measuring, and/or monitoring hydrogen sulfide, its metabolites, and other biomarkers of exposure and 

effect to hydrogen sulfide. The intent is not to provide an exhaustive list of analytical methods. Rather, 

the intention is to identify well-established methods that are used as the standard methods of analysis. 

Many of the analytical methods used for environmental samples are the methods approved by federal 

agencies and organizations such as EPA and the National Institute for Occupational Safety and Health 

(NIOSH). Other methods presented in this chapter are those that are approved by groups such as the 

Association of Official Analytical Chemists (AOAC) and the American Public Health Association 

(APHA). Additionally, analytical methods are included that modify previously used methods to obtain 

lower detection limits and/or to improve accuracy and precision. 

7.1 BIOLOGICAL MATERIALS 

A limited number of analytical techniques have been used for measuring hydrogen sulfide in the breath 

(expired air) and sulfide in biological tissues and fluids including blood and saliva. These include gas 

chromatography coupled with flame ionization detection (GC/FID), gas chromatography coupled with 

flame photometric detection (GC/FPD), iodometric titration, potentiometry with ion-selective electrodes 

(ISE), spectrophotometry, and high-performance liquid chromatography (HPLC). The measurement of 

sulfide concentrations in biological materials is difficult due to its volatility, tendency to undergo 

oxidation, adsorption to glass and rubber, and binding to organic molecules (Richardson et al. 2000). 

Details of commonly used analytical methods for several types of biological media are presented in 

Table 7-1. 

In air, hydrogen sulfide will exist in its molecular form, and methods are available to measure hydrogen 

sulfide in air. However, in aqueous solution, hydrogen sulfide is a weak acid, exhibiting two acid 

dissociation constants. The first dissociation yields bisulfide ion (HS–

), and the second yields sulfide ion 

(S2–), with pKa values for each of these dissociations of 7.04 and 11.96, respectively (O'Neil et al. 2001). 

In biological tissues and fluids, sulfide concentrations typically would be determined. The concentration 

of the un-ionized hydrogen sulfide can be calculated from the concentration of dissolved sulfide 

 


 

	 

	 

	 

HYDROGEN SULFIDE 138 

7. ANALYTICAL METHODS 

Table 7-1. Analytical Methods for Determining Hydrogen Sulfide, Sulfide, and 

Thiosulfate in Biological Samples 

Sample 

Sample Analytical detection Percent 

matrix Preparation method method limita recovery Reference 

Blood Hydrogen sulfide in generated 

in Kipp's apparatus and trapped 

in NaOH solution; pH is 

adjusted to 6.5–6.8, azide and 

excess iodine are added. 

Blood Hydrogen sulfide in generated 

in Kipp's apparatus and trapped 

in NaOH solution; sulfide 

antioxidation buffer is added. 

Blood Liberation of blood sulfide by 

addition of acid; trapping of 

hydrogen sulfide gas in NaOH 

solution. 

Blood and For thiosulfate detection, add 

urine 0.2 mL sample to mixture of 

0.5 mL of 20 mM pentafluorobenzyl bromide (PFBBr) 

solution in acetone, 0.05 mL of 

5% sodium chloride. Vortex for 

1 minute and add 2 mL of 

25 mM iodine solution in ethyl 

acetate and 0.5 mL of internal 

standard solution (40 μM 

1,3,5-tribromobenzene [TBB] in 

ethyl acetate). Vortex for 

30 seconds and centrifuge at 

2,500 rpm for 15 minutes, allow 

to stand for 1 hour. 

Blood and For sulfide detection, add 

urine 0.2 mL sample to mixture of 

0.5 mL of 20 mM PFBBr 

solution in toluene, 2.0 mL of 

internal standard solution 

(10 μM TBB in ethyl acetate), 

and 0.8 mL of 5 mM tetradecyldimethylnenzyl ammonium 

chloride solution in oxygen-free 

water saturated with sodium 

tetraborate. Vortex 1 minute, 

add 0.1 g potassium 

dihydrogenphosphate as a 

buffer. Vortex for 10 seconds, 

centrifuge at 2,500 rpm for 

10 minutes. 

Iodometric 4 μg/L 98–102 Puacz et al. 1995 

method 

Potentiometry NR 98–102 Puacz et al. 1995 

(ISE) 

ISE 10 μg/L NR Lindell et al. 1988 

GC/ECD 3 μmol/L NR Kage et al. 1997 

GC/ECD 0.3 μmol/L NR Kage et al. 1997 

 


 

	 

	 

	 

	 

	 

	 

	 

	 

HYDROGEN SULFIDE 139 

7. ANALYTICAL METHODS 

Table 7-1. Analytical Methods for Determining Hydrogen Sulfide, Sulfide, and 

Thiosulfate in Biological Samples 

Sample 

Sample Analytical detection Percent 

matrix Preparation method method limita recovery Reference 

Urine Freeze and store freshly voided 

urine samples at -25 °C until 

analysis within 24 hours after 

exposure. Analyze urinary 

thiosulfate as its bromobimane 

product. Correct results for the 

excreted creatinine analyzed in 

the same samples. 

Blood and Addition of zinc acetate to trap 

feces sulfide, followed by 

microdistillation into NaOH 

solution to trap evolved 

hydrogen sulfide; analysis by 

ion chromatography. 

Breath Connect Teflon sampling probe 

to analyzer and syringe through 

a sampling valve and loop; 

insert probe 4 cm into mouth 

between closed lips; withdraw 

20 mL over 6 seconds into 

syringe; flush and fill the 

sample loop with 10 mL mouth 

air; carry sample to analysis in 

nitrogen gas. 

Breath Collect air from breathing zone 

using a midget impinger 

containing calcium hydroxidecalcium sulfide-arabinogalactan 

slurry; add solution of N,Ndimethyl-p-phenylenediamine 

and ferric chloride. 

Saliva Collect 3 mL aliquot with sterile 

pipette; introduce into 2-ounce 

glass container and cap; 

incubate 24 hours at 37 °C; 

withdraw through cap with gastight syringe. 

LC NR 

IC/ECD 2.5 μmol/L 

GC/FID 10 μg/m3 

(7 ppb) 

Spectro- 0.20 μg/m3 

photometry (0.1 ppb) 

GC/FID, NR 

microcoulometric titration 

92, 80 Kangas and 

Savolainen 1987 

92–102 Richardson et al. 

(feces) 2000 

79–102 

(blood) 

NR	 Blanchette and 

Cooper 1976 

80 NIOSH 1977a 

NR Solis and Volpe 

1973 

 


 

HYDROGEN SULFIDE 140 

7. ANALYTICAL METHODS 

Table 7-1. Analytical Methods for Determining Hydrogen Sulfide, Sulfide, and 

Thiosulfate in Biological Samples 

Sample 

Sample Analytical detection Percent 

matrix Preparation method method limita recovery Reference 

Brain, lung, 

and 

femoral 

muscle 

Brain, lung, 

and 

femoral 

muscle 

Brain, liver, 

and kidney 

tissue 

(mouse) 

For sulfide detection, add 0.2 g 

sample (minced) to mixture of 

0.5 mL of 20 mM PFBBr 

solution in toluene, 2.0 mL of 

internal standard solution 

(10 μM TBB in ethyl acetate), 

and 0.8 mL of 5 mM tetradecyldimethylnenzyl ammonium 

chloride solution in oxygen-free 

water saturated with sodium 

tetraborate. Vortex 1 minute, 

add 0.1 g potassium 

dihydrogenphosphate as a 

buffer. Vortex for 10 seconds, 

centrifuge at 2,500 rpm for 

10 minutes. 

For thiosulfate detection, add 

0.2 g sample (minced) to 

mixture of 0.5 mL of 20 mM 

PFBBr solution in acetone, 

0.05 mL of 5% sodium chloride 

and 0.5 mL of 200 mM 

L-ascorbic acid. Vortex for 

1 minute and add 2 mL of 

25 mM iodine solution in ethyl 

acetate and 0.5 mL of internal 

standard solution (40 μM TBB 

in ethyl acetate). Vortex 

30 seconds and centrifuge at 

2,500 rpm for 15 minutes, allow 

to stand for 1 hour. 

Weight sample; homogenize in 

aqueous zinc acetate using a 

rotostator at 18,000 rpm for 

20 seconds; dilute with borate 

buffer; convert to methylene 

blue. 

GC/MS NR NR Kage et al. 1998 

GC/MS NR NR Kage et al. 1998 

Ion-interaction nmol/g NR Mitchell et al. 

reversed- 1993 

phase HPLC 

 


 

HYDROGEN SULFIDE 141 

7. ANALYTICAL METHODS 

Table 7-1. Analytical Methods for Determining Hydrogen Sulfide, Sulfide, and 

Thiosulfate in Biological Samples 

Sample 

Sample Analytical detection Percent 

matrix Preparation method method limita recovery Reference 

Brain Homogenization in coid 0.01 M Gas 0.02 μg/g 95–99 (rat Goodwin et al. 

tissue NaOH. Centrifuge and dialysis/ion tissue) 1989 

(rat and resuspend pellet; add zinc chromatohuman) acetate and ascorbic acid; graphy with 

readjust pH; use continuous ECD 

flow gas dialysis system to 

separate sulfide. 

a

Conversion factor: 1 ppm=1.40 mg/m3 

GC/ECD = gas chromatography/electron capture detector; GC/FID = gas chromatography/flame ionization detector; 

GC/MS = gas chromatography/mass spectrometry; HPLC = high performance liquid chromatography; IC = ion 

chromatography; ISE = ion-selective electrode; LC = liquid chromatography; M = molar; NaOH = sodium hydroxide; 

NR = not reported; PFBBr = pentafluorobenzyl bromide; rpm = revolutions per minute; TBB = 1,3,5-tribromobenzene 
HYDROGEN SULFIDE 142 

7. ANALYTICAL METHODS 

components (e.g., HS-, S2-), pH of the solution, and acidity constants for hydrogen sulfide using the 

following equilibrium expressions for the ionization of hydrogen sulfide and bisulfide ion (APHA 1998). 

[HS − (aq)][H + (aq)] Ka1 = [H 2 S(aq)] 

[S 2− (aq)][H + (aq)] Ka2 = [HS − (aq)] 

Puacz et al. (1995) developed a catalytic method, based on the iodine-azide reaction, for the determination 

of sulfide in whole human blood. The method involves the generation of hydrogen sulfide in an 

evolution-absorption apparatus. In addition, the method allows for the determination of sulfide in blood 

without interference from other sulfur compounds in blood. This method is appropriate for the 

determination of sulfide in the concentration range of 4–3,000 μg/L. A percent recovery of 98–102% was 

achieved. Although the accuracy and precision of the catalytic method are comparable to those of the 

ion-selective electrode method, the catalytic method is simpler, faster, and would be advantageous in 

serial analysis. 

Richardson et al. (2000) developed a method for measuring sulfide in whole blood and feces, which 

overcomes the problems of viscosity and turbidity that are typical for these types of samples. Turbidity of 

the sample interferes with colorimetric assays such as methylene blue. In this method, samples are first 

treated with zinc acetate to trap the sulfide as an insoluble zinc complex. Next, a microdistillation 

pretreatment is used to release the complexed sulfide into a sodium hydroxide solution. This 

microdistillation step is coupled to ion chromatography with electron capture detection. A detection limit 

of 2.5 μmol/L (80 μg/L) and percent recoveries of 92–102% (feces) and 79–102% (blood) were reported. 

GC/FPD was employed for measuring hydrogen sulfide in human mouth air with a detection limit of 

7 ppb (Blanchette and Cooper 1976) and included improvements such as calibration of the system with 

permeation tubes, use of a variable beam splitter to produce a wide range of vapor concentrations, and the 

ability to handle samples of limited volume. 

For occupational measurements of airborne concentrations, NIOSH (1977a) recommended the use of a 

midget impinger for sampling breathing zone air and the methylene blue/spectrophotometric method for 

the analysis of hydrogen sulfide. The detection limit was 0.14 ppb. 
HYDROGEN SULFIDE 143 

7. ANALYTICAL METHODS 

GC/FID has been used for quantifying sulfur volatiles such as hydrogen sulfide in human saliva (Solis 

and Volpe 1973). This method included microcoulometric titrations and a procedure for incubation of 

saliva and sampling of headspace sulfur volatile components. The amount of total sulfur volatiles 

detected in control samples of saliva incubated at 37 °C for 24 hours ranged from 4.55 to 13.13 ppm. 

Fresh and frozen mouse tissue samples obtained from brain, liver, and kidney have been analyzed for 

hydrogen sulfide levels by sulfide-derived methylene blue determination using ion-interaction reversedphase HPLC (Mitchell et al. 1993). This method can quantify nmol/g levels of sulfide. Gas dialysis/ion 

chromatography with ECD has been utilized for measurement of sulfide in rat brain tissue with 95–99% 

recovery (Goodwin et al. 1989). Goodwin et al. (1989) also applied this method to human brain tissue 

samples from two suspected hydrogen sulfide fatalities. 

7.2 ENVIRONMENTAL SAMPLES 

The methods most commonly used to detect hydrogen sulfide in environmental samples include GC/FPD, 

gas chromatography with electron capture detection (GC/ECD), iodometric methods, the methylene blue 

colorimetric or spectrophotometric method, the spot method using paper or tiles impregnated with lead 

acetate or mercuric chloride, ion chromatography with conductivity, and potentiometric titration with a 

sulfide ion-selective electrode. Details of commonly used analytical methods for several types of 

environmental samples are presented in Table 7-2. 

Several methods for determining hydrogen sulfide in air have been investigated. GC/FPD has been 

widely used for analyses of hydrogen sulfide at levels ranging from 10-11 to 10-8 grams/0.56 mL (EPA 

1978; Stetter et al. 1977) and for hydrogen sulfide in emissions from tail gas controls units of sulfur 

recovery plants to a sensitivity of 0.5 ppmv (EPA 2000b). Sampling of a standard reference (0.055 ppm 

hydrogen sulfide) with this method resulted in a relative standard deviation of <3% (WHO 1981). The 

sensitivity of hydrogen sulfide detection in air was improved with GC/ECD (Stetter et al. 1977). The 

detector operation is based upon the measurement of the current when hydrogen sulfide is 

electrochemically oxidized at a diffusion electrode. Use of this method resulted in a lower detection limit 

of 3x10-12 grams hydrogen sulfide and a precision of 0.5%. Analyses were achieved within 2 minutes. 

GC/FPD has been used to measure hydrogen sulfide that has been removed from air by activated carbon 

fiber (Choi et al. 1991). Activated carbon fiber, made from coal tar, effectively oxidized hydrogen sulfide 

(200 ppm) to sulfate. 

 


 

	 

	 

	 

	 

	 

	 

HYDROGEN SULFIDE 144 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining Hydrogen Sulfide and Sulfide in 

Environmental Samples 

Sample Analytical Sample Percent 

matrix Preparation method method detection limita recovery Reference 

Air Filter through a 0.5 μm Zefluor; Ion chromato­ 11 μg/sample; NR NIOSH 1994b 

absorb on a solid sorbent tube 

containing shell charcoal; 

desorb with ammonia 

graphy, 

conductivity 

working range 

0.6–14 ppm 

for a 20-L air 

(Method 6013) 

hydroxide and hydrogen 

peroxide; dilute. 

sample 

Air Aspirate through cadmium 

hydroxide; precipitate as 

cadmium sulfide; add 

Spectrophotometry 0.20 μg/m3 80 Adams et al. 

1975; EPA 1978; 

NIOSH 1977a 

STRactan 10®; react with 

N,N-dimethyl-p-phenylenediamine and ferric chloride to 

yield methylene blue. 

Air Aspirate through sodium 

hydroxide and ethanol; react 

with N,N-dimethyl-p-phenylenediamine and ferric chloride 

Spectrophotometry No data NR Van den Berge et 

al. 1985 

to yield methylene blue. 

Air Absorb onto cadmium(II)­

exchange zeolite; precipitate 

as cadmium sulfide; convert to 

PAS 0.01 μg NR NIOSH 1979 

methylene blue; measure at 

750 nm. 

Air Electrochemically oxidize 

sample at potential-controlled 

Teflon-bonded diffusion 

GC/ECD 3 pg NR Stetter et al. 1977 

electrode. 

Air Introduce sampled air and 

carrier gas onto column. 

GC/FPD 5–13 μg/m3

 NR EPA 1978 

Air Introduce sample onto column 

packed with activated carbon 

filter. 

GC/FPD No data NR Choi et al. 1991 

Air Absorb in an impinger 

containing a standardized 

solution of iodine and 

Iodometric 

titration 

No data NR EPA 1978 

potassium iodide; titrate with 

standard sodium thiosulfate 

solution. 

Air Trap H2S in an aqueous NaOH 

and ascorbic acid in a midget 

impinger; titrate resulting 

sulfide ion with CdSO4 solution. 

Potentiometry ppb levels NR Ehman 1976 

 


 

	 

	 

	 

	 

	 

	 

	 

	 

	 

HYDROGEN SULFIDE 145 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining Hydrogen Sulfide and Sulfide in 

Environmental Samples 

Sample Analytical Sample Percent 

matrix Preparation method method detection limita recovery Reference 

Air Aspirate through ammoniacal 

cadmium chloride; strip sulfur 

dioxide by aeration; dissolve 

cadmium sulfide; precipitate in 

concentrated HCl; titrate with 

iodine using a starch indicator. 

Air Filter measured volume of air 

through lead-acetateimpregnated filter paper tape; 

compare optical density with 

unexposed impregnated spot 

of similar area. 

Air Filter measured volume of air 

through mercuric chlorideimpregnated filter paper tape; 

compare optical density with 

unexposed impregnated spot 

of similar area. 

Air Pass air through silver 

membrane filter. 

Air (fuel Hydrogen sulfide is absorbed 

gas on impingers containing 

streams in cadmium sulfate, forming 

petroleum cadmium sulfide, which is 

refineries) measured iodometrically. 

Air A gas sample is extracted from 

(emissions the emission source and 

from diluted with clean dry air. 

stationary 

sources) 

Water Add an amine-sulfuric acid 

reagent and a ferric chloride 

solution to the sample, mix 

gently; after 3–5 minutes add 

(NH4)2HPO4 solution; analyze 

after 3–15 minutes. 

Water For unpreserved samples, add 

solutions of zinc acetate, 

sodium hydroxide, and 

ascorbic acid, shake and let 

stand for 30 minutes; for 

preserved samples, omit the 

zinc acetate step. 

Iodometric 

titration 

Lead-acetateimpregnated 

filter paper 

tape 

Mercuric 

chlorideimpregnated 

filter paper 

tape 

Silver 

membrane 

filters/optical 

density 

measurements 

Iodometric 

titration 

GC/FPD 

Colorimetry 

Spectrophotometry 

0.7 μg/L 

No data 

0.7 μg/m3 

(0.5 ppb) 

No data 

8–740 mg/m3 

(6–520 ppm) 

0.5 ppmv 

Applicable to 

sulfide 

concentrations 

ranging from 

0.1 to 

20.0 mg/L 

Applicable at 

sulfide 

concentrations 

from 0.002 to 

0.100 mg/L 

NR EPA 1978 

NR EPA 1978 

NR EPA 1978 

NR EPA 1978 

NR EPA 2000a 

NR EPA 2000b 

89–92 APHA 1998 

(Methylene Blue 

Method) 

97.6– APHA 1998 (Gas 

104.2 Dialysis, 

Automated 

Methylene Blue 

Method) 

 


 


 


 


 


 

HYDROGEN SULFIDE 146 

7. ANALYTICAL METHODS 

Table 7-2. Analytical Methods for Determining Hydrogen Sulfide and Sulfide in 

Environmental Samples 

Sample 

matrix Preparation method 

Analytical 

method 

Sample 

detection limita 

Percent 

recovery Reference 

Water To the sample, add an excess 

of standard iodine solution; 

back titrate with a sodium 

thiosulfate solution. 

Iodometric 

titration 

Accurate 

method for 

determining 

sulfide 

NR APHA 1998 

(Iodometric 

Method) 

concentrations 

>1 mg/L 

Water Add an alkaline antioxidant 

reagent (AAR) and zinc acetate 

to the sample; measure the 

potential and compare to a 

calibration curve. 

ISE Applicable for 

sulfide 

concentrations 

>0.03 mg/L 

NR APHA 1998 (ISE 

Method) 

Water Collect water sample; acidify; 

strip sample with helium; 

collect gas in nitrogen-cooled 

GC/FPD 0.6 pmol/L NR Radford-Knoery 

and Cutter 1993 

trap. 

Water and 

sludge 

Acidify sample to convert 

sulfide ion to hydrogen sulfide; 

measure hydrogen sulfide 

absorption at 196.0 nm using 

the selenium atomic line. 

AAS 0.25 μg (1– 

10 mL sample 

volume) 

NR Parvinen and 

Lajunen 1994 

Sediment Acidify sample to convert 

sulfide ion to hydrogen sulfide; 

trap hydrogen sulfide in sodium 

hydroxide; sulfide reacts with 

N,N-dimethyl-p-phenylene 

diamine to form methylene 

blue. 

­

Colorimetry 0.01 μmol/g NR Allen et al. 1994 

Sediment Trap in silver nitrate solution as 

insoluble silver sulfide. 

Gravimetry 10 μmol/g NR Allen et al. 1994 

Sediment Trap in a sulfide antioxidant 

buffer. 

Potentiometry/ 

ISE 

No data NR Allen et al. 1994 

a

Conversion factor: 1 ppm=1.40 mg/m3 

AAR = alkaline antioxidant reagent; AAS = atomic absorption spectroscopy; CdSO4 = cadmium sulfate; 

GC/ECD = gas chromatography/electron capture detector; GC/FPD = gas chromatography with flame photometric 

detection; HCl = hydrochloric acid; H2S = hydrogen sulfide; ISE = ion-selective electrode; NaOH = sodium hydroxide; 

NR = not reported; PAS = photoacoustic spectroscopy
 
HYDROGEN SULFIDE 147 

7. ANALYTICAL METHODS 

Methylene blue techniques have been widely utilized for continuous, quantitative monitoring of hydrogen 

sulfide in air and are sensitive to hydrogen sulfide concentrations down to approximately 1–3 ppb 

(NIOSH 1977a). This method provides adequate specificity with good accuracy and precision (WHO 

1981). The amount of sulfide is determined by spectrophotometric or colorimetric measurement of 

methylene blue. The method has been improved to eliminate the formation of the precipitate cadmium 

sulfide, which can result in the obstruction of the sampling impinger (Van Den Berge et al. 1985). Also, 

the simplified method can be used to measure hydrogen sulfide levels in the viscose rayon industry 

because it is not as sensitive to carbon disulfide. Limitations of the methylene blue method include 

potential interferences from light, mercaptans, sulfides, nitrogen dioxide, and sulfur dioxide, and that the 

system is not portable (NIOSH 1977a). Photoacoustic spectroscopy of hydrogen sulfide converted to 

methylene blue has been demonstrated to yield greater sensitivity than standard spectrophotometric 

methods (NIOSH 1979). By maximizing instrument response to the 750-nm peak, it was possible to 

achieve a detection limit of 0.01 μg when collected at 2.0 L/minute for a 1-hour period. 

NIOSH (method 6013) describes the measurement of hydrogen sulfide in the air by ion chromatography 

(NIOSH 1994b). This method has a working range of 0.6–14 ppm for a 20-L air sample and an estimated 

limit of detection of 11 μg per sample. However, sulfur dioxide may interfere with the measurement of 

hydrogen sulfide. 

The iodometric method has been utilized in analyzing hydrogen sulfide in the air (EPA 1978). The 

method is based on the oxidation of hydrogen sulfide by absorption of the gas sample in an impinger 

containing a standardized solution of iodine and potassium iodide. This solution will also oxidize sulfur 

dioxide. The iodometric method is suitable for occupational settings. The accuracy of the method is 

approximately 0.50 ppm hydrogen sulfide for a 30-L air sample (EPA 1978). Another application of the 

iodometric method is for the determination of hydrogen sulfide in fuel gas emissions in petroleum 

refineries (EPA 2000a). In this method, the sample is extracted from a source and passed through a series 

of impingers containing cadmium sulfate. The hydrogen sulfide is absorbed, forming cadmium sulfide, 

which is then measured iodometrically. The sensitivity range of this method is 8–740 mg/m3

 (6– 

520 ppm) (EPA 2000a). 

Paper tapes impregnated with lead acetate have been widely used for air sample measurements of 

hydrogen sulfide in the field (EPA 1978; WHO 1981). The presence of other substances capable of 

oxidizing lead sulfide can lead to errors. This method has been improved by impregnating the paper with 

mercuric chloride or silver nitrate (EPA 1978; WHO 1981). Mercuric chloride paper tape is sensitive and 
HYDROGEN SULFIDE 148 

7. ANALYTICAL METHODS 

reliable for measurement of hydrogen sulfide in air with a sensitivity of 0.7 μg/L (EPA 1978). Tapes 

impregnated with silver nitrate are suitable for determination of hydrogen sulfide concentrations in the 

range of 0.001–50 ppm (WHO 1981). 

Potentiometric titration with a sulfide ion-selective electrode as an indicator has been used to measure 

hydrogen sulfide in the air at ppb levels (Ehman 1976). The method has been shown to have very good 

accuracy and precision. No interference could be found from nitrogen dioxide, sulfur dioxide, or ozone. 

Passive card monitors can be used to detect hydrogen sulfide in workplace environments (Saunders et al. 

2002). These monitors can be categorized as quantitative, semiquantitative, and indicator cards. 

Quantitative cards use an optical reader to assess exposure and calculate a hydrogen sulfide concentration 

in air; the results are digitally displayed. Semiquantitative cards are read by comparing the exposed card 

to a chart or by observing a progressive color development in windows on the card that represent differing 

exposure concentration ranges. The indicator cards change color above a certain threshold concentration 

of hydrogen sulfide. Saunders et al. (2002) reported detection limits of 4–8 and 0.8–4 ppm-hours for two 

commercial quantitative card monitors, 1 and 0.1 ppm-hours for two commercial semiquantitative card 

monitors, and 0.05 and 0.4 ppm-hour for two commercial indicator card monitors. 

Badges that can be worn in a worker’s, breathing zone that change color based on exposure to toxic gases, 

including hydrogen sulfide, are available from American Gas & Chemical Co. The sensitivity for the 

hydrogen sulfide badges is 10 ppm/10 minutes with a color change from white to brown (American Gas 

& Chemical Co. 2005; Ho et al. 2001). Other colorimetric methods for monitoring of hydrogen sulfide 

include handheld colorimetric tubes. Air is drawn through the tube and a color change indicates the 

presence of hydrogen sulfide by reaction with a chemical reagent in the glass tube. Tubes for hydrogen 

sulfide are available from Draeger Safety, Inc. in various measuring ranges from 0–5 ppm to 100– 

2,000 ppm (Draeger Safety 2005). 

Electrochemical sensors are the most commonly used sensors for toxic gases, including hydrogen sulfide, 

and are the best sensor for ambient toxic gas monitoring. These sensors are specific to a particular gas, 

are very accurate, do not get poisoned, and monitor at the ppm level. However, they have a narrow 

temperature range and a short shelf life, particularly in very hot and dry areas. When sensitivity to low 

concentrations of hydrogen sulfide (ppm levels) is needed, semiconductor sensors are one of the best 

sensors. Some advantages of semiconductor sensors for hydrogen sulfide include small size, ruggedness, 
HYDROGEN SULFIDE 149 

7. ANALYTICAL METHODS 

and sensitivity to ppm concentrations. Disadvantages include slow response on aged sensors, requirement 

of a temperature controlled heater, and cost (Delphian Corporation 2005). 

The Iowa Department of Natural Resources (DNR) monitors airborne levels of ammonia, hydrogen 

sulfide, and odor concentrations new animal feeding operations. Approved monitoring methods and 

equipments for the hydrogen sulfide must incorporate a thermal oxidizer and an EPA reference method 

analyzer that is designed for sulfur dioxide. There are several instruments that meet the requirements for 

the Iowa DNR, all of which detect hydrogen sulfide by first oxidizing it to sulfur dioxide, which is then 

measured using a fluorescence detector. The hydrogen sulfide and total reduces sulfide analyzer (Model 

101A) from Advanced Pollution Instrumentation, Inc. has a range of 0–50 ppb to 0–2 ppm for hydrogen 

sulfide. In addition, three hydrogen sulfide analyzers from Thermo Electron Corporation are also 

approved by the Iowa DNR. Minimum detection limits as low as 0.5 ppb can be achieved for models 45C 

and 450C, and 0.06 ppb with model 450C-TL, respectively (API 2005; Iowa DNR 2004, 2005; Thermo 

Electron Corp. 2005a, 2005b, 2005c). 

The APHA (1998) defines three categories of sulfides that must be taken into account for analytical 

methods measuring sulfides in water: total sulfide, dissolved sulfide, and un-ionized hydrogen sulfide. 

Total sulfide includes all sulfide containing species, dissolved hydrogen sulfide, bisulfide ion, and acidsoluble metal sulfides in suspended matter. Dissolved sulfide includes sulfide-containing components 

that remain after suspended solids have been removed. The concentration of the un-ionized hydrogen 

sulfide can be calculated from the concentration of dissolved sulfide components, pH of the solution, and 

the acidity constants for hydrogen sulfide using the equilibrium expressions for the ionization of 

hydrogen sulfide and bisulfide ion (APHA 1998). 

Samples that contain sulfide species can be either analyzed immediately after collection, or preserved 

with a zinc acetate solution for later analysis (APHA 1998). The addition of zinc ion (Zn2+) to the sample 

will precipitate any sulfides as zinc sulfide. A qualitative sulfide test, such as a precipitation test using 

potassium antimony tartrate or testing for hydrogen sulfide vapors using lead acetate paper or silver foil, 

can be useful and are advisable when testing industrial wastes that may contain substances that interfere 

with certain test methods, such as the methylene blue method (APHA 1998). 

The total sulfide concentration in a water sample can be determined using an iodometric titration. In this 

method sulfide is reacted with a measured excess of iodine in an acidic solution; the remaining unreacted 

iodine is then determined by titration with a thiosulfate solution. This method is an accurate method for 
HYDROGEN SULFIDE 150 

7. ANALYTICAL METHODS 

determining sulfide concentrations of >1 mg/L, if interferences are absent and the loss of hydrogen 

sulfide from the solution is avoided. The iodometric method is best suited for the analysis of samples 

freshly taken (i.e., from wells and springs) (APHA 1998). 

The methylene blue method is applicable to sulfide concentrations ranging from 0.1 to 20.0 mg/L. In this 

method, an amine-sulfuric acid reagent and a ferric chloride solution are added to the sample to produce 

methylene blue, which is then quantified colorimetrically. In the automated methylene blue method, a gas 

dialysis technique separates the sulfide from the sample matrix, which removes most inferences (i.e., 

turbidity and color). Addition of ascorbic acid, an antioxidant, improves sulfide recovery. The automated 

methylene blue method is applicable at sulfide concentrations from 0.002 to 0.100 mg/L (APHA 1998). 

Potentiometric methods using a silver electrode are also suitable for determination of sulfide 

concentrations in water and are unaffected by sample color or turbidly. In this method, an alkaline 

antioxidant reagent (AAR) and zinc acetate are added to the sample. The potential of the sample is 

measured using an ion selective electrode (ISE) and the measurement is compared to a calibration curve. 

This method is applicable for sulfide concentrations >0.03 mg/L (APHA 1998). 

Three methods for quantifying acid volatile sulfides in sediment have been described (Allen et al. 1994). 

These include methylene blue/colorimetric methods, gravimetry, and potentiometry with ion-selective 

electrode. Prior to measurement, the acid volatile sulfide in the sample is converted to hydrogen sulfide 

by acidification. The hydrogen sulfide is then purged from the sample and trapped in aqueous solution 

for the colorimetric and potentiometric methods. In the gravimetric method, hydrogen sulfide is trapped 

with silver nitrate (AgNO3), and the mass of the insoluble silver sulfide (Ag2S) that is formed is 

determined. The methylene blue/colorimetric method is generally preferred and is capable of determining 

acid volatile sulfide concentrations in sediment as low as 0.01 μmol/g (0.3 μg/g) dry weight. The 

gravimetric method can be used for samples with moderate or high acid volatile sulfides. However, 

below concentrations of acid volatile sulfides in dry sediment of 10 μmol/g (320 μg/g), accuracy may be 

affected by incomplete recovery of precipitate or by weighing errors. The limit of detection of the ionselective electrode method as applied to measuring hydrogen disulfide in sediment was not reported. 

GC/FPD has been used to measure hydrogen sulfide, free (uncomplexed) sulfide, and dissolved metal 

sulfide complexes in water (Radford-Knoery and Cutter 1993). Hydrogen sulfide was measured in the 

headspace of the sample (100 mL) with a detection limit of 0.6 pmol/L (20 pg/L). A detection limit of 

0.2 pmol/L (6 pg/L) was obtained for total dissolved sulfide. This method allows for the determination of 
HYDROGEN SULFIDE 151 

7. ANALYTICAL METHODS 

the concentration of free sulfide that is in equilibrium with hydrogen sulfide. Complexed sulfide can be 

estimated from the difference between total dissolved sulfide and free sulfide. 

A molecular absorption spectrophotometry method, using a sharp-line irradiation source, has been 

developed for the determination of sulfide (as hydrogen sulfide) in water and sludge samples. The 

method was tested with measurements of real waste water samples. The limit of detection was 0.25 μg 

(1–10 mL sample volume) (Parvinen and Lajunen 1994). 

7.3 ADEQUACY OF THE DATABASE 

Section 104(i)(5) of CERCLA, as amended, directs the Administrator of ATSDR (in consultation with the 

Administrator of EPA and agencies and programs of the Public Health Service) to assess whether 

adequate information on the health effects of hydrogen sulfide is available. Where adequate information 

is not available, ATSDR, in conjunction with NTP, is required to assure the initiation of a program of 

research designed to determine the health effects (and techniques for developing methods to determine 

such health effects) of hydrogen sulfide. 

The following categories of possible data needs have been identified by a joint team of scientists from 

ATSDR, NTP, and EPA. They are defined as substance-specific informational needs that if met would 

reduce the uncertainties of human health assessment. This definition should not be interpreted to mean 

that all data needs discussed in this section must be filled. In the future, the identified data needs will be 

evaluated and prioritized, and a substance-specific research agenda will be proposed. 

7.3.1 Identification of Data Needs 

Methods for Determining Biomarkers of Exposure and Effect. 

Exposure. Methods are available for measuring hydrogen sulfide in expired air (Blanchette and Cooper 

1976; NIOSH 1977a). Methods are available for measuring sulfide in blood (Puacz et al. 1995; 

Richardson et al. 2000) and brain tissue (Goodwin et al. 1989) and measuring sulfur volatiles in saliva 

(Solis and Volpe 1973). Methods are available for measuring thiosulfate levels in urine (Kage et al. 1992; 

Kangas and Savolainen 1987; Milby and Baselt 1999). Analytical methods with satisfactory sensitivity 

and precision are available to determine levels of hydrogen sulfide and thiosulfate in human tissues and 
HYDROGEN SULFIDE 152 

7. ANALYTICAL METHODS 

body fluids. Methods that can quantitatively correlate levels in biological fluids and tissues with 

environmental exposure levels would be helpful in estimating exposure to hydrogen sulfide. 

Effect. No methods have been identified that can be used to directly associate levels of hydrogen sulfide 

in biological samples with the onset of adverse health effects. 

Methods for Determining Parent Compounds and Degradation Products in Environmental 

Media. Methods are available for measuring hydrogen sulfide in air (Ehman 1976; EPA 1978, 2000a, 

2000b; NIOSH 1977a, 1979, 1994b; Stetter et al. 1977; Van Den Berge et al. 1985; WHO 1981). 

Methods are available for measuring sulfide in sediment (Allen et al. 1994), water, (APHA 1998; 

Radford-Knoery and Cutter 1993), and sludge (Parvinen and Lajunen 1994). Ho et al. (2001) reviewed 

sensors and technologies that can be used to monitor various chemicals, including hydrogen sulfide, with 

particular attention to sensors that have the potential to be used for long-term monitoring applications. 

Since hydrogen sulfide is part of the natural environment, dissociates in aqueous solution, and can bind to 

various metal ions in environmental media, in most cases, it would not be possible to distinguish the 

specific source of sulfide ions in environmental media. In the event of a release of hydrogen sulfide, 

increased sulfide concentrations in surrounding environmental media would likely be due to the release. 

7.3.2 Ongoing Studies 

Investigation of novel hydrogen sulfide sensors for portable monitors is underway at CSP Synkera 

Technologies, Inc., Longmont, Colorado; the principal investigator is Stephen S. Williams. Research 

includes optimization of the sensor materials, sensor element fabrication, sensor element packaging, inhouse and external evaluation of the sensors, and establishing the foundation for new instrument 

development. The goal is a low-cost, low-power sensor that can be used in as a personal monitor. This 

research is funded by the National Institutes of Health (FEDRIP 2005). 
HYDROGEN SULFIDE 153 

8. REGULATIONS AND ADVISORIES 

The international, national, and state regulations and guidelines regarding hydrogen sulfide in air, water, 

and other media are summarized in Table 8–1. 

An acute-duration inhalation MRL of 0.07 ppm was derived for hydrogen sulfide. This MRL is based on 

a minimal LOAEL of 2 ppm for a >30% alteration in two measures of lung function that are suggestive of 

bronchial obstruction (airway resistance and specific airway conductance) in 2 out of 10 persons with 

asthma (Jappinen et al. 1990). Although two measures of lung function were altered in two of the 

subjects, there were no statistically significant alterations in lung function for the whole group. The MRL 

was derived by dividing the unadjusted LOAEL by an uncertainty factor of 27 (3 for the use of a minimal 

LOAEL, 3 for human variability, and 3 for database deficiencies). Further details on the derivation of this 

MRL can be found in the MRL worksheets in Appendix A of this profile. 

An intermediate-duration inhalation MRL of 0.02 ppm was derived for hydrogen sulfide. This MRL is 

based on a NOAEL of 10 ppm and a LOAEL of 30 ppm for olfactory neuron loss and basal cell 

hyperplasia in the nasal olfactory epithelium of rats exposed for 6 hours/day, 7 days/week for 10 weeks 

(Brenneman et al. 2000). The NOAEL was adjusted for intermittent exposure and multiplied by the 

regional gas dose ratio (RDGR) for extrathoracic effects to calculate a human equivalent concentration 

(HEC). The MRL was derived by dividing the NOAELHEC by an uncertainty factor of 30 (3 to 

extrapolate from animal to human using dosimetic adjustment and 10 to account for human variability). 

Further details on the derivation of this MRL can be found in the MRL worksheets in Appendix A of this 

profile. 

EPA has derived a chronic inhalation reference concentration (RfC) for chronic exposure to hydrogen 

sulfide. The RfC of 0.002 mg/m3

 (0.001 ppm) is based on a NOAEL of 13.9 mg/m3 (10 ppm) and a 

LOAEL of 41.7 mg/m3

 (30 ppm) for nasal lesions of the olfactory mucosa in rats (Brenneman et al. 

2000). The NOAELHEC of 0.64 mg/m3

 was divided by an uncertainty factor of 300 (3 for interspecies 

extrapolation with dosimetric adjustment from rat to human, 10 for sensitive populations, and 10 for 

subchronic exposure) (IRIS 2006). 
HYDROGEN SULFIDE 154 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Hydrogen Sulfide 

Agency Description Information Reference 

INTERNATIONAL 

Guidelines: 

IARC 

WHO 

Carcinogenicity classification 

Air quality guideline (averaging time of 

24 hours) 

No data 

0.15 mg/m3 

IARC 2006 

 WHO 2000 

Drinking water guideline Not of health concern at 

levels found in drinking 

WHO 2004 

NATIONAL 

Regulations and Guidelines: 

a. Air 

ACGIH TLV (8-hour TWA) 

STEL 

10 ppma 

15 ppma 

 ACGIH 2005 

EPA Accidental release prevention of 

regulated toxic substances; threshold 

quantity 

Interim AEGL-1b 

10,000 pounds EPA 2006b 

40CFR68.130 

EPA 2006a 

10 minutes 0.75 ppm 

30 minutes 0.60 ppm 

60 minutes 0.51 ppm 

4 hours 0.36 ppm 

8 hours 

 Interim AEGL-2c 

0.33 ppm 

10 minutes 41 ppm 

30 minutes 32 ppm 

60 minutes 27 ppm 

4 hours 20 ppm 

8 hours 

 Interim AEGL-3d 

17 ppm 

10 minutes 76 ppm 

30 minutes 59 ppm 

60 minutes 50 ppm 

4 hours 37 ppm 

8 hours 31 ppm 

NIOSH REL (10-minute ceiling TWA) 10 ppm NIOSH 2006 

IDLH 100 ppm 

OSHA Acceptable ceiling concentration 

Acceptable maximum peak above the 

acceptable ceiling concentration for an 

8-hour shift 

20 ppm OSHA 2006d 

29CFR1910.1000, 

Table Z-2 

Concentration 50 ppm 
	 

HYDROGEN SULFIDE 155 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Hydrogen Sulfide 

Agency Description Information Reference 

NATIONAL (cont.) 

Maximum duration 10 minutes once, only if 

no other measured 

exposure occurs 

OSHA PEL (8-hour TWA) for construction 

industry 

10 ppm OSHA 2006b 

29CFR1926.55, 

Appendix A 

PEL (8-hour TWA) for shipyard industry 10 ppm OSHA 2006a 

29CFR1915.1000, 

Table Z 

Highly hazardous chemicals that present 1,500 pounds OSHA 2006c 

a potential for a catastrophic event at or 29CFR1910.119, 

above the threshold quantity Appendix A 

b. Water 

EPA Designated as a hazardous substances Yes EPA 2006c 

pursuant to Section 311(b)(2)(A) of the 40CFR116.4 

Clean Water Act 

Drinking water standards and health No data EPA 2004l 

advisories 

Reportable quantity of hazardous 100 pounds EPA 2006e 

substance designated pursuant to 40CFR117.3 

Section 311 of the Clean Water Act 

Water quality criteria EPA 2006d 

Freshwater CCC 2 μg/L 

Saltwater CCC 2 μg/L 

c. Food 

FDA Generally recognized as safe Yes FDA 2006 

d. Other 

ACGIH Carcinogenicity classification No data ACGIH 2005 

EPA Carcinogenicity classification No datae IRIS 2005 

RfC 2x10-3 mg/m3 

RfD Withdrawn 

Superfund; designated as a hazardous EPA 2006f 

substance pursuant to Section 311(b)(2) 40CFR302.4 

of the Clean Water Act and Section 3001 

of the RCRA 

Reportable quantity 100 pounds 

RCRA waste number U135 

Superfund; extremely hazardous 500 poundsf

 EPA 2006g 

substances; threshold planning quantity 40CFR355, 

Appendix A 

Superfund; toxic chemical release 01/01/94 EPA 2006h 

reporting; effective date 40CFR372.65 

NTP Carcinogenicity classification No data NTP 2005 
	 

	 


 


 


 

	 

	 

	 

HYDROGEN SULFIDE 156 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Hydrogen Sulfide 

Agency Description Information Reference 

STATE 

a. Air 

Arizona Ambient air quality guideline Arizona DEQ 2005 

1 hour 0.045 ppm 

24 hours 0.027 ppm 

Annual No data 

California Ambient air quality standard CalEPA 2005 

Averaging time 1 hour 

Concentration 0.03 ppm 

Delaware Ambient air quality standard Delaware DNREC 

2005 

Average concentration taken over any 0.06 ppm 

consecutive three minutes 

Average concentration taken over any 0.03 ppm 

consecutive 60 minutes 

Maine Hazardous air pollutant and reporting 

threshold 

200 pounds Maine DEP 2005 

Minnesota Ambient air quality standard Minnesota PCA 

2004 

Half-hour average not to be exceeded 0.05 ppm by volume 

over two times a year 

Half-hour average not to be exceeded 0.03 ppm by volume 

over two times in any five consecutive 

days 

Missouri Ambient air monitoring yearly standard 

(30-minute average) 

0.05 ppm Missouri DNR 2005 

Montana Ambient air quality standard (1-hour 

average); not to be exceeded more than 

0.05 ppm Montana DEQ 2005 

once per year 

Nevada Ambient air quality standard (1-hour 

averaging time) 

0.08 ppm Nevada DEP 2005 

New York Ambient air quality standard (1-hour 

averaging time) 

0.01 ppm New York DEC 

2005a 

North Carolina Hazardous and toxic air pollutant Yes North Carolina 

DENR 2005 

Oregon Air toxic Yes Oregon DEQ 2005 

Wisconsin Hazardous air contaminant; acceptable 

ambient concentration for emission rate 

 Wisconsin DNR 

2004 

<25 feet 1.1664 pounds/hour 

≥25 feet 4.8960 pounds/hour 

Ambient air standard (24-hour average) 0.083 ppm 

Hazardous air contaminant Yes 
	 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 


 

HYDROGEN SULFIDE 157 

8. REGULATIONS AND ADVISORIES 

Table 8-1. Regulations and Guidelines Applicable to Hydrogen Sulfide 

Agency Description Information Reference 

STATE (cont.) 

b. Water 

Maine Drinking water guideline 80 μg/L HSDB 2006 

Wisconsin Drinking water guideline 30 μg/L HSDB 2006 

c. Food 

No data 

d. Other 

Iowa Health effects standard 30 ppb Iowa DNR 2004 

New Jersey Hazardous substance Yes New Jersey DEP 

2005 

New York Identification and listing of hazardous Yes New York DEC 

waste 2005b 

New York Land disposal restrictions Yes New York DEC 

2005c 

a

Notice of intended changes: adopted values are those for which changes are proposed. b

AEGL-1 is the airborne concentration of a substance above which it is predicted that the general population, 

including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic nonsensory
 

effects. However, the effects are not disabling and are transient and reversible upon cessation of exposure. c

AEGL-2 is the airborne concentration of a substance above which it is predicted that the general population, 

including susceptible individuals, could experience irreversible or other serious, long lasting adverse health effects or 

an impaired ability to escape. 

d

AEGL-3 is the airborne concentration of a substance above which it is predicted that the general population, 

including susceptible individuals, could experience life-threatening adverse health effects or death. e

Under the Draft Revised Guidelines for Carcinogen Risk Assessment (U.S. EPA, 1999), data are inadequate for an 

assessment of the carcinogenic potential of hydrogen sulfide. No relevant data could be located from which to 

develop an assessment. 

f

Chemicals on the original list that do not meet toxicity criteria but because of their high production volume and 

recognized toxicity are considered chemicals of concern (``Other chemicals''). 

ACGIH = American Conference of Governmental Industrial Hygienists; AEGL = Acute Exposure Guideline Level; 

CCC = Criterion Continuous Concentration; CFR = Code of Federal Regulations; DEC = Department of 

Environmental Conservation; DENR = Department of Environment and Natural Resources; DEP = Department of 

Environmental Protection; DEQ = Department of Environmental Quality; DNR = Department of Natural Resources; 

DNREC = Department of Natural Resources and Environmental Control; EPA = Environmental Protection Agency; 

FDA = Food and Drug Administration; HSDB = Hazardous Substances Data Bank; IARC = International Agency for 

Research on Cancer; IDLH = immediately dangerous to life or health; IRIS = Integrated Risk Information System; 

NIOSH = National Institute for Occupational Safety and Health; NTP = National Toxicology Program; 

OSHA = Occupational Safety and Health Administration; PCA = Pollution Control Agency; PEL = permissible 

exposure limit; RCRA = Resource Conservation and Recovery Act; RfC = reference concentration; RfD = reference 

dose; STEL = short-term exposure limit; TLV = threshold limit values; TWA = time-weighted average; WHO = World 

Health Organization 
HYDROGEN SULFIDE 158 

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HYDROGEN SULFIDE 159 

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HYDROGEN SULFIDE 201 

10. GLOSSARY 

Absorption—The taking up of liquids by solids, or of gases by solids or liquids. 

Acute Exposure—Exposure to a chemical for a duration of 14 days or less, as specified in the 

Toxicological Profiles. 

Adsorption—The adhesion in an extremely thin layer of molecules (as of gases, solutes, or liquids) to the 

surfaces of solid bodies or liquids with which they are in contact. 

Adsorption Coefficient (Koc)—The ratio of the amount of a chemical adsorbed per unit weight of 

organic carbon in the soil or sediment to the concentration of the chemical in solution at equilibrium. 

Adsorption Ratio (Kd)—The amount of a chemical adsorbed by sediment or soil (i.e., the solid phase) 

divided by the amount of chemical in the solution phase, which is in equilibrium with the solid phase, at a 

fixed solid/solution ratio. It is generally expressed in micrograms of chemical sorbed per gram of soil or 

sediment. 

Benchmark Dose (BMD)—Usually defined as the lower confidence limit on the dose that produces a 

specified magnitude of changes in a specified adverse response. For example, a BMD10 would be the 

dose at the 95% lower confidence limit on a 10% response, and the benchmark response (BMR) would be 

10%. The BMD is determined by modeling the dose response curve in the region of the dose response 

relationship where biologically observable data are feasible. 

Benchmark Dose Model—A statistical dose-response model applied to either experimental toxicological 

or epidemiological data to calculate a BMD. 

Bioconcentration Factor (BCF)—The quotient of the concentration of a chemical in aquatic organisms 

at a specific time or during a discrete time period of exposure divided by the concentration in the 

surrounding water at the same time or during the same period. 

Biomarkers—Broadly defined as indicators signaling events in biologic systems or samples. They have 

been classified as markers of exposure, markers of effect, and markers of susceptibility. 

Cancer Effect Level (CEL)—The lowest dose of chemical in a study, or group of studies, that produces 

significant increases in the incidence of cancer (or tumors) between the exposed population and its 

appropriate control. 

Carcinogen—A chemical capable of inducing cancer. 

Case-Control Study—A type of epidemiological study that examines the relationship between a 

particular outcome (disease or condition) and a variety of potential causative agents (such as toxic 

chemicals). In a case-controlled study, a group of people with a specified and well-defined outcome is 

identified and compared to a similar group of people without outcome. 

Case Report—Describes a single individual with a particular disease or exposure. These may suggest 

some potential topics for scientific research, but are not actual research studies. 
HYDROGEN SULFIDE 202 

10. GLOSSARY 

Case Series—Describes the experience of a small number of individuals with the same disease or 

exposure. These may suggest potential topics for scientific research, but are not actual research studies. 

Ceiling Value—A concentration of a substance that should not be exceeded, even instantaneously. 

Chronic Exposure—Exposure to a chemical for 365 days or more, as specified in the Toxicological 

Profiles. 

Cohort Study—A type of epidemiological study of a specific group or groups of people who have had a 

common insult (e.g., exposure to an agent suspected of causing disease or a common disease) and are 

followed forward from exposure to outcome. At least one exposed group is compared to one unexposed 

group. 

Cross-sectional Study—A type of epidemiological study of a group or groups of people that examines 

the relationship between exposure and outcome to a chemical or to chemicals at one point in time. 

Data Needs—Substance-specific informational needs that if met would reduce the uncertainties of human 

health assessment. 

Developmental Toxicity—The occurrence of adverse effects on the developing organism that may result 

from exposure to a chemical prior to conception (either parent), during prenatal development, or 

postnatally to the time of sexual maturation. Adverse developmental effects may be detected at any point 

in the life span of the organism. 

Dose-Response Relationship—The quantitative relationship between the amount of exposure to a 

toxicant and the incidence of the adverse effects. 

Embryotoxicity and Fetotoxicity—Any toxic effect on the conceptus as a result of prenatal exposure to 

a chemical; the distinguishing feature between the two terms is the stage of development during which the 

insult occurs. The terms, as used here, include malformations and variations, altered growth, and in utero 

death. 

Environmental Protection Agency (EPA) Health Advisory—An estimate of acceptable drinking water 

levels for a chemical substance based on health effects information. A health advisory is not a legally 

enforceable federal standard, but serves as technical guidance to assist federal, state, and local officials. 

Epidemiology—Refers to the investigation of factors that determine the frequency and distribution of 

disease or other health-related conditions within a defined human population during a specified period. 

Genotoxicity—A specific adverse effect on the genome of living cells that, upon the duplication of 

affected cells, can be expressed as a mutagenic, clastogenic, or carcinogenic event because of specific 

alteration of the molecular structure of the genome. 

Half-life—A measure of rate for the time required to eliminate one half of a quantity of a chemical from 

the body or environmental media. 

Immediately Dangerous to Life or Health (IDLH)—The maximum environmental concentration of a 

contaminant from which one could escape within 30 minutes without any escape-impairing symptoms or 

irreversible health effects. 
HYDROGEN SULFIDE 203 

10. GLOSSARY 

Immunologic Toxicity—The occurrence of adverse effects on the immune system that may result from 

exposure to environmental agents such as chemicals. 

Immunological Effects—Functional changes in the immune response. 

Incidence—The ratio of individuals in a population who develop a specified condition to the total 

number of individuals in that population who could have developed that condition in a specified time 

period. 

Intermediate Exposure—Exposure to a chemical for a duration of 15–364 days, as specified in the 

Toxicological Profiles. 

In Vitro—Isolated from the living organism and artificially maintained, as in a test tube. 

In Vivo—Occurring within the living organism. 

Lethal Concentration(LO) (LCLO)—The lowest concentration of a chemical in air that has been reported 

to have caused death in humans or animals. 

Lethal Concentration(50) (LC50)—A calculated concentration of a chemical in air to which exposure for 

a specific length of time is expected to cause death in 50% of a defined experimental animal population. 

Lethal Dose(LO) (LDLo)—The lowest dose of a chemical introduced by a route other than inhalation that 

has been reported to have caused death in humans or animals. 

Lethal Dose(50) (LD50)—The dose of a chemical that has been calculated to cause death in 50% of a 

defined experimental animal population. 

Lethal Time(50) (LT50)—A calculated period of time within which a specific concentration of a chemical 

is expected to cause death in 50% of a defined experimental animal population. 

Lowest-Observed-Adverse-Effect Level (LOAEL)—The lowest exposure level of chemical in a study, 

or group of studies, that produces statistically or biologically significant increases in frequency or severity 

of adverse effects between the exposed population and its appropriate control. 

Lymphoreticular Effects—Represent morphological effects involving lymphatic tissues such as the 

lymph nodes, spleen, and thymus. 

Malformations—Permanent structural changes that may adversely affect survival, development, or 

function. 

Minimal Risk Level (MRL)—An estimate of daily human exposure to a hazardous substance that is 

likely to be without an appreciable risk of adverse noncancer health effects over a specified route and 

duration of exposure. 

Modifying Factor (MF)—A value (greater than zero) that is applied to the derivation of a Minimal Risk 

Level (MRL) to reflect additional concerns about the database that are not covered by the uncertainty 

factors. The default value for a MF is 1. 

Morbidity—State of being diseased; morbidity rate is the incidence or prevalence of disease in a specific 

population. 
HYDROGEN SULFIDE 204 

10. GLOSSARY 

Mortality—Death; mortality rate is a measure of the number of deaths in a population during a specified 

interval of time. 

Mutagen—A substance that causes mutations. A mutation is a change in the DNA sequence of a cell’s 

DNA. Mutations can lead to birth defects, miscarriages, or cancer. 

Necropsy—The gross examination of the organs and tissues of a dead body to determine the cause of 

death or pathological conditions. 

Neurotoxicity—The occurrence of adverse effects on the nervous system following exposure to a 

chemical. 

No-Observed-Adverse-Effect Level (NOAEL)—The dose of a chemical at which there were no 

statistically or biologically significant increases in frequency or severity of adverse effects seen between 

the exposed population and its appropriate control. Effects may be produced at this dose, but they are not 

considered to be adverse. 

Octanol-Water Partition Coefficient (Kow)—The equilibrium ratio of the concentrations of a chemical 

in n-octanol and water, in dilute solution. 

Odds Ratio (OR)—A means of measuring the association between an exposure (such as toxic substances 

and a disease or condition) that represents the best estimate of relative risk (risk as a ratio of the incidence 

among subjects exposed to a particular risk factor divided by the incidence among subjects who were not 

exposed to the risk factor). An OR of greater than 1 is considered to indicate greater risk of disease in the 

exposed group compared to the unexposed group. 

Organophosphate or Organophosphorus Compound—A phosphorus-containing organic compound 

and especially a pesticide that acts by inhibiting cholinesterase. 

Permissible Exposure Limit (PEL)—An Occupational Safety and Health Administration (OSHA) 

allowable exposure level in workplace air averaged over an 8-hour shift of a 40-hour workweek. 

Pesticide—General classification of chemicals specifically developed and produced for use in the control 

of agricultural and public health pests. 

Pharmacokinetics—The dynamic behavior of a material in the body, used to predict the fate 

(disposition) of an exogenous substance in an organism. Utilizing computational techniques, it provides 

the means of studying the absorption, distribution, metabolism, and excretion of chemicals by the body. 

Pharmacokinetic Model—A set of equations that can be used to describe the time course of a parent 

chemical or metabolite in an animal system. There are two types of pharmacokinetic models: data-based 

and physiologically-based. A data-based model divides the animal system into a series of compartments, 

which, in general, do not represent real, identifiable anatomic regions of the body, whereas the 

physiologically-based model compartments represent real anatomic regions of the body. 

Physiologically Based Pharmacodynamic (PBPD) Model—A type of physiologically based doseresponse model that quantitatively describes the relationship between target tissue dose and toxic end 

points. These models advance the importance of physiologically based models in that they clearly 

describe the biological effect (response) produced by the system following exposure to an exogenous 

substance. 
HYDROGEN SULFIDE 205 

10. GLOSSARY 

Physiologically Based Pharmacokinetic (PBPK) Model—Comprised of a series of compartments 

representing organs or tissue groups with realistic weights and blood flows. These models require a 

variety of physiological information: tissue volumes, blood flow rates to tissues, cardiac output, alveolar 

ventilation rates, and possibly membrane permeabilities. The models also utilize biochemical 

information, such as air/blood partition coefficients, and metabolic parameters. PBPK models are also 

called biologically based tissue dosimetry models. 

Prevalence—The number of cases of a disease or condition in a population at one point in time. 

Prospective Study—A type of cohort study in which the pertinent observations are made on events 

occurring after the start of the study. A group is followed over time. 

q1*—The upper-bound estimate of the low-dose slope of the dose-response curve as determined by the 

multistage procedure. The q1* can be used to calculate an estimate of carcinogenic potency, the 

incremental excess cancer risk per unit of exposure (usually μg/L for water, mg/kg/day for food, and 

μg/m3

 for air). 

Recommended Exposure Limit (REL)—A National Institute for Occupational Safety and Health 

(NIOSH) time-weighted average (TWA) concentration for up to a 10-hour workday during a 40-hour 

workweek. 

Reference Concentration (RfC)—An estimate (with uncertainty spanning perhaps an order of 

magnitude) of a continuous inhalation exposure to the human population (including sensitive subgroups) 

that is likely to be without an appreciable risk of deleterious noncancer health effects during a lifetime. 

The inhalation reference concentration is for continuous inhalation exposures and is appropriately 

expressed in units of mg/m3 or ppm. 

Reference Dose (RfD)—An estimate (with uncertainty spanning perhaps an order of magnitude) of the 

daily exposure of the human population to a potential hazard that is likely to be without risk of deleterious 

effects during a lifetime. The RfD is operationally derived from the no-observed-adverse-effect level 

(NOAEL, from animal and human studies) by a consistent application of uncertainty factors that reflect 

various types of data used to estimate RfDs and an additional modifying factor, which is based on a 

professional judgment of the entire database on the chemical. The RfDs are not applicable to 

nonthreshold effects such as cancer. 

Reportable Quantity (RQ)—The quantity of a hazardous substance that is considered reportable under 

the Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA). Reportable 

quantities are (1) 1 pound or greater or (2) for selected substances, an amount established by regulation 

either under CERCLA or under Section 311 of the Clean Water Act. Quantities are measured over a 

24-hour period. 

Reproductive Toxicity—The occurrence of adverse effects on the reproductive system that may result 

from exposure to a chemical. The toxicity may be directed to the reproductive organs and/or the related 

endocrine system. The manifestation of such toxicity may be noted as alterations in sexual behavior, 

fertility, pregnancy outcomes, or modifications in other functions that are dependent on the integrity of 

this system. 
HYDROGEN SULFIDE 206 

10. GLOSSARY 

Retrospective Study—A type of cohort study based on a group of persons known to have been exposed 

at some time in the past. Data are collected from routinely recorded events, up to the time the study is 

undertaken. Retrospective studies are limited to causal factors that can be ascertained from existing 

records and/or examining survivors of the cohort. 

Risk—The possibility or chance that some adverse effect will result from a given exposure to a chemical. 

Risk Factor—An aspect of personal behavior or lifestyle, an environmental exposure, or an inborn or 

inherited characteristic that is associated with an increased occurrence of disease or other health-related 

event or condition. 

Risk Ratio—The ratio of the risk among persons with specific risk factors compared to the risk among 

persons without risk factors. A risk ratio greater than 1 indicates greater risk of disease in the exposed 

group compared to the unexposed group. 

Short-Term Exposure Limit (STEL)—The American Conference of Governmental Industrial 

Hygienists (ACGIH) maximum concentration to which workers can be exposed for up to 15 minutes 

continually. No more than four excursions are allowed per day, and there must be at least 60 minutes 

between exposure periods. The daily Threshold Limit Value-Time Weighted Average (TLV-TWA) may 

not be exceeded. 

Standardized Mortality Ratio (SMR)—A ratio of the observed number of deaths and the expected 

number of deaths in a specific standard population. 

Target Organ Toxicity—This term covers a broad range of adverse effects on target organs or 

physiological systems (e.g., renal, cardiovascular) extending from those arising through a single limited 

exposure to those assumed over a lifetime of exposure to a chemical. 

Teratogen—A chemical that causes structural defects that affect the development of an organism. 

Threshold Limit Value (TLV)—An American Conference of Governmental Industrial Hygienists 

(ACGIH) concentration of a substance to which most workers can be exposed without adverse effect. 

The TLV may be expressed as a Time Weighted Average (TWA), as a Short-Term Exposure Limit 

(STEL), or as a ceiling limit (CL). 

Time-Weighted Average (TWA)—An allowable exposure concentration averaged over a normal 8-hour 

workday or 40-hour workweek. 

Toxic Dose(50) (TD50)—A calculated dose of a chemical, introduced by a route other than inhalation, 

which is expected to cause a specific toxic effect in 50% of a defined experimental animal population. 

Toxicokinetic—The absorption, distribution, and elimination of toxic compounds in the living organism. 
HYDROGEN SULFIDE 207 

10. GLOSSARY 

Uncertainty Factor (UF)—A factor used in operationally deriving the Minimal Risk Level (MRL) or 

Reference Dose (RfD) or Reference Concentration (RfC) from experimental data. UFs are intended to 

account for (1) the variation in sensitivity among the members of the human population, (2) the 

uncertainty in extrapolating animal data to the case of human, (3) the uncertainty in extrapolating from 

data obtained in a study that is of less than lifetime exposure, and (4) the uncertainty in using lowestobserved-adverse-effect level (LOAEL) data rather than no-observed-adverse-effect level (NOAEL) data. 

A default for each individual UF is 10; if complete certainty in data exists, a value of 1 can be used; 

however, a reduced UF of 3 may be used on a case-by-case basis, 3 being the approximate logarithmic 

average of 10 and 1. 

Xenobiotic—Any chemical that is foreign to the biological system. 
HYDROGEN SULFIDE 208 

10. GLOSSARY 

This page is intentionally blank. 
HYDROGEN SULFIDE A-1 

APPENDIX A. ATSDR MINIMAL RISK LEVELS AND WORKSHEETS 

The Comprehensive Environmental Response, Compensation, and Liability Act (CERCLA) [42 U.S.C. 

9601 et seq.], as amended by the Superfund Amendments and Reauthorization Act (SARA) [Pub. L. 99– 

499], requires that the Agency for Toxic Substances and Disease Registry (ATSDR) develop jointly with 

the U.S. Environmental Protection Agency (EPA), in order of priority, a list of hazardous substances most 

commonly found at facilities on the CERCLA National Priorities List (NPL); prepare toxicological 

profiles for each substance included on the priority list of hazardous substances; and assure the initiation 

of a research program to fill identified data needs associated with the substances. 

The toxicological profiles include an examination, summary, and interpretation of available toxicological 

information and epidemiologic evaluations of a hazardous substance. During the development of 

toxicological profiles, Minimal Risk Levels (MRLs) are derived when reliable and sufficient data exist to 

identify the target organ(s) of effect or the most sensitive health effect(s) for a specific duration for a 

given route of exposure. An MRL is an estimate of the daily human exposure to a hazardous substance 

that is likely to be without appreciable risk of adverse noncancer health effects over a specified duration 

of exposure. MRLs are based on noncancer health effects only and are not based on a consideration of 

cancer effects. These substance-specific estimates, which are intended to serve as screening levels, are 

used by ATSDR health assessors to identify contaminants and potential health effects that may be of 

concern at hazardous waste sites. It is important to note that MRLs are not intended to define clean-up or 

action levels. 

MRLs are derived for hazardous substances using the no-observed-adverse-effect level/uncertainty factor 

approach. They are below levels that might cause adverse health effects in the people most sensitive to 

such chemical-induced effects. MRLs are derived for acute (1–14 days), intermediate (15–364 days), and 

chronic (365 days and longer) durations and for the oral and inhalation routes of exposure. Currently, 

MRLs for the dermal route of exposure are not derived because ATSDR has not yet identified a method 

suitable for this route of exposure. MRLs are generally based on the most sensitive chemical-induced end 

point considered to be of relevance to humans. Serious health effects (such as irreparable damage to the 

liver or kidneys, or birth defects) are not used as a basis for establishing MRLs. Exposure to a level 

above the MRL does not mean that adverse health effects will occur. 
HYDROGEN SULFIDE A-2 

APPENDIX A 

MRLs are intended only to serve as a screening tool to help public health professionals decide where to 

look more closely. They may also be viewed as a mechanism to identify those hazardous waste sites that 

are not expected to cause adverse health effects. Most MRLs contain a degree of uncertainty because of 

the lack of precise toxicological information on the people who might be most sensitive (e.g., infants, 

elderly, nutritionally or immunologically compromised) to the effects of hazardous substances. ATSDR 

uses a conservative (i.e., protective) approach to address this uncertainty consistent with the public health 

principle of prevention. Although human data are preferred, MRLs often must be based on animal studies 

because relevant human studies are lacking. In the absence of evidence to the contrary, ATSDR assumes 

that humans are more sensitive to the effects of hazardous substance than animals and that certain persons 

may be particularly sensitive. Thus, the resulting MRL may be as much as 100-fold below levels that 

have been shown to be nontoxic in laboratory animals. 

Proposed MRLs undergo a rigorous review process: Health Effects/MRL Workgroup reviews within the 

Division of Toxicology and Environmental Medicine, expert panel peer reviews, and agency-wide MRL 

Workgroup reviews, with participation from other federal agencies and comments from the public. They 

are subject to change as new information becomes available concomitant with updating the toxicological 

profiles. Thus, MRLs in the most recent toxicological profiles supersede previously published levels. 

For additional information regarding MRLs, please contact the Division of Toxicology and 

Environmental Medicine, Agency for Toxic Substances and Disease Registry, 1600 Clifton Road NE, 

Mailstop F-32, Atlanta, Georgia 30333. 
 

 

 

 

 

HYDROGEN SULFIDE A-3 

APPENDIX A 

MINIMAL RISK LEVEL (MRL) WORKSHEET 

Chemical Name: Hydrogen Sulfide 

CAS Numbers: 7783-06-4 

Date: June 2006 

Profile Status: Final Draft 

Route: [x] Inhalation [ ] Oral 

Duration: [x] Acute [ ] Intermediate [ ] Chronic 

Graph Key: 16 

Species: Human 

Minimal Risk Level: 0.07 [ ] mg/kg/day [x] ppm 

Reference: Jäppinen P, Vikka V, Marttila O, et al. 1990. Exposure to hydrogen sulphide and respiratory 

function. Br J Intern Med 47:824-828. 

Experimental design: This study evaluated lung function in three male and seven female subjects with 

bronchial asthma requiring medication for 1–13 years; none of the subjects had severe asthma. The 

subjects were exposed to 2 ppm hydrogen sulfide for 30 minutes. Respiratory function in response to a 

histamine challenge was assessed prior to exposure and after exposure. 

Effect noted in study and corresponding doses: No statistically significant changes in forced vital 

capacity (FVC), forced expiratory volume in 1 second (FEV1), and forced expiratory flow were noted. 

Airway resistance (Raw) and specific airway conductance (SGaw) did not show statistically significant 

changes when examined as a group. In two subjects, there were changes of over 30% in both Raw and 

SGaw; these changes were suggestive of bronchial obstruction. Additionally, 3 of 10 subjects 

complained of headaches after exposure. 

Dose and end point used for MRL derivation: 

[ ] NOAEL [X] LOAEL 

Uncertainty Factors used in MRL derivation: 

[x] 3 for use of a minimal LOAEL 

[ ] 10 for extrapolation from animals to humans 

[x] 3 for human variability 

[x] 3 for database deficiencies 

The 2 ppm concentration was considered a minimally adverse effect level because the changes in airway 

resistance and specific airway conductance were only observed in 2 of 10 subjects. Because the study 

was conducted using asthmatics, who are likely to be a sensitive subpopulation, a partial uncertainty 

factor of 3 was used to account for human variability. An uncertainty factor of 3 was used for database 

deficiencies because of lack of studies on children exposed to hydrogen sulfide and concern for short 

(30 minute) exposure duration in the principal study. 

Was a conversion factor used from ppm in food or water to a mg/body weight dose? No. 

If an inhalation study in animals, list conversion factors used in determining human equivalent dose: No. 
 

 

 

HYDROGEN SULFIDE A-4 

APPENDIX A 

Was a conversion used from intermittent to continuous exposure? 

Other additional studies or pertinent information that lend support to this MRL: Bhambhani et al. (1996b) 

evaluated the acute effects of hydrogen sulfide on the physiological and hematological health of male and 

female volunteers exposed to 5 ppm during two 30-minute sessions of submaximal exercise (50% of 

maximum aerobic power). No significant changes in any parameter were noted in the women, whereas 

the men showed a significant decrease in muscle citrate synthetase as well as nonsignificant changes in 

lactate, lactate dehydrogenase, and cytochome oxidase. Together, these changes were considered 

indicative of compromise of aerobic metabolism. 

No respiratory or cardiovascular effects were observed in 16 male volunteers exposed by oral inhalation 

to hydrogen sulfide at 0.5, 2, or 5 ppm for >16 minutes while exercising (Bhambhani and Singh 1991). 

The end points examined included heart rate, oxygen uptake, carbon dioxide output, and blood gases. 

Airway resistance and conductance were not measured in this study. No significant changes in 

pulmonary function parameters were noted in individuals exposed to 10 ppm hydrogen sulfide for 

15 minutes during exercise (Bhambhani et al. 1996a). 

Respiratory distress was noted in two workers exposed to >40 ppm hydrogen sulfide for under 25 minutes 

(Spolyar 1951). In animals, impacts on the respiratory system such as increases in the cellularity and 

lactate dehydrogenase and alkaline phosphatase activities of bronchial lavage fluids have been seen at 

exposures as low as 10 ppm for 4 hours (Lopez et al. 1987), although without a dose-related trend. 

Moderate to massive pulmonary edema was observed in rats exposed to 375 or 399 ppm for 4 hours 

(Prior et al. 1990). A significant dose-related decrease in lung microsomal cytochrome c oxidase activity 

was seen in rats following a 4 hour exposure to 50, 200, or 400 ppm hydrogen sulfide (Khan et al. 1990). 

Similarly, succinate oxidase activity also decreased in a dose-related fashion; although no affect was 

observed at the lowest dose. Cytochrome oxidase levels returned to normal by 24 hours postexposure in 

animals in the 200 ppm group, but not the 400 ppm group. Exposure at the two higher dose levels was 

also associated with complete abolition of the zymosan-induced stimulation of respiratory rates of 

pulmonary alveolar macrophages and there were significant decreases in the number of viable 

macrophages in lung lavage fluids at the highest dose (Khan et al. 1991). 

Agency Contacts (Chemical Managers): Selene Chou, Mike Fay, and Sam Keith. 
HYDROGEN SULFIDE A-5 

APPENDIX A 

MINIMAL RISK LEVEL (MRL) WORKSHEET 

Chemical Name: Hydrogen Sulfide 

CAS Number: 7783-06-4 

Date: June 2006 

Profile Status: Final Draft 

Route: [x] Inhalation [ ] Oral 

Duration: [ ] Acute [x] Intermediate [ ] Chronic 

Graph Key: 39 

Species: Sprague-Dawley rats 

Minimal Risk Level: 0.02 [ ] mg/kg/day [x] ppm 

Reference: Brenneman KA, James RA, Gross EA, et al. 2000. Olfactory neuron loss in adult male CD 

rats following subchronic inhalation exposure to hydrogen sulfide. Toxicol Pathol 28:326-333. 

Experimental design: Groups of male Sprague-Dawley rats (12/group) were exposed to 0, 10, 30, or 

80 ppm hydrogen sulfide 6 hours/day, 7 days/week for 10 weeks. End points examined were limited to 

the nose; six transverse levels of the nose were examined via light microscopy. 

Effects noted in study and corresponding concentrations: Nasal lesions were limited to the olfactory 

mucosa in rats exposed to 30 or 80 ppm and consisted of multifocal, bilaterally symmetrical olfactory 

neuron loss and basal cell hyperplasia affecting the lining of the dorsal medial meatus and the dorsal and 

medial regions of the ethmoid recess. In most cases, the incidence, mean severity, and distribution of 

exposure-related lesions increased in a concentration-related manner. The severity of the olfactory 

lesions was scored as 1 mild, 2 moderate, or 3 severe. For the olfactory neuron loss, the mild, moderate, 

or severe severity scores corresponded to 26–50, 51–75, and 76–100%, respectively, reduction in the 

normal thickness of the olfactory neuron layer; for the basal cell hyperplasia, mild, moderate, or severe 

severity scores corresponded to 1–33, 34–67, or 68–100% of the normal thickness of the olfactory neuron 

cell layer replaced by basal cells. The basal cell hyperplasia is a regenerative response to the loss of 

olfactory neurons. No olfactory lesions were observed in the controls or rats exposed to 10 ppm. At 

30 ppm, the olfactory neuron loss was observed at nasal levels 4 (11/12, severity 1.4) and 5 (9/12, severity 

1.1) and basal cell hyperplasia was observed at nasal levels 4 (10/12, severity 1.8) and 5 (11/12, severity 

1.3). At 80 ppm, olfactory neuron loss was observed at levels 3 (8/8, severity 2.4), 4 (12/12, severity 2.4), 

5 (11/12, severity 1.5), and 6 (5/12, severity 1.2; incidence not statistically significant) and basal cell 

hyperplasia was observed at nasal levels 4 (12/12, severity 1.2), 5 (11/12, severity 1.3), and 6 (6/12, 

severity 1.0). 

Dose and end point used for MRL derivation: Data from the Brenneman et al. (2000) study for olfactory 

epithelial damage were used to derive an intermediate-duration inhalation MRL for hydrogen sulfide. 

Two approaches for MRL derivation were considered: the traditional NOAEL/LOAEL approach and the 

benchmark dose (BMD) modeling approach. 

NOAEL/LOAEL Approach: 

For the NOAEL/LOAEL approach, the MRL would be derived using the NOAEL of 10 ppm and LOAEL 

of 30 ppm for olfactory neuron loss and basal cell hyperplasia in the nasal olfactory epithelium. 
HYDROGEN SULFIDE A-6 

APPENDIX A 

Benchmark Dose (BMD) Analysis: 

Two data sets were considered for BMD modeling: olfactory neuron loss and basal cell hyperplasia. 

Incidence data were reported for nasal section levels 3 (olfactory neuron loss only) through 6; because the 

highest incidence of lesions in the 30 ppm group was found in level 4, these data were used for the 

benchmark dose analyses; the incidence data are reported in Table A-1. 

Table A-1. Incidence of Olfactory Neuron Loss and Basal Cell Hyperplasia 

Observed in the Nasal Cavity of Male Rats Exposed to Hydrogen Sulfide for 

10 Weeks 

Concentration (ppm) Incidence of olfactory Incidence of basal cell 

neuron loss hyperplasia 

0 0/12 0/12 

10 0/12 0/12 

30 11/12 10/12 

80 12/12 12/12 

Source: Brenneman et al. 2000 

The steepness of the dose-response curve for both lesion types, in particular the lack of intermediate 

response levels, precludes benchmark dose modeling. Therefore, the NOAEL/LOAEL approach was 

used to derive the MRL. 

[x] NOAEL [ ] LOAEL [ ] BMDL 

Uncertainty Factors used in MRL derivation: 

[ ] 10 for use of a LOAEL 

[x] 3 for extrapolation from animals to humans with dosimetric adjustment 

[x] 10 for human variability 

Was a conversion used from ppm in food or water to a mg/body weight dose? None. 

If an inhalation study in animals, list the conversion factors used in determining human equivalent dose: 

NOAELADJ =10 ppm x 6 hour/24 hour x 7 days/7 days=2.5 ppm 

The human equivalent concentration (HEC) was calculated using the following equation (EPA 1994b) for 

category 1 gases: 

NOAELHEC = NOAELADJ x RDGRET 
 

 

 

 

HYDROGEN SULFIDE A-7 

APPENDIX A 

The regional gas dose ratio for the extrathoracic region (RGDRET) of 0.184 was calculated using the 

following equation: 

⎛ V ⎞ E ⎜

⎜

SA ⎟

⎟
 

⎝ ET ⎠rat RGDRET = ⎛ V ⎞

⎜

⎜ E ⎟

⎟

⎝ SAET ⎠human 

Where: 

Ve is the minute volume and SAET is the surface area of the extrathoracic (ET) region of the 

respiratory tract. 

Minute volume (Ve) 

Human: 13.8 L/minute (EPA 1994b) 

Rat: 0.190 L/minute; calculated using the following EPA equation: 

ln(Ve) = b0 + b1ln(BW) 

For rats, b0 equals -0.578 and b1 equals 0.821 

Because a limited amount of body weight data were reported in the study, a reference body 

weight of 0.267 kg (EPA 1988) was used. 

EPA (1994b) rat and human respiratory surface area reference values: 

Extrathoracic 15.0 cm2

 (rat) 200 cm2 (human) 

NOAEL[HEC] = NOAEL (ADJ) x RGDR = 2.5 ppm x 0.184 = 0.46 ppm 

The dosimetric model used to the NOAELHEC takes into account species differences in the surface area of 

the upper respiratory tract and inhalation rates. However, the model does not take into consideration that 

a larger portion of the rat nasal cavity is lined with olfactory epithelium compared to humans (50% in rats 

compared to 10% in humans) and differences in air flow patterns. A computational fluid dynamics model 

of the rat nasal epithelium developed for hydrogen sulfide (Moulin et al. 2002) found a strong correlation 

between the amount of hydrogen sulfide reaching the olfactory tissue and the severity of the lesions. A 

human computational fluid dynamics model has not been identified; thus, there is some uncertainty 

whether the dosimetric adjustments used to calculate the MRL over- or underestimates the risk to humans. 

Other additional studies or pertinent information which lend support to this MRL: There are limited data 

on the toxicity of hydrogen sulfide in humans following intermediate-duration exposure. Acute- and 

chronic-duration studies suggest that the respiratory tract, cardiovascular system, and nervous system are 

sensitive targets of hydrogen sulfide. 

Intermediate-duration animal studies support the identification of the respiratory tract and nervous system 

as sensitive targets; cardiovascular effects have not been reported in intermediate-duration animal studies. 

Exposure of rats and mice to low hydrogen sulfide concentrations have resulted in histological damage to 

the upper respiratory tract. Brenneman et al. (2000) reported significant concentration-related increases 

in the incidence and severity of lesions to the nasal olfactory epithelium in rats exposed to hydrogen 

sulfide for 10 weeks. The effects consisted of olfactory neuron loss and basal cell hyperplasia in rats 

exposed to 30 ppm and higher, 6 hours/day, 7 days/week for 10 weeks; no adverse effects were observed 

at 10 ppm. Earlier studies conducted by CIIT (1983b, 1983c) did not find significant alterations in the 
HYDROGEN SULFIDE A-8 

APPENDIX A 

nasal turbinates of Sprague-Dawley or F-344 rats exposed to ≤80 ppm hydrogen sulfide 6 hours/day, 

5 days/week for 13 weeks. Inflammation of the squamous portion of the nasal mucosa was observed in 

mice exposed to 80 ppm hydrogen sulfide 6 hours/day, 5 days/week for 13 weeks (CIIT 1983a); the 

NOAEL for this effect is 30 ppm. However, a re-examination of the histological specimens from this 

study (Dorman et al. 2004) revealed significant increases in the incidence of olfactory neuron loss in male 

and female Sprague-Dawley rats, F-344 rats, and B6C3F1 mice exposed to 30 or 80 ppm; the NOAEL 

was 10 ppm. Additionally, significant increases in the incidence of bronchiolar epithelial hypertrophy 

and hyperplasia were observed in female Sprague-Dawley rats exposed to 30 or 80 ppm and male 

Sprague-Dawley rats and male F-344 rats exposed to 80 ppm. The sensitivity of the olfactory epithelium 

has been confirmed by acute-duration studies. Degeneration of the olfactory epithelium was observed in 

rats exposed to 400 ppm hydrogen sulfide for 4 hours (Lopez et al. 1988b), rats exposed to 200 ppm for 

3 hours (Brenneman et al. 2002), and rats exposed to 80 ppm 3 hours/day for 5 days (Brenneman et al. 

2002). Data collected using a computational fluid dynamics model of the rat nasal epithelium (Moulin et 

al. 2002) suggest that the olfactory epithelium is more sensitive than the nasal respiratory epithelium 

despite the higher hydrogen sulfide flux (a surrogate for dose) to the regions lined with respiratory 

epithelium compared to regions lined with olfactory epithelium. Within the areas of the nose lined with 

olfactory epithelium, a high correlation between predicted hydrogen sulfide flux and the incidence of 

olfactory lesion was found. 

The neurotoxicity of hydrogen sulfide following intermediate-duration exposure has not been adequately 

tested in mature animals; the data are limited to studies assessing brain weight, neurological function 

(posture, gait, tone of facial muscles, and pupillary reflexes), and histopathology. A 5% decrease in 

absolute brain weight was observed in Sprague-Dawley rats exposed to 80 ppm hydrogen sulfide 

6 hours/day, 5 days/week for 13 weeks; no alterations were observed at 30 ppm (CIIT 1983c). No 

alterations in histopathology or neurological function were observed in Sprague-Dawley rats (CIIT 

1983c), F-344 rats (CIIT 1983b), or B6C3F1 mice (CIIT 1983a) exposed to concentrations up to 80 ppm 

6 hours/day, 5 days/week for 13 weeks. Neurodevelopmental toxicity studies have found some alterations 

that are suggestive of neurotoxicity. The suggestive findings in the offspring of rats exposed to 20 ppm 

7 hours/day on gestational day 5 through postnatal day 21 include alterations in the architecture and 

growth characteristics of Purkinje cell dendritic fields (Hannah and Roth 1991), decreases in 

norepinephrine and increases in serotonin in the frontal cortex (Skrajny et al. 1992), and decreases in 

brain amino acid levels at 75 ppm (Hannah et al. 1989, 1990). However, no alterations in 

neurobehavioral performance (assessed via motor activity, passive avoidance, acoustic startle, functional 

observation battery) were observed in the offspring of rats exposed for 2 weeks prior to mating, during 

mating, on gestational days 5–19, and on postnatal days 5–18 (Dorman et al. 2000). These data suggest 

that exposures of 20–80 ppm may result in subclinical alterations in neurochemistry. 

Agency Contacts (Chemical Managers): Selene Chou, Mike Fay, and Sam Keith. 
	 

	 

	 

HYDROGEN SULFIDE B-1 

APPENDIX B. USER'S GUIDE 

Chapter 1 

Public Health Statement 

This chapter of the profile is a health effects summary written in non-technical language. Its intended 

audience is the general public, especially people living in the vicinity of a hazardous waste site or 

chemical release. If the Public Health Statement were removed from the rest of the document, it would 

still communicate to the lay public essential information about the chemical. 

The major headings in the Public Health Statement are useful to find specific topics of concern. The 

topics are written in a question and answer format. The answer to each question includes a sentence that 

will direct the reader to chapters in the profile that will provide more information on the given topic. 

Chapter 2 

Relevance to Public Health 

This chapter provides a health effects summary based on evaluations of existing toxicologic, 

epidemiologic, and toxicokinetic information. This summary is designed to present interpretive, weightof-evidence discussions for human health end points by addressing the following questions: 

1.	 What effects are known to occur in humans? 

2. What effects observed in animals are likely to be of concern to humans? 

3. What exposure conditions are likely to be of concern to humans, especially around hazardous 

waste sites? 

The chapter covers end points in the same order that they appear within the Discussion of Health Effects 

by Route of Exposure section, by route (inhalation, oral, and dermal) and within route by effect. Human 

data are presented first, then animal data. Both are organized by duration (acute, intermediate, chronic). 

In vitro data and data from parenteral routes (intramuscular, intravenous, subcutaneous, etc.) are also 

considered in this chapter. 

The carcinogenic potential of the profiled substance is qualitatively evaluated, when appropriate, using 

existing toxicokinetic, genotoxic, and carcinogenic data. ATSDR does not currently assess cancer 

potency or perform cancer risk assessments. Minimal Risk Levels (MRLs) for noncancer end points (if 

derived) and the end points from which they were derived are indicated and discussed. 

Limitations to existing scientific literature that prevent a satisfactory evaluation of the relevance to public 

health are identified in the Chapter 3 Data Needs section. 

Interpretation of Minimal Risk Levels 

Where sufficient toxicologic information is available, ATSDR has derived MRLs for inhalation and oral 

routes of entry at each duration of exposure (acute, intermediate, and chronic). These MRLs are not 
HYDROGEN SULFIDE B-2 

APPENDIX B 

meant to support regulatory action, but to acquaint health professionals with exposure levels at which 

adverse health effects are not expected to occur in humans. 

MRLs should help physicians and public health officials determine the safety of a community living near 

a chemical emission, given the concentration of a contaminant in air or the estimated daily dose in water. 

MRLs are based largely on toxicological studies in animals and on reports of human occupational 

exposure. 

MRL users should be familiar with the toxicologic information on which the number is based. Chapter 2, 

"Relevance to Public Health," contains basic information known about the substance. Other sections such 

as Chapter 3 Section 3.9, "Interactions with Other Substances,” and Section 3.10, "Populations that are 

Unusually Susceptible" provide important supplemental information. 

MRL users should also understand the MRL derivation methodology. MRLs are derived using a 

modified version of the risk assessment methodology that the Environmental Protection Agency (EPA) 

provides (Barnes and Dourson 1988) to determine reference doses (RfDs) for lifetime exposure. 

To derive an MRL, ATSDR generally selects the most sensitive end point which, in its best judgement, 

represents the most sensitive human health effect for a given exposure route and duration. ATSDR 

cannot make this judgement or derive an MRL unless information (quantitative or qualitative) is available 

for all potential systemic, neurological, and developmental effects. If this information and reliable 

quantitative data on the chosen end point are available, ATSDR derives an MRL using the most sensitive 

species (when information from multiple species is available) with the highest no-observed-adverse-effect 

level (NOAEL) that does not exceed any adverse effect levels. When a NOAEL is not available, a 

lowest-observed-adverse-effect level (LOAEL) can be used to derive an MRL, and an uncertainty factor 

(UF) of 10 must be employed. Additional uncertainty factors of 10 must be used both for human 

variability to protect sensitive subpopulations (people who are most susceptible to the health effects 

caused by the substance) and for interspecies variability (extrapolation from animals to humans). In 

deriving an MRL, these individual uncertainty factors are multiplied together. The product is then 

divided into the inhalation concentration or oral dosage selected from the study. Uncertainty factors used 

in developing a substance-specific MRL are provided in the footnotes of the levels of significant exposure 

(LSE) tables. 

Chapter 3 

Health Effects 

Tables and Figures for Levels of Significant Exposure (LSE) 

Tables and figures are used to summarize health effects and illustrate graphically levels of exposure 

associated with those effects. These levels cover health effects observed at increasing dose 

concentrations and durations, differences in response by species, MRLs to humans for noncancer end 

points, and EPA's estimated range associated with an upper- bound individual lifetime cancer risk of 1 in 

10,000 to 1 in 10,000,000. Use the LSE tables and figures for a quick review of the health effects and to 

locate data for a specific exposure scenario. The LSE tables and figures should always be used in 

conjunction with the text. All entries in these tables and figures represent studies that provide reliable, 

quantitative estimates of NOAELs, LOAELs, or Cancer Effect Levels (CELs). 

The legends presented below demonstrate the application of these tables and figures. Representative 

examples of LSE Table 3-1 and Figure 3-1 are shown. The numbers in the left column of the legends 

correspond to the numbers in the example table and figure. 
	 

	 

HYDROGEN SULFIDE B-3 

APPENDIX B 

LEGEND 

See Sample LSE Table 3-1 (page B-6) 

(1) Route of Exposure. One of the first considerations when reviewing the toxicity of a substance 

using these tables and figures should be the relevant and appropriate route of exposure. Typically 

when sufficient data exist, three LSE tables and two LSE figures are presented in the document. 

The three LSE tables present data on the three principal routes of exposure, i.e., inhalation, oral, 

and dermal (LSE Tables 3-1, 3-2, and 3-3, respectively). LSE figures are limited to the inhalation 

(LSE Figure 3-1) and oral (LSE Figure 3-2) routes. Not all substances will have data on each 

route of exposure and will not, therefore, have all five of the tables and figures. 

(2) Exposure Period. Three exposure periods—acute (less than 15 days), intermediate (15– 

364 days), and chronic (365 days or more)—are presented within each relevant route of exposure. 

In this example, an inhalation study of intermediate exposure duration is reported. For quick 

reference to health effects occurring from a known length of exposure, locate the applicable 

exposure period within the LSE table and figure. 

(3) Health Effect. The major categories of health effects included in LSE tables and figures are 

death, systemic, immunological, neurological, developmental, reproductive, and cancer. 

NOAELs and LOAELs can be reported in the tables and figures for all effects but cancer. 

Systemic effects are further defined in the "System" column of the LSE table (see key number 

18). 

(4) Key to Figure. Each key number in the LSE table links study information to one or more data 

points using the same key number in the corresponding LSE figure. In this example, the study 

represented by key number 18 has been used to derive a NOAEL and a Less Serious LOAEL 

(also see the two "18r" data points in sample Figure 3-1). 

(5) Species. The test species, whether animal or human, are identified in this column. Chapter 2, 

"Relevance to Public Health," covers the relevance of animal data to human toxicity and 

Section 3.4, "Toxicokinetics," contains any available information on comparative toxicokinetics. 

Although NOAELs and LOAELs are species specific, the levels are extrapolated to equivalent 

human doses to derive an MRL. 

(6) Exposure Frequency/Duration. The duration of the study and the weekly and daily exposure 

regimens are provided in this column. This permits comparison of NOAELs and LOAELs from 

different studies. In this case (key number 18), rats were exposed to “Chemical x” via inhalation 

for 6 hours/day, 5 days/week, for 13 weeks. For a more complete review of the dosing regimen, 

refer to the appropriate sections of the text or the original reference paper (i.e., Nitschke et al. 

1981). 

(7) System. This column further defines the systemic effects. These systems include respiratory, 

cardiovascular, gastrointestinal, hematological, musculoskeletal, hepatic, renal, and 

dermal/ocular. "Other" refers to any systemic effect (e.g., a decrease in body weight) not covered 

in these systems. In the example of key number 18, one systemic effect (respiratory) was 

investigated. 

(8) NOAEL. A NOAEL is the highest exposure level at which no harmful effects were seen in the 

organ system studied. Key number 18 reports a NOAEL of 3 ppm for the respiratory system, 
	 

HYDROGEN SULFIDE B-4 

APPENDIX B 

which was used to derive an intermediate exposure, inhalation MRL of 0.005 ppm (see 

footnote "b"). 

(9) LOAEL. A LOAEL is the lowest dose used in the study that caused a harmful health effect. 

LOAELs have been classified into "Less Serious" and "Serious" effects. These distinctions help 

readers identify the levels of exposure at which adverse health effects first appear and the 

gradation of effects with increasing dose. A brief description of the specific end point used to 

quantify the adverse effect accompanies the LOAEL. The respiratory effect reported in key 

number 18 (hyperplasia) is a Less Serious LOAEL of 10 ppm. MRLs are not derived from 

Serious LOAELs. 

(10) Reference. The complete reference citation is given in Chapter 9 of the profile. 

(11) CEL. A CEL is the lowest exposure level associated with the onset of carcinogenesis in 

experimental or epidemiologic studies. CELs are always considered serious effects. The LSE 

tables and figures do not contain NOAELs for cancer, but the text may report doses not causing 

measurable cancer increases. 

(12) Footnotes. Explanations of abbreviations or reference notes for data in the LSE tables are found 

in the footnotes. Footnote "b" indicates that the NOAEL of 3 ppm in key number 18 was used to 

derive an MRL of 0.005 ppm. 

LEGEND 

See Sample Figure 3-1 (page B-7) 

LSE figures graphically illustrate the data presented in the corresponding LSE tables. Figures help the 

reader quickly compare health effects according to exposure concentrations for particular exposure 

periods. 

(13) Exposure Period. The same exposure periods appear as in the LSE table. In this example, health 

effects observed within the acute and intermediate exposure periods are illustrated. 

(14) Health Effect. These are the categories of health effects for which reliable quantitative data 

exists. The same health effects appear in the LSE table. 

(15)	 Levels of Exposure. Concentrations or doses for each health effect in the LSE tables are 

graphically displayed in the LSE figures. Exposure concentration or dose is measured on the log 

scale "y" axis. Inhalation exposure is reported in mg/m3

 or ppm and oral exposure is reported in 

mg/kg/day. 

(16) NOAEL. In this example, the open circle designated 18r identifies a NOAEL critical end point in 

the rat upon which an intermediate inhalation exposure MRL is based. The key number 18 

corresponds to the entry in the LSE table. The dashed descending arrow indicates the 

extrapolation from the exposure level of 3 ppm (see entry 18 in the table) to the MRL of 

0.005 ppm (see footnote "b" in the LSE table). 

(17) CEL. Key number 38m is one of three studies for which CELs were derived. The diamond 

symbol refers to a CEL for the test species-mouse. The number 38 corresponds to the entry in the 

LSE table. 
	 

	 

HYDROGEN SULFIDE B-5 

APPENDIX B 

(18)	 Estimated Upper-Bound Human Cancer Risk Levels. This is the range associated with the upperbound for lifetime cancer risk of 1 in 10,000 to 1 in 10,000,000. These risk levels are derived 

from the EPA's Human Health Assessment Group's upper-bound estimates of the slope of the 

cancer dose response curve at low dose levels (q1*). 

(19)	 Key to LSE Figure. The Key explains the abbreviations and symbols used in the figure. 
3 

4 

SAMPLE 

1 → Table 3-1. Levels of Significant Exposure to [Chemical x] – Inhalation 

LOAEL (effect) Exposure 

Key to frequency/ NOAEL Less serious Serious (ppm) 

figurea Species duration System (ppm) (ppm) Re

2 → INTERMEDIATE EXPOSURE 

5 

→ Systemic ↓

18 Rat 

→

CHRONIC EXPOSURE 

Cancer 38 Rat 39 Rat 40 Mouse 

6 7 8 9 

↓ ↓ ↓ ↓

3b 13 wk Resp 10 (hyperplasia) 

5 d/wk 6 hr/d 

11 ↓

18 mo 20 5 d/wk 7 hr/d 89–104 wk 10 5 d/wk 6 hr/d 79–103 wk 10 5 d/wk 6 hr/d 

(CEL, multiple organs) (CEL, lung tumors, nasal tumors) (CEL, lung tumors, hemangiosarcomas) 

10 

↓

NitWNTNT

12 → a The number corresponds to entries in Figure 3-1. b Used to derive an intermediate inhalation Minimal Risk Level (MRL) of 5x10-3 ppm; dose adjusted for intermittent ex

by an uncertainty factor of 100 (10 for extrapolation from animal to humans, 10 for human variability). 

HYDROGEN SULFIDE B-8 

APPENDIX B 

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HYDROGEN SULFIDE C-1 

APPENDIX C. ACRONYMS, ABBREVIATIONS, AND SYMBOLS 

ACGIH American Conference of Governmental Industrial Hygienists 

ACOEM American College of Occupational and Environmental Medicine 

ADI acceptable daily intake 

ADME absorption, distribution, metabolism, and excretion 

AED atomic emission detection 

AFID alkali flame ionization detector 

AFOSH Air Force Office of Safety and Health 

ALT alanine aminotransferase 

AML acute myeloid leukemia 

AOAC Association of Official Analytical Chemists 

AOEC Association of Occupational and Environmental Clinics 

AP alkaline phosphatase 

APHA American Public Health Association 

AST aspartate aminotransferase 

atm atmosphere 

ATSDR Agency for Toxic Substances and Disease Registry 

AWQC Ambient Water Quality Criteria 

BAT best available technology 

BCF bioconcentration factor 

BEI Biological Exposure Index 

BMD benchmark dose 

BMR benchmark response 

BSC Board of Scientific Counselors 

C centigrade 

CAA Clean Air Act 

CAG Cancer Assessment Group of the U.S. Environmental Protection Agency 

CAS Chemical Abstract Services 

CDC Centers for Disease Control and Prevention 

CEL cancer effect level 

CELDS Computer-Environmental Legislative Data System 

CERCLA Comprehensive Environmental Response, Compensation, and Liability Act 

CFR Code of Federal Regulations 

Ci curie 

CI confidence interval 

CL ceiling limit value 

CLP Contract Laboratory Program 

cm centimeter 

CML chronic myeloid leukemia 

CPSC Consumer Products Safety Commission 

CWA Clean Water Act 

DHEW Department of Health, Education, and Welfare 

DHHS Department of Health and Human Services 

DNA deoxyribonucleic acid 

DOD Department of Defense 

DOE Department of Energy 

DOL Department of Labor 

DOT Department of Transportation 
HYDROGEN SULFIDE C-2 

APPENDIX C 

DOT/UN/ Department of Transportation/United Nations/ 

NA/IMCO North America/International Maritime Dangerous Goods Code 

DWEL drinking water exposure level 

ECD electron capture detection 

ECG/EKG electrocardiogram 

EEG electroencephalogram 

EEGL Emergency Exposure Guidance Level 

EPA Environmental Protection Agency 

F Fahrenheit 

F1 first-filial generation 

FAO Food and Agricultural Organization of the United Nations 

FDA Food and Drug Administration 

FEMA Federal Emergency Management Agency 

FEV1 forced expiratory volume in 1 second 

FIFRA Federal Insecticide, Fungicide, and Rodenticide Act 

FVC forced vital capacity 

FPD flame photometric detection 

fpm feet per minute 

FR Federal Register 

FSH follicle stimulating hormone 

g gram 

GC gas chromatography 

gd gestational day 

GLC gas liquid chromatography 

GPC gel permeation chromatography 

HPLC high-performance liquid chromatography 

HRGC high resolution gas chromatography 

HSDB Hazardous Substance Data Bank 

IARC International Agency for Research on Cancer 

IDLH immediately dangerous to life and health 

ILO International Labor Organization 

IRIS Integrated Risk Information System 

Kd adsorption ratio 

kg kilogram 

kkg metric ton 

Koc organic carbon partition coefficient 

Kow octanol-water partition coefficient 

L liter 

LC liquid chromatography 

LC50 lethal concentration, 50% kill 

LCLo lethal concentration, low 

LD50 lethal dose, 50% kill 

LDLo lethal dose, low 

LDH lactic dehydrogenase 

LH luteinizing hormone 

LOAEL lowest-observed-adverse-effect level 

LSE Levels of Significant Exposure 

LT50 lethal time, 50% kill 

m meter 

MA trans,trans-muconic acid 

MAL maximum allowable level 
HYDROGEN SULFIDE C-3 

APPENDIX C 

mCi millicurie 

MCL maximum contaminant level 

MCLG maximum contaminant level goal 

MF modifying factor 

MFO mixed function oxidase 

mg milligram 

mL milliliter 

mm millimeter 

mmHg millimeters of mercury 

mmol millimole 

mppcf millions of particles per cubic foot 

MRL Minimal Risk Level 

MS mass spectrometry 

NAAQS National Ambient Air Quality Standard 

NAS National Academy of Science 

NATICH National Air Toxics Information Clearinghouse 

NATO North Atlantic Treaty Organization 

NCE normochromatic erythrocytes 

NCEH National Center for Environmental Health 

NCI National Cancer Institute 

ND not detected 

NFPA National Fire Protection Association 

ng nanogram 

NHANES National Health and Nutrition Examination Survey 

NIEHS National Institute of Environmental Health Sciences 

NIOSH National Institute for Occupational Safety and Health 

NIOSHTIC NIOSH's Computerized Information Retrieval System 

NLM National Library of Medicine 

nm nanometer 

nmol nanomole 

NOAEL no-observed-adverse-effect level 

NOES National Occupational Exposure Survey 

NOHS National Occupational Hazard Survey 

NPD nitrogen phosphorus detection 

NPDES National Pollutant Discharge Elimination System 

NPL National Priorities List 

NR not reported 

NRC National Research Council 

NS not specified 

NSPS New Source Performance Standards 

NTIS National Technical Information Service 

NTP National Toxicology Program 

ODW Office of Drinking Water, EPA 

OERR Office of Emergency and Remedial Response, EPA 

OHM/TADS Oil and Hazardous Materials/Technical Assistance Data System 

OPP Office of Pesticide Programs, EPA 

OPPT Office of Pollution Prevention and Toxics, EPA 

OPPTS Office of Prevention, Pesticides and Toxic Substances, EPA 

OR odds ratio 

OSHA Occupational Safety and Health Administration 

OSW Office of Solid Waste, EPA 
HYDROGEN SULFIDE C-4 

APPENDIX C 

OTS Office of Toxic Substances 

OW Office of Water 

OWRS Office of Water Regulations and Standards, EPA 

PAH polycyclic aromatic hydrocarbon 

PBPD physiologically based pharmacodynamic 

PBPK physiologically based pharmacokinetic 

PCE polychromatic erythrocytes 

PEL permissible exposure limit 

pg picogram 

PHS Public Health Service 

PID photo ionization detector 

pmol picomole 

PMR proportionate mortality ratio 

ppb parts per billion 

ppm parts per million 

ppt parts per trillion 

PSNS pretreatment standards for new sources 

RBC red blood cell 

REL recommended exposure level/limit 

RfC reference concentration 

RfD reference dose 

RNA ribonucleic acid 

RQ reportable quantity 

RTECS Registry of Toxic Effects of Chemical Substances 

SARA Superfund Amendments and Reauthorization Act 

SCE sister chromatid exchange 

SGOT serum glutamic oxaloacetic transaminase 

SGPT serum glutamic pyruvic transaminase 

SIC standard industrial classification 

SIM selected ion monitoring 

SIR standardized incidence ratio 

SMCL secondary maximum contaminant level 

SMR standardized mortality ratio 

SNARL suggested no adverse response level 

SPEGL Short-Term Public Emergency Guidance Level 

STEL short term exposure limit 

STORET Storage and Retrieval 

TD50 toxic dose, 50% specific toxic effect 

TLV threshold limit value 

TOC total organic carbon 

TPQ threshold planning quantity 

TRI Toxics Release Inventory 

TRS total reduced sulfur 

TSCA Toxic Substances Control Act 

TWA time-weighted average 

UF uncertainty factor 

U.S. United States 

USDA United States Department of Agriculture 

USGS United States Geological Survey 

VOC volatile organic compound 

VO

2 oxygen uptake 
HYDROGEN SULFIDE C-5 

APPENDIX C 

VCO2 carbon dioxide uptake 

WBC white blood cell 

WHO World Health Organization 

> greater than ≥ greater than or equal to 

= equal to 

< less than ≤ less than or equal to 

% percent α alpha β beta γ gamma δ delta μm micrometer μg microgram q1

* cancer slope factor 

– negative 

+ positive 

(+) weakly positive result 

(–) weakly negative result 
HYDROGEN SULFIDE C-6 

APPENDIX C 

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HYDROGEN SULFIDE D-1 

APPENDIX D. INDEX 

absorbed dose ..............................................................................................................................................................92 

adsorption ..................................................................................................................................................................137 

aerobic .............................................................................................................................................................57, 61, 97 

ambient air......................................................................................................................... 117, 124, 125, 126, 129, 134 

anaerobic........................................................................................................................................ 15, 86, 119, 120, 128 

anemia .................................................................................................................................................................57, 102 

aspartate aminotransferase...........................................................................................................................................57 

biomarker......................................................................................................................................... 91, 92, 93, 105, 137 

body weight effects..........................................................................................................................................60, 73, 74 

breast milk .................................................................................................................................................128, 131, 132 

cancer......................................................................................................................................... 4, 5, 12, 71, 72, 90, 102 

carcinogen..................................................................................................................................................................102 

carcinogenic...........................................................................................................................................14, 21, 102, 157 

carcinogenicity ....................................................................................................................................................12, 102 

cardiac arrhythmia ...........................................................................................................................................10, 54, 55 

cardiovascular.............................................................................................................................. 24, 54, 55, 72, 74, 100 

cardiovascular effects ....................................................................................................................................53, 54, 100 

cognitive function..................................................................................................................................................64, 98 

death ...............................................................................21, 22, 23, 25, 26, 72, 73, 77, 78, 86, 100, 101, 104, 128, 157
 

dermal effects ..............................................................................................................................................................58 

deoxyribonucleic acid..................................................................................................................................................92 

endocrine ...................................................................................................................................................58, 72, 74, 88 

endocrine effects..........................................................................................................................................................58 

erythema ......................................................................................................................................................................59 

fetus .....................................................................................................................................................................89, 132 

gastrointestinal effects .....................................................................................................................................55, 56, 72 

general population ........................................................................................................... 3, 6, 10, 91, 95, 117, 129, 157 

genotoxic .....................................................................................................................................................................21 

genotoxicity .........................................................................................................................................................75, 102 

groundwater....................................................................................................................................... 118, 119, 121, 133 

half-life ........................................................................................................................................................................91 

hematological effects...................................................................................................................................................56 

hepatic effects..............................................................................................................................................................57 

hydroxyl radical.................................................................................................................................................117, 122 

immunological................................................................................................................................... 21, 61, 62, 74, 100 

immunological effects .................................................................................................................................................62 

Kow .............................................................................................................................................................................111 

lymphoreticular..............................................................................................................................................61, 74, 100 

metabolic effects..............................................................................................................................................14, 61, 72 

milk..............................................................................................................................................................97, 128, 132 

musculoskeletal effects................................................................................................................................................57 

neurobehavioral ......................................................................................................... 11, 13, 16, 62, 66, 70, 89, 90, 103 

neurodevelopmental.....................................................................................................................................................18 

neurotransmitter...........................................................................................................................................................91 

norepinephrine.......................................................................................................................................................17, 71 

nuclear .......................................................................................................................................................................114 

ocular effects .................................................................................................................................................11, 60, 100 

odds ratio .........................................................................................................................................................46, 47, 49 

pharmacodynamic........................................................................................................................................................83 

pharmacokinetic................................................................................................................... 76, 83, 84, 85, 89, 101, 102
 

rate constant.......................................................................................................................................................117, 122 

renal effects .................................................................................................................................................................58 

 


 


 


 


 


 


 


 


 

HYDROGEN SULFIDE D-2 

APPENDIX D 

retention.................................................................................................................................................................63, 93

serum glutamic oxaloacetic transaminase (see SGOT)................................................................................................57 

SGOT (see serum glutamic oxaloacetic transaminase)..........................................................................................57, 70 

solubility...................................................................................................................................... 75, 102, 121, 127, 133 

thyroid .........................................................................................................................................................................58 

toxicokinetic ..................................................................................................................................................21, 88, 106 

tremors...........................................................................................................................................................18, 62, 104

vapor phase................................................................................................................................................................128 

volatility.....................................................................................................................................................................137