Unned States FINAL DRAFT
Environmental Protection ECAO-CIN-6088
A9encv April. 1990
2-EPA Research and
Development
HEALTH AND ENVIRONMENTAL EFFECTS DOCUMENT
FOR HYDROGEN SULFIDE
Prepared for
OFFICE OF SOLID WASTE AND
EMERGENCY RESPONSE
Prepared by
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Cincinnati, OH 45268
DRAFT: 00 NOT CITE OR QUOTE
NOTICE
This document I* a preliminary draft. It has not been formally released
by the U.S. Environmental Protection Agency and should not at this stage be
construed to represent Agency policy. It Is being circulated for comments
on Its technical accuracy and policy Implications.
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DISCLAIMER
This report Is an external draft for review purposes only and does not
constitute Agency policy. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
11
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PREFACE
Health and Environmental Effects Documents (HEEDs) are prepared for the
Office of Solid Waste and Emergency Response (OSWER). This document series
Is Intended to support listings under the Resource Conservation and Recovery
Act (RCRA) as well as to provide health-related limits and goals for emer-
gency and remedial actions under the Comprehensive Environmental Response,
Compensation and Liability Act (CERCLA). Both published literature and
Information obtained for Agency Program 'Office files are evaluated as they
pertain to potential human health, aquatic life and environmental effects of
hazardous waste constituents. The literature searched for In this document
and the dates searched are Included In "Appendix: Literature Searched."
Literature search material 1s current up to 8 months previous to the final
draft date listed on the front cover. Final draft document dates (front
cover) reflect the date the document 1s sent to the Program Officer (OSWER).
Several quantitative estimates are presented provided sufficient data
are available. For systemic toxicants, these Include Reference doses (RfDs)
for chronic and subchronlc exposures for both the Inhalation and oral
exposures. The subchronlc or partial lifetime RfD Is an estimate of an
exposure level that would not be expected to cause adverse effects when
exposure occurs during a limited time Interval I.e., for an Interval that
does not constitute a significant portion of the llfespan. This type of
exposure estimate has not been extensively used, or rigorously defined as
previous risk assessment efforts have focused primarily on lifetime exposure
scenarios. Animal data used for subchronlc estimates generally reflect
exposure durations of 30-90 days. The general methodology for estimating
subchronlc RfDs Is the same as traditionally employed for chronic estimates,
except that subchronlc data are utilized when available.
In the case of suspected carcinogens, a carcinogenic potency factor, or
q-|* (U.S. EPA, 1980), Is provided. These potency estimates are derived
for both oral and Inhalation exposures where possible. In addition, unit
risk estimates for air and drinking water are presented based on Inhalation
and oral data, respectively. An RfD may also be derived for the noncarclno-
genlc health effects of compounds that are also carcinogenic.
Reportable quantities (RQs) based on both chronic toxlclty and carclno-
genlclty are derived. The RQ Is used to determine the quantity of a hazard-
ous substance for which notification Is required In the event of a release
as specified under the Comprehensive Environmental Response, Compensation
and Liability Act (CERCLA). These two RQs (chronic toxlclty and carclno-
genlclty) represent two of six scores developed (the remaining four reflect
Ignltablllty, reactivity, aquatic toxlclty, and acute mammalian toxlclty).
Chemical-specific RQs reflect the lowest of these six primary criteria. The
methodology for chronic toxlclty and cancer based RQs are defined In U.S.
EPA, 1984 and 1986d, respectively.
111
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EXECUTIVE SUMMARY
Hydrogen sulflde Is a colorless, flammable gas wUh an odor of rotten
eggs (Wlndholz, 1983). It Is soluble In water, forming a slightly acidic
solution (pH 4.1) (Weast, 1980). It Is oxidized by many oxidizing agents;
1n water, hydrogen sulflde Is slowly converted Into elemental sulfur by the
action of dissolved oxygen (Vllndholz, 1983). A common reaction of hydrogen
sulflde Is with metal Ions In which Insoluble sulfldes are formed (Well,
1983).
Hydrogen sulflde occurs naturally; It Is produced by the mlcroblal
degradation of sulfates under anaerobic conditions and the bacterial
decomposition of proteins (Well, 1983). It Is present 1n the gases from
many volcanoes, swamps, stagnant bodies of water, undersea vents, coal pits,
gas wells (sour gas) and sulfur springs (Hawley. 1981; Well, 1983).
Hydrogen sulflde may be produced by the action of dilute acids of Iron
sulflde or other sulfldes, by the direct combination of sulfur and hydrogen
or by heating sulfur with paraffin (Well, 1983). Most hydrogen sulflde used
commercially In the United States Is either a by-product of crude oil
refining or obtained from sour natural gas (Well, 1983). Sulfldes naturally
occur In crude oil and are removed by a process In which the sulfur-rich
fraction of the crude oil and hydrogen gas are passed through a fixed-bed
catalyst. In this process. 80-90% of the sulfur compounds are converted to
hydrogen sulflde (Well, 1983).
No recent U.S. production data for hydrogen sulflde were located. Most
of the hydrogen sulflde recovered from crude oil or natural gas Is converted
to elemental sulfur and sulfurlc acid (Well, 1983). While elemental sulfur
was listed as being produced by refineries or from natural gas by numerous
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companies, only four were listed as producers of hydrogen sulflde (SRI,
1989; CMR, 1988). In addition to being an Intermediate In the production of
elemental sulfur and sulfurlc acid, hydrogen sulflde Is used as a reagent In
the manufacture of Inorganic sulflde (e.g., sodium sulflde and sodium
hydrosulfIde) which Is used In the manufacture of dyes, plastics, leather
products, rubber chemicals, Pharmaceuticals and organosulfur products (e.g.,
mercaptans) (Well, 1989; Chemlcyclopedla, 1988). Hydrogen sulflde Is also
used for separating metals, In metallurgical waste treatment and recovery,
In analytical chemistry and 1n the calibration of analytical Instruments
(Wlndholz, 1983; Chemlcyclopedla, 1988).
Hydrogen sulflde may occur In sewage as a result of Industrial
discharges or may be formed by the mkroblal reduction of sulfate under
anaerobic conditions. It Is a weak acid with a pK, of 7.04. Between pH 6
and 8, the lonlzatlon of hydrogen sulflde ranges from 10-90%. Hydrogen
sulflde reacts with oxldants such as dissolved oxygen and hydrogen peroxide
In water to produce elemental sulfur, thlosulfate and sulfate (Balls and
Llss, 1983). Because It Is a gas with a high Henry's Law constant, hydrogen
sulflde will have a strong tendency to volatilize from water. Both oxida-
tion and volatilization are pH dependent. At pH 8 and 25°C, the oxldatlve
half-lives In air-saturated water and seawater are 50 and 25 hours, respec-
tively (Mlllero et al.. 1987). At 20°C and at relatively low oxygen concen-
trations, oxidation was mildly pH dependent; the half-life ranged from 43
hours at pH 6 to 63 hours at pH 8 (Balls and Llss. 1983). Volatilization Is
the more significant transport process. The volatilization half-life of
hydrogen sulflde In a body of water 1 m deep was 16.3 hours at pH 6 and 1.9
hours at pH 8 (Balls and Llss, 1983).
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Hydrogen sulflde reacts with photochemlcally produced hydroxyl radicals
In the troposphere; the rate constant for this reaction Is 4.8xlO~12
cm3/molecule-sec (Cox, 1975). Assuming an average hydroxyl radical
concentration of IxlO6 per cm3, the half-life of hydrogen sulflde In the
troposphere will be 38 hours. During summer daylight hours, the half-life
will be 3.8 hours. The reaction products are sulfur dioxide and sulfate
(Sze and Ko, 1980). Reaction of hydrogen sulflde with atmospheric ozone Is
too slow to be a significant sink for hydrogen sulflde. Hydrogen sulflde Is
relatively soluble In water and should be removed from the atmosphere by
rain.
Soil appears to be an Important natural sink for hydrogen sulflde.
Adsorption Is rapid, and the ability of soil to adsorb hydrogen sulflde and
the rate of adsorption are not significantly correlated with soil properties
like pH, clay content, organic-matter content or the presence of soil micro-
organisms. Soil moisture had little effect on sorptlon capacity; 15.4-65.2
rag of hydrogen sulflde sorbed to a gram of air-dried soil, while 11.0-62.5
mg of hydrogen sulflde sorbed to a gram of moist soil (Smith et al., 1973).
The mean adsorptlvltles of the dry and moist soils were 50.7 and 44.7 mg/g,
respectively. Pertinent data regarding abiotic and blotlc reactions of
hydrogen sulflde In soil were not located In the available literature cited
In Appendix A. It Is probable that hydrogen sulflde will be oxidized In
soil by oxygen and other oxidizing agents.
Pertinent data regarding hydrogen sulflde In drinking water were not
located In the available literature cited In Appendix A. Hydrogen sulflde
Is produced under anoxlc conditions by sulfate-reduclng bacteria and Is
mainly emitted from soil near coastal areas such as salt marshes (Aneja et
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al., 1982). It Is likely that hydrogen sulflde Is found In these waters,
although no levels of hydrogen sulflde In surface water were reported In the
available literature.
Hydrogen sulflde Is a naturally occurring chemical produced by the
mlcroblal metabolism of protein and also In the Intestines as a result of
bacterial action (NIOSH, 1977). Trace amounts of hydrogen sulflde have been
Identified In the breast meat of freshly killed chickens, roasted peanuts
and cheese (Grey and Shrlmpton, 1967; Young, 1985; Rlchter and Vanderzant,
1987; Dumont and Adda, 1978}. It Is probable that humans arc exposed to
some hydrogen sulflde In food, although no estimation of quantity of
hydrogen sulflde Ingested Is possible.
Hydrogen sulflde Is a gas produced naturally and emitted by Industrial
sources and numerous other nonpolnt anthropogenic sources. Blogenlc sulfur
compounds are emitted from soils with coastal wetlands having the greatest
potential for emitting significant quantities of hydrogen sulflde Into the
atmosphere. Emissions exhibit a diurnal variation, which peak around noon
when soil temperature and solar Irradiation are at a maximum (Cooper et al.,
1987). Industrial sources and other anthropogenic sources are believed to
contribute -10% of the hydrogen sulflde entering the atmosphere (U.S. EPA,
1986a). Nonpolnt anthropogenic sources are ubiquitous. Including dlesel
engines and motor vehicles, especially those In which carburetors or
catalytic converters are not functioning properly (Hayano et al., 1985; U.S.
EPA, 1986a). Concentrations of hydrogen sulflde In West Germany, Miami, FL
(polluted air), Illinois, Missouri and the North Sea range from 0.035-1.65
Mg/m* of hydrogen sulflde (Aneja et al., 1982; Sze and Ko, 1980). Lower
concentrations (0.008-0.17 yg/m3) were observed In urban Miami, FL,
France and Boulder, CO. Much higher levels (80 jig/m3} were found In the
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air above a tidal marsh In North Carolina, near an Industrial source (1000
pg/m3) and near a geothermal vent In New Zealand (0.008-2.9 mg/m3)
(Aneja et a!., 1982; U.S. EPA, 1986a).
NIOSH (1977) lists 73 occupations that potentially expose workers to
hydrogen sulflde. These Include workers In coke oven plants, employees In
petroleum production and refining Industries, dye makers, tanners, textile
workers, sewage plant operators, rayon makers, paper makers, fermentation
plant operators and livestock farmers. Hydrogen sulflde has been detected
In pulp and paper factories, oil Industries, wastewater treatment plants,
synthetic fibers and agricultural areas (Kangas and Ryosa, 1988; NIOSH,
1987). According to statistical estimates, 94,922 workers, Including 6519
women, are potentially exposed to hydrogen sulflde In the workplace (NIOSH,
1989). Concentrations of hydrogen sulflde In selected workplaces Include
0.002-0.016 ppm In a sewage treatment plant, 0.054 ppm In a sulfate pulp
mill, 0.216-0.933 ppm In the sewage plant of a sulflte pulp mill and <15 ppm
In a viscose rayon plant; occasionally, levels reached 100 ppm (Kangas and
Ryosa, 1988; NIOSH, 1977). There are several reports of worker exposure to
high levels of hydrogen sulflde as a result of accidents or leaks resulting
In serious Injury or death. In these cases, hydrogen sulflde may have been
monitored after some of the gas had dissipated. The maximum level of
hydrogen sulflde reported In these accidents was 17,000 mg/m3 (12,000 ppm).
The acute toxlclty of hydrogen sulflde was similar In most species of
freshwater fish examined, with LC5Q values ranging from 0.003 mg/i in
whlteflsh, C_. clupeaformls (Fung and Bewick, 1980) to 3.0 mg/a In mosquito
fish, G. afflnls (Prasad. 1980b). The latter was the only fish with an
LC5Q >1. Representatives from >14 genera of fish have been assayed for
acute toxlclty from hydrogen sulflde (Adelman and Smith, 1970, 1972; Bonn
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and Follls. 1967; BrodeMus et al., 1977; Fung and Bewick, 1980; Oseld and
Smith, 1974a; Prasad, 1980a,b; Reynolds and Halnes, 1980; Smith, 1970; Smith
and Oseld, 1970, 1972. 1975; Smith et al., 1976a.b,c; Van Horn et al..
1949). Some acclimation occurs with Initial low-level exposure of bluegllls
to hydrogen sulflde (Smith et al., 1976a).
Freshwater and marine Invertebrates were less sensitive to hydrogen
sulflde than were fish. Variation of response within the Invertebrates was
slight. LC.- values ranged from 0.02 mg/l In the mayfly, B. vaqans
(Smith- et al., 1976a; Oseld and Smith, 1974b), to 6 mg/l In the clam. M.
balthlca (Caldwell, 1975), for all Invertebrates tested. The one exception
was Chlronomus sp., with an LC5Q of 550 (Prasad, 1980a).
Chronic studies with freshwater animals yielded LOECs ranging from
0.0010-0.429 mg/l. Little difference was noted between fish and Inverte-
brates (Reynolds and Halnes, 1980; Oseld and Smith. 1974a; Smith, 1970;
Smith and Oseld. 1975; Smith et al., 1976a). Prespawnlng adult L. macro-
chlrus were the most sensitive group, suffering reproductive stress with
exposure to 0.0010 mg/l for 90 days (Smith, 1970; Smith et al., 1976a).
Field tests with I., punctatus Indicated that exposure to 1 mg/l at pH 7.0
adversely affects reproduction (Bonn and Follls, 1967).
Available data Indicate that criteria based on protection of freshwater
fish would be protective of fresh and saltwater Invertebrates. The
currently recommended criterion of 2 jig/l hydrogen sulflde for fresh and
saltwater life (U.S.EPA/OURS, 1986) may not be protective for all life
stages of L_. macrochlrus. It does, however, appear to be protective for
other species.
Terrestrial plants fumigated with 0.25 ml/l for <14 days may suffer
reduced growth and altered leaf morphology (Haas et al., 1987).
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Absorption by humans of Inhaled hydrogen sulflde can be Inferred from
excretion of thlosulfate following human exposure to hydrogen sulflde gas
(Kangas and Savolalnen, 1987), and from toxic effects following acute and
occupational exposure (see Chapter 6). Absorption through the respiratory
tracts and skin of animals can be Inferred from toxic effects following
respiratory and dermal exposure (Laug and Dralze, 1942; Walton and
WUherspoon, 1925). Studies using rats suggest that gastrointestinal
absorption Is rapid and virtually complete (Curtis et al., 1972). U.S. EPA
(1986b) concluded that the most common route of entry for hydrogen sulflde
1s the lung.
Wide distribution to the brain, liver, kidneys, pancreas and small
Intestines has been shown hlstochemlcally after Inhalation exposure of
guinea pigs and rats (Volgt and Mullet, 1955). Distribution to the gastro-
intestinal tract, cartilaginous tissues, lungs, brain and blood has been
shown autoradlographlcally following oral, Intraperltoneal, and Intravenous
administration of hydrogen sulflde to rats (Curtis et al., 1972). Warenycla
et al. (1989) reported that the highest concentration of sulflde In the
brain was found In the bralnstem following Intraperltoneal doses of sodium
hydrosulfIde.
Three separate metabolic pathways exist for hydrogen sulflde: 1) oxida-
tion to sulfate, 2) methylatlon, and 3) reaction with metallo- or dlsulflde-
contalnlng proteins (Beauchamp et al., 1984). Oxidation and methylatlon
detoxify hydrogen sulflde, while the reaction of hydrogen sulflde with
essential proteins results In Its toxic effects.
The predominant route of excretion of hydrogen sulflde In humans and
rats Is In the urine as metabolites (sulfate or thlosulfate) (Kangas and
Savolalnen, 1987; Curtis et al., 1972). Urinary levels of thlosulfate, a
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metabolite of hydrogen sulflde, have been correlated with exposure levels of
hydrogen sulflde In workers (Kangas and Savolalnen. 1987).
Hydrogen sulflde acts by Inhibiting oxldatlve metabolism; consequently,
the tissues with the greatest oxygen need (such as the nervous system) are
most severely affected (Ammann, 1986). Toxic effects resulting from acute
Inhalation exposure Increase 1n severity with Increasing exposure levels:
at low levels (50-200 ppm), effects such as respiratory and eye Irritation
occur, at higher levels (200-250 ppm), pulmonary edema Is observed, and at
concentrations above 1000-2000 ppm, respiratory paralysis and death result
(Ammann, 1986; Deng and Chang, 1987; Vannatta, 1982). Death In guinea pigs
and rabbits followed dermal exposure to hydrogen sulflde (Walton and
Wither spoon, 1925; Laug and Dralze. 1942). Following subchronlc (1 year)
exposure of an Infant to up to 0.6 ppm hydrogen sulflde, reversible neuro-
logical damage was found (Galtonde et al., 1987). In occupatlonally exposed
workers, eye effects were Induced by 10 ppm (Nesswetha, 1969) and levels of
20 ppm and above resulted In unconsciousness, headaches, nausea/vomiting.
disequilibrium and neurophyslcal effects (Arnold et al., 1985). Poda (1966)
reported no adverse effects In workers occupatlonally exposed to up to 10
/
ppm hydrogen sulflde.
A study Investigating the correlation between the Incidence of sponta-
neous abortions 1n women, with their occupations and the occupations of
their husbands did not conclusively Implicate hydrogen sulflde In develop-
mental toxlclty (Hemmlnkl and Nleml, 1982), since 1) only an Insignificant
Increase In the Incidence of spontaneous abortions was found In women
exposed to >4 yg/m3 hydrogen sulflde and 2} confounding factors (such as
exposure to other agents) could not be controlled.
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Animal studies support the findings that the nervous and respiratory
systems are the targets of hydrogen sulflde administered by the Inhalation
and Intraperltoneal routes (Toxlgenlcs, 1983a,b,c; Lopez et al., 1987.
1988a,b, 1989; Komblan et al., 1988). The Inhalation studies suggest that
rats are more sensitive than mice. Mice showed neurological signs when
Intermittently exposed to 80 but not to 30.5 ppm for 90 days (Toxlgenlcs,
1983a). Clinical signs of Irritation and toxlclty were observed In rats In
the same study Intermittently exposed to 10.1 ppm, the lowest concentration
tested. Subchronlc dietary exposure to 15, but not 3.1 mg/kg/day resulted
In digestive disturbances and reduced body weight In pigs (Wetterau et al..
1964).
Only one study on the mutagenlc potential of hydrogen sulflde was
available In the literature. Hughes et al. (1984) determined that hydrogen
sulflde was not mutagenlc. with or without activation. In three strains of
Salmonella typhlmurlum.
Because of the lack of cancer data 1n either humans or animals, hydrogen
sulflde was placed In U.S. EPA group D, not classifiable as to human
carclnogenlclty. Data were Insufficient for estimation of cancer potencies
or for assignment of an RQ for carclnogenlclty.
A subchronlc Inhalation RfD of 8 yg/m3 hydrogen sulflde was derived
from the LOAEL of 0.836 yg/m3 for neurotoxlc effects 1n an Infant
exposed to hydrogen sulflde for one year (Galtonde et al., 1987). An
uncertainty factor of 100 was applied, 10 to estimate a NOAEL from a LOAEL
and 10 to reflect deffIclendes In the study. The subchronlc RfD was
adopted as the RfD for chronic Inhalation exposure. A subchronlc oral RfD
of 0.03 mg/kg/day and a chronic oral RfD of 0.003 mg/kg/day were derived
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from the NOAEL for weight changes "in a pig feeding study (Wetterau et a "I.,
1964; U.S. EPA, 1989). An uncertainty factor of 100 (for Intra- and Inter-
species variation) was used In the subchronlc derivation and an uncertainty
factor of 1000 (100 for Intra- and Interspecles variation and 10 for the use
of a subchronlc study) was used In the chronic derivation. An RQ of 100 for
chronic toxlclty was calculated based on the neurotoxlc effects found In the
infant In the Galtonde et al. (19B7) study.
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TABLE OF CONTENTS
Page
1. INTRODUCTION 1
1.1. STRUCTURE AND CAS NUMBER 1
1.2. PHYSICAL AND CHEMICAL PROPERTIES 1
1.3. PRODUCTION DATA 2
1.4. USE DATA 5
1.5. SUMMARY 5
2. ENVIRONMENTAL FATE AND TRANSPORT 7
2.1. AIR 7
2.2. WATER 7
2.3. SOIL 8
2.4. SUMMARY 9
3. EXPOSURE 11
3.1. WATER 11
3.2. FOOD 11
3.3. INHALATION 12
3.4. DERMAL 14
3.5-. SUMMARY 14
4. ENVIRONMENTAL TOXICOLOGY 17
4.1. AQUATIC TOXICOLOGY 17
4.1.1. Acute Toxic Effects on Fauna 17
4.1.2. Chronic Effects on Fauna 24
4.1.3. Effects on Flora 27
4.1.4. Effects on Bacteria 27
4.2. TERRESTRIAL TOXICOLOGY 27
4.2.1. Effects on Fauna 27
4.2.2. Effects on Flora 27
4.3. FIELD STUDIES .- 28
4.4. AQUATIC RISK ASSESSMENT 28
4.5. SUMMARY 30
5. PHARMACOKINE1CS 33
5.1. ABSORPTION 33
5.2. DISTRIBUTION 34
5.3. METABOLISM 35
5.4. EXCRETION 38
5.5. SUMMARY 39
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TABLE OF CONTENTS (cont.)
Page
6. EFFECTS 41
6.1. SYSTEMIC TOXICITY 41
6.1.1. Inhalation Exposure 41
6.1.2. Oral Exposure 46
6.1.3. Other Relevant Information 46
6.2. CARC1NOGENICITY 49
6.2.1. Inhalation 49
6.2.2. Oral 49
6.2.3. Other Relevant Information 49
6.3. MUTAGENICITY 49
6.4. DEVELOPMENTAL TOXICITY 49
6.5. OTHER REPRODUCTIVE EFFECTS 49
6.6. SUMMARY 50
7. EXISTING GUIDELINES AND STANDARDS 52
7.1. HUMAN 53
7.2. AQUATIC 53
8. RISK ASSESSMENT 54
8.1. CARCINOGENICITY 54
8.1.1. Inhalation 54
8.1.2. Oral 54
8.1.3. Other Routes 54
8.1.4. Height of Evidence 54
8.1.5. Quantitative Risk Estimates 54
8.2. SYSTEMIC TOXICITY 54
8.2.1. Inhalation Exposure 54
8.2.2. Oral Exposure 57
9. REPORTA8LE QUANTITIES 58
9.1. BASED ON SYSTEMIC TOXICITY 58
9.2. BASED ON CARCINOGENICITY 61
10. REFERENCES 63
APPENDIX A: LITERATURE SEARCHED 81
APPENDIX B: SUMMARY TABLE FOR HYDROGEN SULFIDE 84
APPENDIX C: DOSE/DURATION RESPONSE GRAPH(S) FOR EXPOSURE TO
HYDROGEN SULFIDE 85
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LIST OF TABLES
No. Title Page
1-1 Manufacturers of Hydrogen SulHde In the United States
as of January, 1988 4
4-1 Acute Lethality of Hydrogen SulMde to Aquatic Fauna 18
4-2 Chronic Toxldty of Hydrogen Sulflde to Aquatic Fauna .... 25
9-1 Toxldty Summary for Hydrogen Sulflde 59
9-2 Composite Scores for Hydrogen Sulflde 60
9-3 . Hydrogen Sulflde: Minimum Effective Dose (MED) and Reportable
Quantity (RQ) 62
LIST OF FIGURES
No. Title Page
4-1 Organization Chart for Listing GMAVs. GMCVs and BCFs
Required to Derive Numerical Water Quality Criteria by
the Method of U.S. EPA/OWRS (1986) to Protect Freshwater
Aquatic Life from Exposure to Hydrogen Sulflde 29
4-2 Organization Chart for Listing GMAVs, GMCVs and BCFs
Required to Derive Numerical Water Quality Criteria by
the Method of U.S. EPA/OWRS (1986) to Protect Saltwater
Aquatic Life from Exposure to Hydrogen Sulflde 31
5-1 Metabolism of Hydrogen Sulflde 36
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LIST OF ABBREVIATIONS
AEL Adverse effecte level
CAS Chemical Abstract Service
CS Composite score
PEL Frank effect level
KOW Octanol/water partition coefficient
LC5Q Concentration lethal to SOX of recipients
(and all other subscripted dose levels)
LOAEL Lowest-observed-adverse-effect level
LOEC Lowest-observed-effect concentration
NOEC No-observed-effect concentration
NOEL No-observed-effect level
ppm Parts per million
RfD Reference dose
RQ Reportable quantity
RV
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1. INTRODUCTION
1.1. STRUCTURE AND CAS NUMBER
Hydrogen sulflde Is also known as dlhydrogen sulflde, sulfur hydride,
sulfureted hydrogen and hydrosulfurlc acid (Chemline, 1989). It Is avail-
able as a liquified gas with purity >99.0%. Hydrogen sulflde Is sold In low
concentration mixtures with argon, hydrogen, helium, nitrogen or methane
(Chemlcyclopedla, 1988). Hydrogen sulflde occurs naturally; It Is produced
by the mlcroblal degradation of sulfates under anaerobic conditions and the
bacterial decomposition of proteins (Well. 1983). It 1s present In the
gases from many volcanoes, swamps, stagnant bodies of water, undersea vents,
coal pits, gas wells (sour gas) and sulfur springs (Hawley, 1981; Well,
1983). The structure, molecular formula, molecular weight and CAS registry
number for hydrogen sulflde are as follows:
H-S-H
Molecular formula: H_S
Molecular weight: 34.08
CAS Registry number: 7783-06-4
1.2. PHYSICAL AND CHEMICAL PROPERTIES
Hydrogen sulflde Is a colorless, flammable gas with an odor of rotten
eggs {Wlndholz, 1983). It Is soluble In water, forming a slightly acidic
solution (pH 4.1) (Weast. 1980). Hydrogen sulflde Is also soluble in many
polar organic solvents such as methano1, ethanol. acetone, ether, glycerol
and amines (Wlndholz, 1983; Well, 1983). It Is oxidized by agents Including
oxygen, ozone, hydrogen peroxide, sulfur dioxide and oxidizing acids (Well
1983). In water, hydrogen sulflde Is slowly oxidized by dissolved oxygen;
the solution becomes turbid with the formation of elemental sulfur
0238d -1- 11/06/89
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(Wlndholz. 1983). Many metalllclons react with hydrogen sulflde to form
Insoluble sulMde (Well, 1983). Selected physical properties of hydrogen
sulflde are listed below:
Boiling point:
Melting point:
Density (g/cm3):
Vapor pressure (atm):
Specific gravity (gas):
Vapor density (g/SL):
Explosive limits:
Autolgnltlon temperature:
Mater solubility (g/l):
pKlf pK2:
Log Kow:
Henry's Law constant:
(atm-m3/mol)
Conversion factor:
-60.33°C
-85.49°C
0.993 (-60°C)
20.5 (25°C)
10.2 (0°C)
0.72 (-20°C)
1.19 (air = 1.00)
1.5392 (0°C, 760
torr.)
4.3-46 (% by
volume when
mixed with air)
260°C
4.13 (20°C)
3.36 {25°C)
7.04, 11.96 (18°C)
not available
2.91 (25°C)
9.0X10'3 (20°C)
1 ppm = 1.518 mg/m3
1 mg/m3 = 0.659 ppm
Windholz, 1983
Wlndholz, 1983
Well. 1983
Daubert and Danner, 1985
Well, 1983
Well, 1983
Wlndholz, 1983
Wlndholz, 1983
Wlndholz, 1983
Wlndholz, 1983
Wlndholz, 1983
Barrett et al.. 1988
Weast, 1980
Yoo et al.. 1986
Balls and Llss, 1983
The Henry's Law constant, 2.91 atm-mVmol, was converted from 9.78
kg-atm/mol (Yoo et al., 1986) by dividing by the water solubility, 3.36
kg An3 (Barrett et al.. 1983).
1.3. PRODUCTION DATA
Hydrogen sulflde can be readily produced In the laboratory by the action
of dilute adds on Iron sulflde, calcium sulflde, zinc sulflde or sodium
0238d
-2-
11/06/89
-------
hydrosulMde (Weil. 1983). Laboratory quantities may be produced by heating
sulfur with a nonvolatile aliphatic hydrocarbon, such as paraffin. Hydrogen
sulflde has been produced commercially by the direct combination of hydrogen
and sulfur vapor In the presence of a catalyst. The reaction occurs at
~500°C (Well, 1983).
Host hydrogen sulflde used commercially 1n the United States Is either a
by-product of crude oil refining or obtained from sour natural gas. The
crude oil refined In the United States contains ~0.04-5 weight % of sulfur,
generally In the form of acyllc or cyclic organic sulfldes. These sulfldes
are removed In a hydrodesulfurlzatlon process In which the sulfur-rich
fraction of the crude oil and hydrogen gas are passed through a fixed-bed
catalyst. In this process, 80-90% of the sulfur compounds are converted to
hydrogen sulflde (Well. 1983).
The four companies listed by SRI (1989) as manufacturers of hydrogen
sulflde In the United States are found In Table 1-1. The number of
companies producing hydrogen sulflde as a byproduct Is much higher. The
Chemical Manufacturing Association lists 24 companies (138 locations) having
a production capacity of elemental sulfur derived from refineries or natural
gas >80,000 long tons (CHR, 1988). In 1987, production capacity for
elemental sulfur from these sources was 10 million long tons, and demand for
elemental sulfur was 11.4 million long tons. Since hydrogen sulflde Is the
raw material or an Intermediate In the production of elemental sulfur, the
amount of hydrogen sulflde produced may be -10 million long tons.
According to the 1977 1SCA Inventory, hydrogen sulflde was produced al
71 locations In the United Slates In quantities >10,000 pounds. The total
production volume reported In 1977 was ~8600 million pounds (4.3 million
tons) (TSCAPP, 1989).
0238d -3- 11/06/89
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TABLE 1-1
Manufacturers of Hydrogen Sulflde In the United States
as of January, 1988*
Manufacturer
Location
Mobil Corporation
Montana Sulfur & Chemical Co.
Pennwalt Corporation
PGG Industries, Inc.
Beaumont, TX
East Billings. MT
Houston. TX
Natrium. WV
'Source: SRI, 1989
0238d
-4-
09/11/89
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1.4. USE DATA
Most of the hydrogen sulflde recovered from crude oil or natural gas 1s
converted to elemental sulfur and sulfurlc acid (Well, 1983). Hydrogen
sulflde Is used as a reagent \n the manufacture of Inorganic sulflde (e.g.,
sodium sulflde and sodium hydrosulfIde), which Is used In the manufacture of
dyes, plastics, leather products, rubber chemicals, Pharmaceuticals and
organosulfur products (e.g., mercaptans) (Well, 1989; Chemlcyclopedla,
1988). Hydrogen sulflde Is also used for separating metals and In metal-
lurgical waste treatment and recovery. It has applications In analytical
chemistry and In the calibration of analytical Instruments (Wlndholz, 1983;
Chemlcyclopedia, 1988).
1.5. SUMMARY
Hydrogen sulflde Is a colorless, flammable gas with an odor of rotten
eggs {Wlndholz, 1983). It Is soluble In water, forming a slightly acidic
solution (pH 4.1) (Weast, 1980). It Is oxidized by many oxidizing agents;
In water, hydrogen sulflde 1s slowly converted Into elemental sulfur by the
action of dissolved oxygen (Wlndholz, 1983). A common reaction of hydrogen
sulflde Is with metal Ions In which Insoluble sulMdes are formed (Well,
1983).
Hydrogen sulflde occurs naturally; It Is produced by the mlcroblal
degradation of sulfates under anaerobic conditions and the bacterial
decomposition of proteins (Well, 1983). It Is present In the gases from
many volcanoes, swamps, stagnant bodies of water, undersea vents, coal pits,
gas wells (sour gas) and sulfur springs (Hawley. 1981; Well, 1983).
Hydrogen sulflde may be produced by the action of dilute acids of Iron
sulflde or other sulfldes, by the direct combination of sulfur and hydrogen
or by heating sulfur with paraffin (Well, 1983). Most hydrogen sulflde used
0238d -5- 11/06/89
-------
commercially In the United States Is either a by-product of crude oil
refining or obtained From sour natural gas (Well, 1983). SulFldes naturally
occur In crude oil and are removed by a process In which the sulFur-rlch
Fraction of the crude oil and hydrogen gas are passed through a Fixed-bed
catalyst. In this process. 80-90% oF the sulFur compounds are converted to
hydrogen sulFlde (Well. 1983).
No recent U.S. production data For hydrogen sulFlde were located. Most
oF the hydrogen sulFlde recovered From crude oil or natural gas Is converted
to elemental sulFur and sulFurlc add (Well, 1983). While elemental sulFur
was listed as being produced by refineries or From natural gas by numerous
companies, only Four were listed as producers oF hydrogen sulFlde (SRI,
1989; CMR, 1988). In addition to being an Intermediate In the production oF
elemental sulFur and sulFurlc acid, hydrogen sulFlde Is used as a reagent In
the manufacture oF Inorganic sulFlde (e.g., sodium sulFlde and sodium
hydrosulf1de), which Is used In the manuFacture oF dyes, plastics, leather
products, rubber chemicals, Pharmaceuticals and organosulFur products (e.g.,
mercaptans) (Well, 1989; Chemlcyclopedla, 1988). Hydrogen sulFlde Is also
used For separating metals. In metallurgical waste treatment and recovery.
In analytical chemistry and In the calibration oF analytical Instruments
(Wlndholz. 1983; Chemlcyclopedla, 1988).
0238d _6- 11/06/89
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2. ENVIRONMENTAL FATE AND TRANSPORT
2.1. AIR
Since hydrogen sulflde does not absorb UV radiation at wavelengths
reaching the earth's surface. It will not photolyze directly. It reacts
with photochemlcally produced hydroxyl radicals; the rate constant for this
reaction Is 4.8xlO~12 cmVmolecule-sec. The mean half-life of hydrogen
sulflde In the troposphere will be 38 hours, assuming the concentrations of
hydroxyl radicals as IxlOVcm3. Peak hydroxyl radical concentrations In
the summer reach IxlOVcm3 and during this period, the half-life of
hydrogen sulflde will be 3.8 hours (Cox, 1975). The reaction eventually
leads to the formation of sulfur dioxide and sulfate (Sze and Ko, 1980).
The Initial product of the reaction Is the HS», which may then react with
N02, 03 or H02 to form HSO (Cox, 1975; Sze and Ko, 1980). The HS-
may react with compounds containing reactive hydrogens to reform H_S, but
experimental evidence Is lacking (Sze and Ko, 1980). Reaction of hydrogen
sulflde wUh atmospheric ozone Is too slow to be a significant sink for
hydrogen sulflde (Cox, 1975). Hydrogen sulflde Is relatively soluble In
water and should be removed from the atmosphere by rain.
2.2. HATER
Hydrogen sulflde may occur In sewage as a result of Industrial
discharges. It may be formed by the mlcroblal reduction of sulfate under
anaerobic conditions. Hydrogen sulflde Is a weak acid and Is partially
dissociated In water. Its pK] Is 7.04; therefore, at pH 7, half of the
chemical Is dissociated. At pH 6 and 8, 10 and 90% of the chemical Is
dissociated. Hydrogen sulflde reacts with oxldants such as dissolved oxygen
and hydrogen peroxide In water to produce elemental sulfur, thlosulfate and
sulfate (Balls and Llss, 1983). Because hydrogen sulflde Is a gas with a
0238d -7- 11/06/89
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high Henry's Law constant, H will have a strong tendency to volatilize from
water. Since volatilization Involves the undlssoclated molecule, water-gas
transfer will be pH dependent. The oxldatlve half-life of H2$ In air-
saturated water and seawater was studied as a function of temperature, pH
and Ionic strength. "the resulting half-lives In water and seawater at pH 8
and 25°C were 50 and 26 hours, respectively (Mlllero et al., 1987). The
rate of oxidation of hydrogen sulflde at 20°C In a circulating tank In which
salinity simulated that of seawater was studied. The rate of oxidation was
reported as first order and only mildly dependent on pH (Balls and Llss,
1983). At the high sulflde to oxygen ratio employed, 5:1, the oxldatlve
half-life of hydrogen sulflde varied from 43 hours at pH 6 to 63 hours at pH
8. The overall water-to-aIr transfer rate varied from 4.24-36.9 cm/hour
from pH 6-8. The respective half-lives would be 16.3 and 1.9 hours for a
body of water 1 m deep. For natural waters of pH <6, hydrogen sulflde Is
characteristic of an unreactlve gas with Us volatilization rate limited by
Its diffusion through water. As the pH of the water Increases, diffusion
through the gas phase becomes more significant. The presence of Ionic
species In the boundary layer between the water and air significantly
enhances volatilization. Based on a model for estimating mass transfer
(Thomas, 1982), using a Henry's Law constant of 2.91 or 0.979xlO~2
atm-rWmol, the volatilization half-life for hydrogen sulflde In a model
river 1 m deep, flowing at 1 m/sec, with a wind velocity of 3 m/sec can be
calculated as 1.7 and 1.8 hours, respectively.
2.3. SOIL
Soil appears to be an Important natural sink for hydrogen sulflde. The
adsorption of hydrogen sulflde by soils was studied using six soils with
widely varying properties. Ninety-five percent of the gas was adsorbed onto
0238d -8- 11/06/89
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son In 2-49 minutes with a mean value of 14 minutes. Experiments with
air-dry soils Indicate that 15.4-65.2 mg (mean 50.7 mg) of hydrogen sulflde
gas may be adsorbed by each gram of soil (Smith et a!., 1973). Moisture had
little effect on the sorptlon capacity of the soil. The corresponding
capacity for soil at 50% of Its water holding capacity Is 11.0-62.5 mg/g
soil (mean, 44.7 mg/g). The ability of soil to adsorb hydrogen sulflde and
the rate of adsorption Is not significantly correlated with soil properties
like pH, clay content, organic-matter content or the presence of soil micro-
organisms. Pertinent data regarding abiotic and blotlc reactions of
hydrogen sulflde In soil were not located In the available literature cited
In Appendix A. It Is probable that hydrogen sulflde will be oxidized In
soil by oxygen and other oxidizing agents.
2.4. SUMMARY
Hydrogen sulflde may occur In sewage as a result of Industrial
discharges or may be formed by the mlcroblal reduction of sulfate under
anaerobic conditions. It Is a weak acid with a pK.. of 7.04. Between pH 6
and 8, the lonlzatlon of hydrogen sulflde ranges from 10-90%. Hydrogen
sulflde reacts with oxldants such as dissolved oxygen and hydrogen peroxide
In water to produce elemental sulfur, thlosulfate and sulfate (Balls and
Llss, 1983). Because It Is a gas with a high Henry's Law constant, hydrogen
sulflde will have a strong tendency to volatilize from water. Both oxida-
tion and volatilization are pH dependent. At pH 8 and 25°C, the oxldatlve
half-lives In air-saturated water and seawater are 50 and 25 hours, respec-
tively (Mlllero et al., 1987). At 20°C and at relatively low oxygen concen-
trations, oxidation was mildly pH dependent; the half-life ranged from 43
hours at pH 6 to 63 hours at pH 8 (Balls and Llss, 1983). Volatilization Is
0238d -9- 11/06/89
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the more significant transport process. The volatilization half-life of
hydrogen sulflde In a body of water 1 m deep was 16.3 hours at pH 6 and 1.9
hours at pH 8 (Balls and Llss, 1983).
Hydrogen sulflde reacts with photochemlcally produced hydroxyl radicals
In the troposphere; the rate constant for this reaction Is 4.8xlO~12
cm3/molecule-sec (Cox, 1975). Assuming an average hydroxyl radical
concentration of 1x10* per cm3, the half-life of hydrogen sulflde In the
troposphere will be 38 hours. During summer daylight hours, the half-life
will be 3.8 hours. The reaction products are sulfur dioxide and sulfate
(Sze and Ko, 1980). Reaction of hydrogen sulflde with atmospheric ozone Is
too slow to be a significant sink for hydrogen sulflde. Hydrogen sulflde Is
relatively soluble In water and should be removed from the atmosphere by
rain.
Soil appears to be an Important natural sink for hydrogen sulflde.
Adsorption Is rapid, and the ability of soil to adsorb hydrogen sulflde and
the rate of adsorption are not significantly correlated with soil properties
like pH, clay content, organic-matter content or the presence of soil micro-
organisms. Soil moisture had little effect on sorptlon capacity; 15.4-65.2
mg of hydrogen sulflde sorbed to a gram of air-dried soil, while 11.0-62.5
mg of hydrogen sulflde sorbed to a gram of moist soil (Smith et al., 1973).
The mean adsorptlvltles of the dry and moist soils were 50.7 and 44.7 mg/g,
respectively. Pertinent data regarding abiotic and blotlc reactions of
hydrogen sulflde In soil were not located In the available literature cited
In Appendix A. It Is probable that hydrogen sulflde will be oxidized In
soil by oxygen and other oxidizing agents.
0238d -10- 11/06/89
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3. EXPOSURE
3.1. WATER
Pertinent data regarding hydrogen sulflde In drinking water were not
located In the available literature cited In Appendix A. Hydrogen sulflde
Is produced under anoxlc conditions by sulfate-reduclng bacteria and Is
mainly emitted from soil near coastal areas such as salt marshes (Aneja et
al., 1982). Therefore, It Is likely that hydrogen sulflde Is found In these
waters, although pertinent data regarding levels of hydrogen sulflde In
surface water were not located In the literature. The highest level of
hydrogen sulflde In natural water was found In Framvaren, an extremely
anoxlc fjord In southern Norway. Because of unusual geomorphologlcal
features, the hydrogen sulflde concentration In the fjord ranges from
100-170 mi/i below 100 m depth (Skel, 1983). The fjord Is meromlctlc,
therefore the lower anoxlc layers of water do not mix with the surface water.
3.2. FOOD
Hydrogen sulflde Is a naturally occurring chemical produced by the
mlcroblal metabolism of protein and also In the Intestines as a result of
bacterial action (NIOSH, 1977). Data are lacking regarding the presence of
hydrogen sulflde In food. Trace amounts of hydrogen sulflde have been
Identified In breast meat of freshly killed chickens; however, none was
detected In meat that had been kept 4 days at 10-20°C (Grey and Shrlmpton,
1967). It has also been reported as a volatile component of roasted peanuts
(Young, 1985), Cheddar cheese (Rlchter and Vanderzant, 1987) and aged
Beaufort cheese manufactured In the French Alps (Dumont and Adda, 1978).
Although It Is probable that humans are exposed to some hydrogen sulflde In
food, It Is not possible to estimate the extent of exposure.
0238d -11- 11/06/89
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3.3. INHALATION
Blogenlc sulfur compounds are emitted from soils. Coastal wetlands
particularly have a potential for extremely high emissions of reduced sulfur
compounds Into the environment. Emissions of hydrogen sulflde from five
wetland soils characterized by different vegetation In Florida ranged from
0.1-152 yg S/m2-hour (Cooper et al., 1987). Only one site with moist,
peaty soil and a water table just below the soil surface had a hydrogen
sulflde emission rate >8.4 yg/m2-hour. In a study by Aneja et al.
(1982) average hydrogen sulflde emission rates ranged from 0.001-77 g
S/mVyear, with maximum rates of 1.4-2000 g S/mVyear. Hydrogen sulflde
Is produced by sulfate-reduclng bacteria under anaerobic conditions.
Emission shows a diurnal variation, which peaks around noon when soil
temperature and solar Irradiation are at a maximum (Cooper et al., 1987).
The concentration of hydrogen sulflde In the nonurban atmosphere 1s
estimated as 4 ppb (6 yg/m3) using a mass balance approach (Graedel and
Allara, 1977). Although natural emissions of hydrogen sulflde exhibit
diurnal variations, no significant fluctuations 1n hydrogen sulflde concen-
tration are predicted. Field data are sparse and measurements conducted
before 1972 are considered unreliable (Aneja et al., 1982). Ambient air
concentrations, removed from significant sources, have been found to be much
lower than the estimated 6 yg/m3. Investigators reported 0.035-1.65
yg/m3 of hydrogen sulflde over West Germany. Similar concentrations,
0.17-1.15, 0.12-0.3 and 0.1 yg/m3, were found In polluted air near
Miami. FL; Illinois; Missouri; and over the North Sea (Aneja et al.. 1982;
Sze and Ko, 1980). Lower concentrations were observed In urban Miami. FL
(0.008-0.08 yg/m3}. France (0.017-0.17 yg/m3) and Boulder. CO (0.04
yg/m3). Concentrations of hydrogen sulflde as high as 80 yg/m3 were
0238d -12- 11/06/89
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found In the air above a tidal marsh In North Carolina. Long-term
concentrations >1000 pg/m3 were reported 0.4-11.3 km from an Industrial
source. Similar high concentrations of hydrogen sulflde were measured In
the early 1960s over a highly polluted, shallow backwater. The ambient
concentration of hydrogen sulflde near a geothermal vent In New Zealand
ranged from 0.005-1.9 ppm (0.008-2.9 mg/m3) (U.S. EPA, 1986a).
NIOSH (1977) lists 73 occupations that potentially expose workers to
hydrogen sulflde. These Include workers In coke oven plants, employees In
petroleum production and refining Industries, dye makers, tanners, textile
workers, sewage plant operators, rayon makers, paper makers, fermentation
plant operators and livestock farmers. Hydrogen sulflde has been detected
In pulp and paper factories, oil Industries, wastewater treatment plants and
agricultural areas (Kangas and Ryosa, 1988). Hydrogen sulflde also enters
the air from dlesel engines and motor vehicles, especially those In which
carburetors or catalytic converters are not functioning properly (Hayano et
a!., 1985; U.S. EPA, 19863).
According to statistical estimates, 94,922 workers, Including 6519
women, are potentially exposed to hydrogen sulflde In the workplace (NIOSH,
1989). Measurements of hydrogen sulflde In selected workplaces resulted In
0.016 and 0.002 ppm hydrogen sulflde In the pretreatment and sludge treat-
ment areas of a sewage treatment plant. 0.054 ppm at the chip chute of a
sulfate pulp mill and 0.216, 0.515 and 0.933 ppm at three sites of a sewage
plant of a sulflte pulp mill (Kangas and Ryosa, 1988). In a viscose rayon
plant, workers were exposed to hydrogen sulflde concentrations of <20
mg/m3 (15 ppm) (NIOSH, 1977). Occasionally, levels In the plant reached
-140 mg/m3 (100 ppm). There are several reports of worker exposure to
high levels of hydrogen sulflde as a result of accidents or leaks resulting
In serious Injury or death. In some cases, hydrogen sulflde was not
0238d -13- 11/06/89
-------
monitored until after some of the gas may have dissipated. The maximum
level of hydrogen sulflde reported In these accidents was 17,000 mg/m3
(12,000 ppm).
3.4. DERMAL
Pertinent data regarding dermal contact with hydrogen sulflde were not
located In the available literature cited In Appendix A.
3.5. SUMMARY
Pertinent data regarding hydrogen sulflde In drinking water were not
located In the available literature cited In Appendix A. Hydrogen sulflde
Is produced under anoxlc conditions by sulfate-reduclng bacteria and Is
mainly emitted from soil near coastal areas such as salt marshes (Aneja et
al.. 1982). It Is likely that hydrogen sulflde Is found In these waters,
although no levels of hydrogen sulflde In surface water were reported In the
available literature.
Trace amounts of hydrogen sulflde have been Identified In the breast
meat of freshly killed chickens, roasted peanuts and cheese (Grey and
Shrlmpton, 1967; Young, 1985; Rlchter and Vanderzant, 1987; Oumont and Adda,
1978). It 1s probable that humans are exposed to some hydrogen sulflde In
food, although no estimation of quantity of hydrogen sulflde Ingested Is
possible.
Hydrogen sulflde Is a gas produced naturally and emitted by Industrial
sources and numerous other nonpolnt anthropogenic sources. Blogenlc sulfur
compounds are emitted from soils with coastal wetlands having the greatest
potential for emitting significant quantities of hydrogen sulflde Into the
atmosphere. Emissions exhibit a diurnal variation, which peak around noon
when soil temperature and solar Irradiation are at a maximum (Cooper et al.,
1987). Industrial sources and other anthropogenic sources are believed to
contribute -10% of the hydrogen sulflde entering the atmosphere (U.S. EPA,
0238d -14- 11/06/89
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1986a). Nonpolnt anthropogenic sources are ubiquitous. Including dlesel
engines and motor vehicles, especially those In which carburetors or
catalytic converters are not functioning properly (Hayano et al., 1985; U.S.
EPA, 1986a). Concentrations of hydrogen sulflde In West Germany, Miami, FL
(polluted air), Illinois. Missouri and the North Sea range from 0.035-1.65
ug/m3 of hydrogen sulflde (Aneja et al., 1982; Sze and Ko, 1980}. Lower
concentrations (0.008-0.17 vQ/m3) were observed 1n urban Miami, FL,
France and Boulder, CO. Much higher levels (80 »»g/ni3) were found In the
air above a tidal marsh 1n North Carolina, near an Industrial source (1QOO
vg/m3) and near a geothermal vent In New Zealand (0.008-2.9 mg/m3)
(Aneja et al., 1982; U.S. EPA, 1986a).
NIOSH (1977) lists 73 occupations that potentially expose workers to
hydrogen sulflde. These Include workers In coke oven plants, employees in
petroleum production and refining Industries, dye makers, tanners, textile
workers, sewage plant operators, rayon makers, paper makers, fermentation
plant operators and livestock farmers. Hydrogen sulflde has been detected
In pulp and paper factories, oil Industries, wastewater treatment plants,
synthetic fibers and agricultural areas (Kangas and Ryosa, 1968; NIOSH,
1987). According to statistical estimates, 94,922 workers, Including 6519
women, are potentially exposed to hydrogen sulflde In the workplace (NIOSH,
1989). Concentrations of hydrogen sulflde In selected workplaces include
0.002-0.016 ppm In a sewage treatment plant, 0.054 ppm In a sulfate pulp
mill, 0.216-0.933 ppm In the sewage plant of a sulfUe pulp mill and <15 ppm
in a viscose rayon plant; occasionally, levels reached 100 ppm (Kangas and
Ryosa, 1988; NIOSH, 1977). There are several reports of worker exposure to
high levels of hydrogen sulflde as a result of accidents or leaks resulting
0238d -15- 11/06/89
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In serious Injury or death. In these cases, hydrogen sulflde may have been
monitored after some of the gas had dissipated. The maximum level of
hydrogen sulflde reported In these accidents was 17,000 mg/m3 (12,000 ppm).
0238d -16- 11/06/89
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-vll
. trfects on Fauna. Acute toxlclty test
.* have been conducted with at least 12 freshwater \
representatives from 14 genera of freshwater fUh and six mar
brate species (Table 4-1). In studies where more than one llf-
assayed, results for the most sensitive stage are presented. The
consistently show the egg stage to be less sensitive than fry and
cases, swim-up fry tended to be more sensitive than sac fry, lepomj
chlrus. (Smith et al., 19?6a) and Salvellnus fontanalls (Smith and
1975}. The data Indicate that the most sensitive life stage differs f
species.
The 96-hour LC5Q ranged from 0.02-550 rag/8, among freshwater inve
brates and from 0.003-3 mg/i for freshwater fish. The toxlclty range
marine Invertebrates was 0.2-6.0 mg/i. Of the 33 tested species, all b
9 had 96-hour LC5Q values of <1 mg/i. The mosquito fish, Gambusl
afflnls. was the only vertebrate with an LC5Q >1 mg/l. These data
Indicate that Invertebrates are less acutely sensitive than fJsh to hydrogen
sulflde toxlclty and little difference exists between fresh and saltwater
forms. Chlronoffius sp., which showed extreme resistance to hydrogei\ sulflde
1n two separate assays (Van Horn et al., 1949; Prasad, 1980a), may exemplify
an adaptive advantage. Benthlc forms may be exposed to high levels of
hydrogen sulflde under natural conditions since high concentrations often
occur where organic material Is undergoing decomposition (Smith and Qseld,
1970).
Threshold LC5Q values have been reported for several freshwater fish
species. These range from 0.006 mg/SL over a 6-day period for Plmephales
0238d -17- 11/06/89
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TABLF 4-1
Acute Lethality of Hydrogen Sulflde to Aquatic Fauna
u
CO
Q.
LCjo Concentration (mg/t) Hardness Water
^
CD
1
~^
"s.
O
CO
US
Species No./
Group
FRESHWATER INVERTEBRATES
Procanfbarus 25
clarklt
Crayfish
Canbarus dlogenes 10
Crayfish
Asellus mllltarus NR
Isopod
Crangon»« NR
Mchmondensls
Amphlpod
Baetls vagani NR
Mayfly
Ephemera slmulans NR
Mayfly
Henagenla llmbata NR
Mayfly
Gamiarus NR
pseudollmnaeus
Scud"
G. pseudollmnaeus NR
Scud "
Test NOECa LOEC» pH (as
Type 24-Hour 48-Hour 72-Hour 96-Hour (mg/t) (mg/t) CaC03)
flow- NR NR NR 0.0851 NR NR 7.65» 220
through 0.04
measured
flow- NR NR NR 0.1403 NR NR 7.69* 220
through 0.01
measured
flow- NR NR NR 1.07 NR NR 7.5 220
through
measured
flow- NR NR NR 0.64 NR NR 7.4 220
through
measured
flow- NR NR NR 0.020 NR NR 7.6 220
through
measured
flow- NR NR NR 0.316 NR NR 7.4 220
through
measured
flow- NR NR NR 0.111 NR NR 7.7 220
through
measured
flow- NR NR NR 0.022 NR NR 7.7- 220
through 1-9
flow- NR NR NR 0.030 NR NR NR 2?0
through
measured
02 Temperature Comment
CC)
NR 20 »2 Geometric mean
LC«|o for two
tests; first two
Instars
NR 13.9-22.0 Subadults; mean
carapace length:
25.4 am
NR 15.1 5-13 mm
NR 15*0.1 6-15 mm
NR 14.8 4-6 mn mean of
two tests calcu-
lated by authors
NR 15.0 Nymphs; 13-21 mm
NR 15.0 Nymphs; 14-35 nm;
mean of seven
tests calculated
by authors
NR 18*0.02 15-17 days old
NR 12.4 Length: 0-16 mm
Reference
Smith et al..
1976a
Smith et al..
1976a
Smith et al.,
1976a; Oseld
and Smith.
1974b
Smith et al
!9/6a; Oselo
and Smith.
1974b
Smith et al.
1976a; Oselo
and Smith.
1974b
Smith et al .
1976a; Oseld
and Smith.
19746
Smith et al .
I976a; Osetd
and Smith.
19746
Oseld and
Smith. 1974a
Smith et al..
19/fca
-------
r\j
00
Q.
1
to
o
CD
IO
Species No./
Group
Chlronomus sp. 2
Nidge
C. sp. NR
Nidge
Cic Top sp. NR
Copepod plank-
tonlc
Bosmlna sp. NR
Cladoceran
planktonlc
Daphnla sp. NR
Mater flea
FRESHWATER VERTEBRATES
Notropli sp. 1-5
Shiners
Sambusla afflnls 10
Mosquito fish
Ictalurus 10
punctatus
Channel catfish
Lepoals 25
macrochlrus
Bluegll) sunflsh
I. macrochlrus 10
Bluegtll sunflsh
LCjg Concentration (mg/t)
Test NOfC*
Type 24-Hour 48-Hour 72-Hour 96-Hour (mg/l)
Static NR NR NR NR NR
Static NR NR NR 550 NR
static NR NR NR 2 NR
Static NR NR NR 2 NR
static NR NR NR 3 NR
Static NR NR NR NR NR
static IB 10 6 3 NR
static NR NR NR NR 0.5
measured
72-hour
lethality
flow- NR NR NR 0.0159 NR
through
measured
static NR NR NR NR 0.8
measured
72 -hour
lethality
lOtCb pH
Jng/O
750 7.6-
7.8
NR 7.0-
7.5
NR 7.0-
7.5
NR 7.0-
7.5
NR 7.0-
7.5
1.0 7.6-
7.B
NR B.3
0.6 7.0
NR 7.8-
8.0
0.9 7.0
Hardness
(as 02
CaCOj)
hard HR
(not
quanti-
fied)
80-B5 7.6
80-85 T.B
80-85 7.8
80-85 7.8
hard NR
(not
quanti-
fied)
84 7.9
NR NR
220 6.2-
6.5
NR NR
Hater
Temperature Comment Reference
CC)
18 Larvae; stage NR Van Horn
et al.. 1949
1300 Larvae; stage NR Prasad. 1980a
30O Age NR Prasad. 19BOa
30*1 Age NR Prasad. T9BOa
30 »l Age NR Prasad. 1980a
IB Adults Van Horn
et al.. 1949
30 Age NR Prasad. 19806
25-30 30 nra fry Bonn and
Follls. 1967
20»1 Geometric mean Smith et al..
LCjo of two W6c
tests with fry
mean length: 0.3-
0.8 en
27*2 30 mm fry Bonn and
folMs. I9H
-------
TABLE 4-1 (cont.)
0
INJ
LJ
00
Q.
Species
L. macrochlrus
Blueglll sunflsh
Esox luclus
Northern pike
E. luclus
Northern pike
E_. luclus
Northern pike
i
£> Plmephales
i promelas
Fathead minnows
Plmephales
promelas
Fathead minnows
Carasslus auratus
Goldfish
C. auratus
Goldfish
Stliostedlon
vltreum
Hall eye
^ S. vltreum
° Walleye
\
00
S vtlreum
Walleye
No./
Group
NR
33-50
NR
100-
1000
10-20
20
NR
8
5
100-
1000
NR
LCjQ Concentration (mg/l)
Test NOECa LOECD
Type 24 -Hour 48-Hour 72-Hour 96 -Hour (mg/l) (mg/t)
flow- NR NR NR 0.0090 NR NR
through
measured
flow- 0.160 0.047 0.030 0.026 0.006 NR
through
flow- 0.159 NR 0.0190 0.0153 NR NR
through
flow- NR 0.059 0.0395 0.0354 NR NR
through
measured
flow- NR NR NR 0.057 NR NR
through (0.05-
0.06)
flow- 0.0208 NR NR 0.0070 0.0061 NR
through
measured
flow- NR NR NR 0.025 0.0306 NR
through •
measured
flow- NR NR NR 0.065 NR NR
through
flow- 0.0413 0.0535 0.0198 0.0192 0.010 NR
through
measured
flow- NR 0.0740 0.0616 0.0676 NR NR
through
measured
flow- NR NR 0.017 0.007 NR NR
through
pH
7.6-
8.0
7.68-
7.75
7.6-
8.0
7.6-
8.0
7.1
7.9
7.62
7.65
7.9*
o.r
7.6-
8.0
7.6-
8.0
Hardness Water
(as 02 Temperature
CaC03) CO
210
290-
300
hard
210
220
220
220
220
220
210
Hard
NR 22
1.9- 13.1*0.1
6.0
2.0- 17»1
6.0
3.0- 13
6.0
7.4- 20
7.6
5.4- 24
6.2
8.72 22O
7.5- 20
8.0
5.9- 15*1
6.8
3.0- 13»2
6.0
3.0- 17.1
6.0
Comment
Swim-up fry.
length NR
Geometric mean
LC50 of six
tests with sac
fry
Fry length NR
geometric mean
LCjo of two
tests with eggs
13 weeks old
Geometric mean
USD of three
tests with fry
length: 5. 6-5. 9mm
fry
Adults age 4
monlhs-2.5 years
Geometric mean
LCjQ of up to 4
tests with Juve-
niles 89-100 mm
Geometric mean
LCjo of up to 5
tests with eggs
Fry. size NR
Reference
Smith. 1979;
Smith and
Oseld. 1975
Adelman and
Smith. 1970
Smith and
Osetd, 1970
Smith and
Osetd. 1972
Broderlus
et al.. 1977
Smith et at..
1976a,b;
Smith. 1970;
Smith and
Oseld. 1975
Smith et al..
1976a
Adelman and
Smith. 1972
Smith et al.,
1976a
Smith and
Oseld. 1972
Smith and
Oseld. 1970
-------
MBit 4-1 (conl.)
to
to
CD
O.
1
ro
i
V.
o
CD
OS
Species
Salvellnus
fontlnalls
Brook trout
S. fontlnalls
Brook trout
Salmo galrdnerl
Rainbow trout
S. galrdnerl
Rainbow trout
Salmo trutta
Brown trout
Salmo qalrdnerl
Rainbow trout
S. galrdnerl
Rainbow trout
Catostomus
conmrsonl
While sucker
C. coomersonl
While sucker
C. Conner sonl
White sucker
Choregonus
c lupcaf ormls
WhHeMsh"
No./
Group
NR
NR
NR
100-
1000
NR
10
10
10
100-
1000
NR
30-40
LC5Q Concentration (mg/l)
Test NOF.C*
Type 24-Hour 48-Hour 72-Hour 96 -Hour (mg/i)
flow- NR NR NR 0.0224 NR
through
measured
flow- NR NR NR 0.0216 NR
through
flow- NR NR 0.020 NR NR
through
flow- NR NR 0.0663 0.049 NR
through
measured
flow- NR NR NR 0.007 NR
through
measured
flow- NR NR NR 0.013 NR
through
measured
flow- 0.026 0.0222 0.013 0.013 NR
through
flow- 0.029 0.0206 0.0212 0.0215 NR
through
measured
flow- NR NR MR 0.0215 NR
through
measured
flow- 0.034 NR 0.020 0.0198 NR
through
flow- 0.0073 0.0047 0.0039 0.0033 NR
through
Hardness
LOF,Cb pH (as 02
(mg/t) CaC03)
NR 7.68< 220
0.01~
NR 7.6- 210
8.0
NR 7.6- hard
8.0
NR 7.6- 210
8.0
NR 7.1* 127.2
o.r
NR 7.7 220
NR 7.5- 104
8.0
NR 7.9 220
NR 7.6- 210
8.0
NR 7.6- hard
8.0
NR 8 104
NR
NR
6.0
6.0
9.7
6.4-
8.4
10.7
5.9-
6.2
3.0-
6.0
3.0-
6.0
10.0
Water
Temperature
13.5
12.5
16-18
10-15
130
13.80.5
8.50.5
200
13-15
16-18
10
Comment
Geometric mean
LCjQ of four
tests with 48-
hour -old sac fry
Swim-up fry
Fry, length NR
Geometric mean
LCjg 'rom "P to
2 tests with eggs
Sac fry
Geometric mean
LCjQ. two tests
with juveniles.
length: 45-54 im
Geometric mean
LCjQi two tests
with juveniles.
6-8 im
Geometric mean
LCjQ for up to
4 tests; Juve-
niles; length:
33-124 im
Eggs tested
Fry. length not
reported
Geometric mean
Uc0f 4 tests
with sac fry
Reference
Smith ct al..
I976a
Smith and
Oseld. 1975
Smith and
Oseld. 1970
Smith and
Oseld. 1972
Reynolds and
Halnes. 1980
Smith et al..
1976a
Fung and
Bewick, 19flO
Smith et al..
1976a
Smith and
Oseld. 1972
Smith and
Oseld. 1970
Fung and
Bewick. 1980
-------
TABLE 4-1 (cont.)
OJ
00
I
i ro
Species No./
Group
Perca f lavescens 30-40
Yellow perch
Nlcropterns 30-40
sa lino Ides
largemouth bass
SALTWATER INVERTEBRATES
Cancer maglster 10
Oungeness crab
Gnorlmosphaeroma 10
oregonensls
Isopod
Antsoqanmarui 10
confervlcola
Amphlpod
Corophlum 10
salmonls
Amphlpod
Nacoma ballhlca 10
Clam
Crassostrea glgas 10
LCso Concentration (mg/l)
Test NOEC'
Type 24-Hour 48-Hour 72-Hour 96-Hour (mg/l
flow- 0.0190 0.0079 0.0055 0.0045 NR
through
flow- 0.01BB 0.0182 0.1817 0.1817 NR
through
flow- 0.7 0.6 NR 0.5 NR
through
measured
flow- 6.8 6.0 NR 5.2 NR
through
measured
flow- 3.2 0.8 NR 0.2 NR
through
measured
flow- 1.4 <1.0 NR <1.0 NR
through
measured
flow- >10.0 8.0 NR 6.0 NR
through
measured
flow- 3.3 2.6 NR 1.4 NR
through
measured
Hardness Hater
LOEC" pH (as Oj Temperature Comment
} (mg/l) CaC03) CC)
NR 7.5- 104
8.0
NR 7.5- 104
8.0
NR 8.1* NR
0.2
NR 1.8- NR
8.6
NR 7.8- NR
8.7
NR NR
NR 7.8- NR
8.6
NR 7.8- NR
8.7
8.4 10-20 Sac fry
8.1 15-20 Sac fry
7.1* 14*0.5 Zoeae stage
0.6"
4.3* 17.3 NC
4
5.1* 17.5*0.5 NC
3
5.4* 17.5*0.5 NC
3
5.7* 17.3*0.5 NC
3
5.4* 17.4*1 NC
3
Reference
fung and
Bewick. 1980
Fung and
Bewick. I9BO
Caldwell. 1975
Caldwell. 1975
Caldwell. 1975
Caldwell, 1975
Caldwell, 1975
Caldwell. 1975
'NOEC - No effect noted at this concentration or below
DLOEC . Lowest concentration at which an effect was noted
—• NR • Not reported; NC - no comment
\
o
GO
10
-------
promelas to 0.060 for 11 days 1n Carasslus auratus (Smith, 1970; Smith and
Oseld, 1975). These fall within the same range as 96-hour LC™ values
and, therefore, would be protected by criteria based on 96-hour LC,.
levels. Values did not decrease significantly after 48-hour exposures. An
acclimation test In which flngerllngs were exposed to serial concentrations
of hydrogen sulflde varying from 0.0144-0.0308 mg/4 Indicated that fish
became acclimated to Us presence, provided that the Initial concentrations
were not acutely toxic within 48 hours (Smith et al., 1976a).
The Influence of temperature and oxygen on hydrogen sulflde toxldty
with goldfish, C. auratus. was tested. Results show a negatively
logarithmic relation between toxldty and temperature over the range of
6.5-25°C. The mean 96-hour LC5Q at 6°C was 530 yg/l, and at 25°C, 4
M9/1. The highly significant linear regression Is described by the
equation, log Y' = -1.8527 log X * 4.2325, where y" = 96-hour IC™ and x =
temperature (Adelman and Smith, 1972).
Decreasing oxygen concentrations Increased toxldty In bloassays
conducted with and without prior oxygen acclimation. Without acclimation,
mean LCrgS were 71 and 53 yg/1 at oxygen concentrations of 6 and 1.5
respectively. The following equation describes this significant
linear regression: Y1 = 4.08x * 46.52, where Y1 Is the 96-hour LC5Q and x
Is the oxygen concentration. With acclimation, mean LC5Qs were 62 and 48
for the same oxygen conditions. This equally significant linear regression
Is described as Y1 = 2.83x * 44.28, where Y' and x are used as above. A
similar oxygen/hydrogen sulflde toxldty relationship was reported for Esox
ludus {Adelman and Smith, 1970).
Summer felt and Lewis (1967) performed an avoidance test of hydrogen
sulflde with 30 green sunflsh, Lepomls cyanellus. and determined that
concentrations <40 mg/i for <15 minutes did not repel fish.
0238d -23- 11/06/89
-------
4.1.2. Chronic Effects on Fauna.
4.1.2.1. TOXICITY — The chronic toxlclty of hydrogen sulflde has
been examined with three or more freshwater Invertebrates and eight fresh-
water fish {Table 4-2). Exposure for <196 days resulted In LOECs ranging
from 0.0071-0.429 mg/i for Invertebrates. Chronic exposure for <826 days
produced effects at concentrations ranging from 0.0010-0.03 mg/l for
freshwater fish. The lowest LOEC was from a test started with prespawnlng
adults of the blueglll. L.. macrochlrus. continuously exposed for 97 days.
The full data set Indicate this 1s the most sensitive species tested. For
most test species, decreased growth and survival were the most sensitive
endpolnts monitored. Reproduction was adversely affected at the toxlclty
threshold In brooktrout and bluegllls and was commonly noted in other
species at higher exposures. Newly hatched Stlzostedlon vltreum and
Catostomus commersonl had dose-related deformities (lordosls, congestion
around veins, gelatinous lesions and uneven resorptlon of yolk) after
exposure at the egg stage to concentrations ranging from 0.006-0.062 mg/l
for <20 days (Smith and Oseld, 1972). Similar deformities were noted by
Adelman and Smith (1970) In E_. luclus among fry hatched from eggs exposed
/
<96 hours to high concentrations of hydrogen sulflde. These deformities
eventually caused death.
Some sublethal effects were noted, but not quantified, and Include
reduced activity and Increased respiratory movements (Reynolds and Halnes,
1980). Growth enhancement was noted In Sal mo trutta. C_. commersonl and P.
promelas by Reynolds and Halnes (1980), Smith and Oseld (1972) and Smith et
al. (1976a), respectively. The authors speculated that one of the
antibiotic properties of hydrogen sulflde may be growth enhancement.
0238d -24- 11/06/89
-------
lABLf 4-2
ro
CO
oo
0.
1
ro
in
i
11/06/89
Chronic loxlclty of Hydrogen Sulflde to Aquatic Fauna
Species Exposure
Duration
FRESHWATER INVERTEBRATES
Hexagenla 138
llmbata
Nayfly
Procambarus 196
clarkll
Crayfish
Gammarus 105
pseudollmnaeus
Scud
FRESHWATER VERTEBRATES
Salmo 100
galrdnerl
Rainbow Trout
S. trutta 22
Brown trout
Salvcllnus 120
fontlnalls
brook trout
S. fontlnalls 120
Brook trout
Plmephales 297
promelas
fathead minnow
P promelas 29 /
Fathead minnow
P. promelas 373
fathead minnow
Stage at Start
of Test
nymph
juvenl le
15-17 days old
sac fry
sac fry
0.5 g
finger ling
5 g flngerllng
sac fry
juveniles
juveniles
Concentration* (roq/t)
Toxic Effect
NOECD LOECC
0.0225 0.429 decreased
survival
0.0062 0.010 decreased
survival
0.0029 0.0071 decreased
survival
0.0047 0.0110 decreased
growth
5 NR decreased
survival
0.0092 0.0125 decreased
reproduction
0.007 0.009 decreased
growth
0.0049 0.0101 decreased
growth
0.0049 0.009? decreased
survival
0.0066 0.0194 decreased
growth and
survival
Comment
pH-7.7;
temp*17.6*C
pHt7.65»0.04;
pH, 7. 6-8.0;
terap.20»2*C
02*7.8-9.4;
pH*7. 6-8.0;
temp.!4.7*C
Op. 9. 3; pH.7;
tempi 1 30 *C
Op NR;
pH, 7. 6-8.0;
temp*13*C
Op NR; pH=7.S;
tenp-13'C
02=5.2-6.3;
pH,7. 6-8.0;
Op^S.2-6.3;
pH=7.7-7 8;
temp-23*O.I*C
Op. pH NR;
lemp'2l.3*C
Reference
Smith et al..
1976a
Smith et al..
I976a
Osetd and
Smith. 1974J
Smith et al..
1976a
Reynolds and
Halnes. 1980
Smith et al..
19?6a
Smith. 1978;
Smith and
Oseld. 1975
Smith et al..
1976a
Smith. 1976b
Smith and
Oseld, 197S;
Smith, 1978
-------
IABK 4-2 (cont.)
ro
CD
CX
OJ
i
Species
Carasslus
auratus
Goldfish
Lepomls
macrochlrus
BlueglM
I. Mcrochlrus
Blueglll
L. macrochlrus
Blueglll
L. macrochlrus
BlueglM
Stliostedlon
vltreum
Walleye
S. vllreum
Walleye
Cat os (onus
Conner son 1
White sucker
Exposure Stage al Start
Duration of lest
294 Juveniles
14B juveniles
316 eggs
826 Juveniles
97 pre-spawnlng
adults
225 Juvenile
20 eggs
1? eggs
Cone cntratlon8 (mq/i)
To*1c Effect
0.0140 0.0350 decreased
growth and
survival
0.0006 0.0023 decreased
reproduction
NR 0.0022 decreased
growth and
survival
O.OOIS 0.0034 decreased
growth and
survival
NR 0.0010 decreaied
egg pro-
duction
0.0043 0.0071 decreased
growth
NR 0.013 decreaied
growth
0.012 0.028 decreased
growth
Comment
07'4.9-6.6;
pH=7. 6-8.0;
temp.!8.6*C
Oj-6. 2-9.0;
pH. 1.6-8.0;
te«p.?4-C
02«6. 2-9.0;
pHrl.6-8 0;
temp.?2.4*C
0? *R;
pH.l. 6-8.0;
temp.M.8*C
0?.6. 2-9.0:
pM. 1. 6-8.0;
temp>20-25*C
0;.8.l-8.3;
pH.7. 6-8.0;
temp-H.B'C
02. 3. 0-6.0;
pH «B;
lempU2*C
0^.3.0-6.0;
pH. 7. 6-8.0;
temp.!3*C
Reference
Smith et al..
I976a
Smith et al..
Smith et al..
I976c; Smith
and Oseld. 1975
Smith and
Oseld. 1975;
Smith. 1978
Smith et al..
1976c; Smith.
19r8
Smith et al..
Smith and
Oteld. 1972
Smith and
(Meld. 1972
o
-------
4.1.2.2. BIOACCUHULATION/BIOCONCENTRATION — Pertinent data regarding
the bloaccumulatlon/bloconcentratlon potential of hydrogen sulflde In
aquatic fauna were not located In the available literature cited In
Appendix A.
4.1.3. Effects on Flora.
4.1.3.1. TOXICITY -- Pertinent data regarding the toxic effects of
exposure of aquatic flora to hydrogen sulflde were not located In the
available literature cited In Appendix A.
4.1.3.2. BIOCONCENTRATION — Pertinent data regarding the bloconcen-
tratlon potential of hydrogen sulflde In aquatic flora were not located In
the available literature cited In Appendix A.
4.1.4. Effects on Bacteria. Pertinent data regarding the effects of
exposure of aquatic bacteria to hydrogen sulflde were not located In the
available literature cited In Appendix A.
4.2. TERRESTRIAL TOXICOLOGY
4.2.1. Effects on Fauna. Pertinent data regarding the effects of
exposure of terrestrial fauna to hydrogen sulflde were not located In the
available literature cited In Appendix A.
4.2.2. Effects on Flora. Effects of hydrogen sulflde on growth,
morphology, transpiration and sulfur content of spinach, Splnacla oleracea.
have been Investigated. Haas et al. (1987) exposed plants to 0.25 yi/a.
of hydrogen sulflde for 11-14 days at temperatures ranging from 15-20eC
under controlled light conditions (10-hour days). Results based on fresh
weight of the plants were compared with untreated controls. Relative growth
rate was significantly reduced by fumigation (by 26, 47 and 60% at 15, 18
and ?5°C, respectively). Shoot-to-root ratios were significantly reduced In
plants treated at 18 and 25°C. After 14 days of exposure, an Increased
0238d -27- 11/06/89
-------
transpiration rate, Increased plant content of sulfhydryl compounds and
sulfate, and alterations In leaf morphology were noted. Alterations In leaf
morphology were characterized by tightly packed and smaller cells, higher
chlorophyll content than In controls and smaller and fewer air spaces; these
effects were especially pronounced at leaf edges.
4.3. FIELD STUDIES
Bonn and Follls (1967) conducted field tests with channel catfish,
Ictalurus punctatus. In 10 lakes having natural populations ranging from
excellent to very poor (authors' descriptions). Two lakes were stocked with
10 marked wild adult catfish/acre. Other stocks were laboratory-reared,
acclimated to lake conditions before stocking, and reared the following
summer. One hundred catfish fry were placed In a test pen at Lake Ferndale
to serve as controls for the laboratory-reared stock. Catfish survival,
hydrogen sulflde concentrations, unionized and Ionized forms and pH were
monitored.
The transplanted adult catfish grew rapidly. A check of sexual condi-
tion showed that many had spent gonads; young were not harvested In repeated
collection attempts. Acute toxlclty tests Identified LC^-s of 1.0 mg/a.
at pH 7.0 for flngerllngs, 1.3 for advanced flngerllngs and 1.4 for adults
exposed to un-lonlzed hydrogen sulflde. Its toxic form. Maximum concentra-
tions of this compound were naturally produced In the spring at levels <5.66
mg/a (pH 6.0) In water from Glass Lake station 1. Ihls level was found to
be above the toxic threshold to catfish fry.
4.4. AQUATIC RISK ASSESSMENT
The lack of pertinent data regarding the effects of exposure of aquatic
fauna and flora to hydrogen sulflde precludes the development of a fresh-
water criterion by the method of U.S.EPA/OURS (1986) (Figure 4-1).
0238d -28- 11/06/89
-------
Family
11
Chordate (Salmonid-f ish)
12
Chordate (warwwater fish)
13
Chordate (fish or amphibian)
Crustacean (planktonic)
*5
Crustacean (benthic)
#6
Insectan
17
non-Arthropod/-Chordate
#6
New Insectan or phylum
representative
19
algae
TEST TYPE
CMAV* CMCVa
0.016b 0.0072h
0.011C 0.0016*
0.003d 0.0069^
NA NA
O.C256 NA
0.02f 0.098*
NA NA
O.lllg NA
XXXXXXXXXXXX
XXXXXXXXXXXX NA
BCF*
NA
NA
NA
NA
NA
NA
NA
NA
NA
no
Vascular plant
XXXXXXXXXXXX
xxxxxxxxxxxx
NA
aNA=Not Available; ^Mean 96-h LC50 for rainbow trout, S.qairdneri;
cKean 96-h LC^Q for fathead minnows, P. oromelas; d96-h LCsp for
whitefish, C. cluoeafonnis; eMean LCgo f°r scud, G. pseudolnnnaeus:
*96-h LC50 for the mayfly, B. vaaans; 996-h LCs0 for the nayfly,
E. simulans; "Mean chronic value for the rainbow trout, S. aaird-
neri: AMean chronic value for bluegills, L. macrochirus; 3Mean
chronic value for fathead minnows, P. promelasi KMean chronic value
for the mayfly, H. limbata.
FIGURE 4-1
Organization Chart for Listing GMAVs, GHCVs and BCfs Required to Derive
Numerical Water Quality Criteria by the Method of U.S. EPA/OURS (1986) to
Protect Freshwater Aquatic Life from Exposure to Hydrogen Sulflde
02380
-29-
09/11/89
-------
Available data Indicate that concentrations >0.001 mg/i may be chronically
toxic to freshwater fauna. Additional data required for the developmejU of
a freshwater criterion Include the results of acute assays with a planktonlc
crustacean and a nonarthropod and nonchordate species. The development of a
freshwater criterion also requires data from chronic toxlclty tests with two
species of fauna and one species of algae or vascular plant and at least one
bloconcentratlon study.
The lack of pertinent data regarding the effects of exposure of aquatic
fauna-and flora to hydrogen sulflde prevented the development of a saltwater
criterion by the method of U.S.EPA/OURS {1986} (Figure 4-2). Available data
indicate that concentrations as low as 0.2 mg/a. may be toxic to saltwater
fauna. Additional data required for the development of a saltwater
criterion Include the results of acute assays with two chordate species, a
mysld or panaeld crustacean and one other species of marine fauna. The
development of a saltwater criterion also requires data from chronic
toxlclty tests with two species of fauna and one species of algae or
vascular plant and at least one bloconcentratlon study.
4.5. SUMMARY
The acute toxldty of hydrogen sulflde was similar In most species of
freshwater fish examined, with LC5Q values ranging from 0.003 mg/l In
whlteflsh, C. clupeaformls (Fung and Bewick, 1980) to 3.0 mg/i In mosquito
fish. G. afflnls (Prasad, 1980b). The latter was the only fish with an
LC5Q >1. Representatives from >14 genera of fish have been assayed For
acute toxlclty from hydrogen sulflde (Adelman and Smith, 1970, 1972; Bonn
and FolUs, 1967; Broderlus et al.. 1977; Fung and Bewick, 1980; Oseld and
Smith, 1974a; Prasad, 1980a,b; Reynolds and Halnes, 1980; Smith, 1970;
0238d -30- 11/06/89
-------
TEST TYPE
Family
11
Chordate
«2
• Chordate
13
non-Arthropod/-Chordate
«4
Crustacean (Kysid/Panaeid)
*5
non-Chordate
16
non-Chordate
#7
non-Chordate
#8
other
*9
algae
110
Vascular plant
aNA»Not Available; b96-h LC50
c56-h LCso 'or the amphipod,
cunaeness crab. C. maaister:
CMAV*
(Bg/D
NA
NA
1.4*
NA
°.2C
0.5^
6.0e
NA
xxxxxxxxxxxx
xxxxxxxxxxxx
xxxxxxxxxxxx
xxxxxxxxxxxx
for the Pacific
A. confervicola;
*96-h LCcn for tl
CMCVa
(»g/L)
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
oyster, c_._
d96-h LC50
le clan, M.
Bcra
NA
NA
NA
NA
NA
NA
NA
NA
NA
NA
qiqas :
for the
balthic£
FIGURE 4-2
ni. r ' GMCVs and 8CFs "equtred to DerWe
i, Qu.alUy CrUeMa "y th^ Method of U.S. EPA/OWRS (1986) to
Saltwater Aquatic Life from Exposure to Hydrogen Sulflde
0?38d
-31-
11/06/89
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Smith and Oseld, 1970, 1972, 1975; SmHh et al., 1976a,b,c; Van Horn et al.,
1949). Some acclimation occurs with Initial low-level exposure of bluegllls
to hydrogen sulflde (SmHh, et al., 1976a).
Freshwater and marine Invertebrates were less sensitive to hydrogen
sulflde than were fish. Variation of response within the Invertebrates was
slight. LC50 values ranged from 0.02 mg/l In the mayfly, B. vagans
(Smith et al., 1976a; Oseld and SmHh, 1974b), to 6 mg/a. In the clam, M.
balthlca (Caldwell, 1975), for all Invertebrates tested. The one exception
was CMronomus sp.t wHh an LC5Q of 550 (Prasad, 1980a).
Chronic studies with freshwater animals yielded LOECs ranging from
0.0010-0.429 mg/i. Little difference was noted between Msn and Inverte-
brates (Reynolds and Halnes, 1980; Oseld and Smith, 1974a; SmHh, 1970;
Smith and Oseld, 1975; SmHh et al., 1976a}. Prespawnlng adult L.
macrochlrus were the most sensitive group, suffering reproductive stress
with exposure to 0.0010 mg/i. for 90 days (SmHh, 1970; SmHh et al.,
1976aj. Field tests with ]_. punctatus Indicated that exposure to 1 mg/t
at pH 7.0 adversely affects reproduction (Bonn and Follls, 1967).
Available data Indicate that criteria based on protection of freshwater
fish would be protective of fresh and saltwater Invertebrates. The
currently recommended criterion of 2 yg/l hydrogen sulflde for fresh and
saltwater life (U.S.EPA/OWRS, 1986) may not be protective for all life
stages of L. roacrochlrus. It does, however, appear to be protective for
other species.
Terrestrial plants fumigated with 0.25 ml/a for <14 days may suffer
reduced growth and altered leaf morphology (Haas et al., 1987).
0238d -32- 11/06/89
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5. PHARMACOKINETICS
5.1. ABSORPTION
Kangas and Savolalnen (1987) correlated human exposure (concentration
multiplied by duration of exposure) to hydrogen sulflde with urinary levels
of thlosulfate, an oxidized form of sulflde (Section 5.4.). Respiratory
tract absorption was Inferred by the authors from exposure-related levels of
thlosulfate In the urine. However, the authors reported no precautions
against dermal absorption. Absorption Is also Implied by the toxic effects
reported In human Inhalation studies (Chapter 6). U.S. EPA (1986a) con-
cluded that the most common route of entry for hydrogen sulflde Is the lung.
No animal Inhalation studies measuring the absorption of hydrogen
sulflde were located, but absorption through the respiratory tract can be
Inferred from toxlclty studies (Chapter 6).
Curtis et al. (1972) administered 2.02 mg/kg sodium 35S-sulf1de orally
or Intraperltoneally to rats and measured the radioactivity excreted In
feces and urine over a 48-hour period. The results, described In Section
5.4., suggest that orally-administered 35S-sulf1de Is rapidly and almost
completely absorbed from the gastrointestinal tract.
Absorption of hydrogen sulflde through the skin has been demonstrated by
dermal toxldty studies In animals (Laug and Dralze, 1942; Walton and
WHherspoon, 1925). Walton and Wltherspoon (1925) determined that death In
two guinea pigs but not In one dog (sex and strains not reported) resulted
from 45 minutes of dermal exposure of approximately half of the animals'
body surface to pure hydrogen sulflde. Laug and Draize (1942) exposed the
clipped, moist, Intact or abraded skin of throe male rabbits (strain not
reported) to unreported concentrations of hydrogen sulflde gas. Dermal
absorption was qualitatively Indicated by the presence of hydrogen sulflde
0238d -33- 11/06/89
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In exhaled air after 7 minutes of exposure and by mortalities In two of
three rabbits 1n 100-135 minutes after the onset of exposure.
5.2. DISTRIBUTION
In the only study of the distribution of Inhaled hydrogen sulflde, Volgt
and Muller (1955) exposed rats and guinea pigs to unreported concentrations
of hydrogen sulflde for 1 minute to 10 hours and presented hlstochemlcal
evidence of the presence of sulflde In the brain, liver, kidneys, pancreas
and small Intestines.
Curtis et al. (1972) Injected sodium «S-sulf1de (2.02 mg/kg) Intra-
perltoneally Into young M.R.C. hooded rats (4-6 weeks, number of animals not
reported), sacrificed them at Intervals ranging from 3 minutes to 6 hours
after administration and determined the radioactive distribution by whole-
body radloautography. Sulflde was widely distributed In the body, Including
the gastrointestinal tract and cartilaginous tissues. Following administra-
tion of sodium 3SS-sulf1de, other areas of accumulation, listed according
to their relative levels of radioactivity, were the lung, blood and brain.
Curtis et al. (1972) also determined that the maximum blood accumulation
after oral and Intravenous administration was 10.7% of the administered
Intravenous dose or 4.7% of the oral dose. The authors deduced that sulflde
has only a transient existence In blood. Both j£ vivo (Intravenously and
orally) and In vitro, the majority of the radioactivity In the blood was
associated with the plasma and not the blood cells. In. vivo, most radio-
activity In the blood was In the form of Inorganic 35S-sulfate. In vitro.
most radioactivity was associated with plasma and blood cell proteins. When
sodium 3*S-sulflde-enr1ched whole blood was used to perfuse Isolated
livers, protein-associated radioactivity declined rapidly and was replaced
0238d -34- 11/06/89
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by 35S-sulfate. The authors concluded that the transient existence of
sulftde In the blood was rapidly followed by Us uptake and oxidation In
tissues.
Warenycla et al. (1989) reported the brain distribution of Intraperlto-
neally Injected doses (7.5-50 mg/kg) of sodium hydrosulflde In male Sprague-
Dawley rats. In untreated rat brains, an endogenous sulflde level of 1.57
vg/gm was found. When sections of the brain were analyzed separately, the
bralnstero had the lowest levels of endogenous sulflde (1.23 yg/g), but It
had the greatest net uptake of Injected sulflde (3.02 yg/g). Subcellular
fractlonatlon of the brain found that sulflde localized In the fractions
containing myelln, synaptosomes and mitochondria, with -25J4 of the total
endogenous concentration of sulflde in the mUochondrlal fraction. After
Injection with sodium hydrosulflde, the sulflde concentration In these three
subcellular fractions Increased 2- to 3-fold.
5.3. METABOLISM
Three major pathways exist for the metabolism of hydrogen sulflde:
1) oxidation to sulfate; 2) methylatlon; and 3) reaction with metallo- or
dlsulflde-contalnlng proteins (Figure 5-1) (Beauchacnp et al., 1984). The
Interaction of the sulflde with essential proteins, especially the
Iron-containing proteins of the respiratory chain. Is largely responsible
for the toxlclty of hydrogen sulflde. The other two pathways, oxidation and
methylatlon, represent modes of detoxification.
The oxidation of the sulflde to the sulfate Is the major metabolic
pathway. Sulflde oxldase In the mitochondria of rat liver and kidneys
catalyzes the oxidation of sulflde to thlosulfate, possibly through poly-
sulflde Intermediates (Der-Garabedian, 1945a,b; Baxter and Van Keen, 1958;
0238d -35- 11/22/89
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TXIOL S-MCTMVL
MtTALLOMOTIINl
CHjlM
»> 1 MfTMIMOCLOIIh.
PCRftiTih
9CATAIASI
HHOKlOAJl
fcXClUlC DIM YOHO«NAIt
CO*.»tool'., i:
»DITOXi'lCATiO»»
»TOIICITY
>TOHCITV |?i
ATOXICITY IT)
MEOUCTASE
FIGURE 5-1
Metabolism of Hydrogen
Source: Beauchamp et al.. 1984
02380
11/06/89
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Baxter el al.. 1958; Sorbo, 1958; Baxter and Van Reen, 1958). The thlo-
sulfate Is oxidized to sulfate by sulfUe oxldase with the participation of
glutathlone (Bartholomew et al.. 1980; Curtis et al., 1972; KoJ et al.,
1967; MacLeod et al., 1961a,b). Curtis et al. (1972) determined that sodium
35S-sulf1de, Incubated \n_ vitro with rat blood, rapidly bound to blood
proteins In the plasma and on the cells. However, the primary site of
sulflde oxidation Is the mitochondria of liver, kidney and heart
(Bartholomew et al., 1980; MacLeod et al., 1961a,b). Little or none Is
oxldfzed to sulfate In the lungs (Curtis et al., 1972; MacLeod et al.,
1961a,b; Bartholomew et al., 1980). Results of Iji vivo studies In rats
(Section 5.4.) suggest that oxidation to sulfate occurs rapidly and accounts
for the bulk of administered sulflde.
Hydrogen sulflde formed from anaerobic bacteria In the gastrointestinal
tract Is sequentially methylated to methanethlol and then to dlmethylsulf1de
(see Figure 5-1) by thlol-S-methyltransferase, In the gastric mucosa and the
liver (Welslger and Jakoby, 1979). Methylatlon results In detoxification,
since both methylated products are less toxic than hydrogen sulflde
(Beauchamp et al., 1984).
The third metabolic pathway, the reaction with metallo- and dlsulflde-
contalnlng proteins, Is the source of the toxlclty of hydrogen sulflde
(Beauchamp et al.. 1984). The mechanism Is briefly discussed In Section 6.3.
In mice (Ui vivo) and human blood (\r± vitro), the reaction of hydrogen
sulflde with methemoglobln (produced by the Interaction of sodium nitrate
and hemoglobin) results In a detoxification of hydrogen sulflde (Smith and
Gosselln, 1966; Beck et al., 1981) by the formation of sulfmethemoglobln,
which Is less toxic than hydrogen sulflde. Similarly, ferrHIn detoxifies
sulflde by oxidation to the sulfate (Baxter and Van Reen, 1958).
0238d -37- 11/06/89
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5.4. EXCRETION
Volunteers working In a pelt processing plant (number not reported) were
exposed to concentrations of 8, 18 or 30 ppm hydrogen sulflde gas for 30-45
minutes and the urinary levels of thlosulfate were determined In every urine
sample voided within 24 hours after exposure (Kangas and Savolalnen, 1987).
A group of 29 unexposed men served as controls. A positive correlation was
found between exposure to hydrogen sulflde (expressed as the product of
concentration and time) and urinary thlosulfate, with peak levels of
thlosulfate found 15 hours after exposure. Studies of excretion by animals
following Inhalation of hydrogen sulflde were not located.
Following IntraperUoneal, Intravenous and oral administration of sodium
3SS-sulf1de, most of the administered radioactive dose was oxidized to
35S-sulfate and excreted In the urine, with the bulk of excretion within
12 hours of administration. Curtis et al. (1972) administered sodium
35S-sulf1de (2.02 mg/kg) to M.R.C. hooded rats Intraperltoneally (three
males and three females) or orally by gavage (throe males and throe females)
and determined the excretion of radioactivity In the urine and feces <48
hours after administration. Most of the urinary radioactivity was excreted
In the first 12 hours. At 48 hours, most administered radioactivity was
found In the urine following both Intraperltoneal (84-93% of the given dose)
and oral administration (52-69%). Fecal excretion accounted for 5-19% of
the administered radioactivity following Intraperltoneal Injection and for
3-19% following oral administration. The major radioactive component
excreted In the urine was Inorganic 3SS-sulfate. In a similar experiment,
sodium 35S-sulflde (2.05 mg/kg) was administered Intravenously to two male
rats cannulated In ureters and bile ducts. Over a period of 6 hours, 45 and
5% of the administered radioactivity was excreted In the urine and bile,
respectively. The biliary radioactivity was not sulfate, but the majority
0238d -38- 11/06/89
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of the radioactivity excreted In the urine was Inorganic 35S-sulfate.
Unidentified materials present In traces after 5 hours constituted -15% of
the total radioactive dose. Curtis et al. (1972) concluded that the
principal terminal fate of administered sulflde In rats Is oxidation to
sulfate and excretion In urine.
5.5. SUMMARY
Absorption by humans of Inhaled hydrogen sulflde can be Inferred from
excretion of thlosulfate following human exposure to hydrogen sulflde gas
(Kangas and Savolalnen, 1987), and from toxic effects following acute and
occupational exposure (Chapter 6}. Absorption through the respiratory
tracts and skin of animals can be Inferred from toxic effects following
respiratory and dermal exposure (Laug and Dralze, 1942; Walton and
WHherspoon, 1925). Studies using rats suggest rapid and virtually complete
gastrointestinal absorption (Curtis et al., 1972). U.S. EPA (1986b) con-
cluded that the most common route of entry for hydrogen sulflde Is the lung.
Wide distribution to the brain, liver, kidneys, pancreas and small
Intestines has been shown hlstochemlcally after Inhalation exposure of
guinea pigs and rats (Volgt and Mullet, 1955). Distribution to the gastro-
intestinal tract, cartilaginous tissues, lungs, brain and blood has been
shown autoradlographlcally following oral, Intraperltoneal and Intravenous
administration of hydrogen sulflde to rats (Curtis et al.. 1972). Warenycla
et al. (1989) reported that the highest concentration of sulflde In the
brain was In the bralnstem following Intraperltoneal doses of sodium
hydrosulfIde.
Three separate metabolic pathways exist for hydrogen sulflde: 1) oxida-
tion to sulfate; 2) methylatlon; and 3) reaction with metallo- or dlsulflde-
contalnlng proteins (Beauchamp et al., 1984). Oxidation and methylatlon
0238d -39- 11/06/89
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detoxify hydrogen sulflde, while the reaction of hydrogen sulflde with
essential proteins results In Its toxic effects.
The predominant route of excretion of hydrogen sulflde In humans and
rats Is In the urine as metabolites (sulfate or thlosulfate) (Kangas and
Savolainen. 1987; Curtis et al.. 1972). Urinary levels of thlosulfate, a
metabolite of hydrogen sulflde, have been correlated with exposure levels of
hydrogen sulflde In workers (Kangas and Savolainen, 1987).
0238d -40- 11/06/89
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6. EFFECTS
6.1. SYSTEHIC TOXICITY
6.1.1. Inhalation Exposure.
6.1.1.1. SUBCHRONIC — Galtonde et al. (1987) described a case of
subacutc encephalopathy in a 20-month-old child exposed to >0.6 ppm hydrogen
sulflde For -12 months. The child's family lived beside a colliery where a
burning tip had been emitting hydrogen sulflde for ~1 year. The maximum
recorded hydrogen sulflde level found In the family's house was 0.6 ppm,
although the number of measurements taken and the range of concentrations
measured were not reported. The Initial symptom was Intermittent tonic
deviation of the eyes, followed a few months later by Involuntary movements
of the whole body and frequent falls. When the child was admitted to the
hospital, gross ataxla and dystonla were evident and the child could not
stand. Computed tomographs of the brain showed areas of low density 1n both
basal ganglia and 1n the surrounding white matter, suggesting toxic encepha-
lopathy. After admission, the child's condition Improved and a normal
tomograph was taken after 10 weeks, suggesting reversibility of the
condition. The concentration of 0.6 ppm hydrogen sulflde can be considered
a LOAEL for neurological effects.
Ninety-day Inhalation studies using B6C3F1 mice, Sprague-Dawley rats and
F344 rats were conducted with hydrogen sulflde vapor (loxlgenlcs,
1983a,b,c). The mice (groups of 10 males and 12 females) and both strains
of rats (15 animals/sex/group) were exposed to TWA concentrations of 0,
10.1, 30.5 or 80.0 ppm for 6 hours/day, 5 days/week for 90 days. In the
mice, no compound-related effects (mortality, body weight, food consumption,
ophthalmoscoplc abnormalities, neurological function and gross or
histopathologlcal examination) were observed In the 10.1 and 30.5 ppm
groups. In the mice exposed to 80.0 ppm hydrogen sulflde, a biologically
0238d -41- 11/22/89
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significant decrease In body weight gain and significant differences In food
consumption were noted. Also In this group, two mice did not respond to
light stimulus. Two mice In this group were sacrificed during the course of
the study because of prostration, hypoactlvlty and alopecia. At
termination, hlstopathologlcal examination revealed that 89% of the males
and 78% of the females In the high-dose group showed compound-related
Inflammation of the nasal mucosa. This lesion was also present In the two
high-dose mice that died during the course of the study. However, this
effect was not observed In the other treated groups or In the controls.
Further details of the experiment and Individual animal data were not
reported (Toxlgenlcs, 1983a).
Clinical observations In both strains of exposed rats Included crusti-
ness associated with the ear tag, the nose, the eye and the muzzle, lacrlma-
tlon and red-stained fur. Additional observations in the Sprague-Dawley
rats were Irritability and swollen ears, muzzle and eyes and, In the F344
rats, yellow/brown-stained fur.
A significant lag In body weight gain was found In all treated F344
groups compared with controls after the first week of exposure; the body
weights continued to be lower over the following 12 weeks. Depressed body
weight gain and depressed brain weight was found In the high-dose group of
Sprague-Dawley rats. No significant differences In food consumption,
ophthalmology, clinical pathology, neurological function or gross or
hlstopathologlcal examination were found In any of the treated animals from
either species of rat. Neuropathologlc studies on the fibers of the tlblal
nerve in both species of rat showed no effects from exposure to hydrogen
sulflde. Further details of the studies and Individual animal data were not
reported (Toxlgenlcs 1983b,c).
0238d -42- 11/22/89
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Hale Sprague-Dawley rats (10/group) were exposed by Inhalation to 0 or
50 ppm hydrogen sulflde, 5 days/week for 25 weeks (Gagnalre et al., 1986).
The animals were examined for effects on sensory and motor nerve conduction
velocity. No neurological effects on the rats were found In the group
treated with hydrogen sulflde.
Duan (1959) examined effects of hydrogen sulflde on the nervous system
In groups of 10 rats exposed to 0. 0.014 or 7 ppm for 3 months (12
hours/day, 5 days/week}. The study examined the muscular galvanic response
and hlstologlcally examined the dendrltes In the neurons of the cerebral
cortex. In the group exposed to 7 ppm, some swelling of the dendrltes was
Found, but this effect may have been an artifact (NIOSH, 1977).
6.1.1.2. CHRONIC — Arnold et al. (1985) reported a 5-year retrospec-
tive study of 250 workers that filed compensation claims during a 4-year
period following exposure to unreported concentrations of hydrogen sulflde
for unreported lengths of time. Symptoms of neurological toxlclty were the
most common complaints among the workers. Major neurological effects
Included unconsciousness (54% of the workers), headache (26%). nausea/vomit-
ing (24.8%). disequilibrium (21.6%) and neurophyslologlcal effects, such as
agitated behavior and amnesia (8.0%). Respiratory effects [dyspnea (22.8%L
sore throats/cough (16.4%). chest pain (7.2%) and pulmonary edema (5.6%)]
and opnthalmologlc effects [conjunctivitis (18.4%)] were also observed. The
overall fatality rate was 2.8%.
Ahlborg (1951) noted that workers occupatlonally exposed dally to -20
ppm hydrogen sulflde In the shale oil Industry experienced changes In
personality, Intellect and memory, Irritation of the eyes and respiratory
tract and disorders of the gastrointestinal tract. Of the workers employed
>2 years, 59% of exposed workers and 42% of unexposed workers complained of
fatigue, and In workers employed <2 years. 35% of exposed workers and 22% of
0238d -43- 11/06/89
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unexposed workers complained of fatigue. Poda (1966) reported no adverse
effects In workers occupatlonally exposed to 10 ppm hydrogen sulflde.
Nesswetha (1969) reported eye Irritation (spinner's eye) in 6500 workers
Industrially exposed to hydrogen sulflde. Symptoms of Irritation developed
after 6-7 hours at 15 mg/m3 (10 ppm) and after 4-5 hours at 20 mg/m3 {14
ppm). Workers stressed by the presence of carbon dlsulflde, thloformalde-
hyde and other Irritating chemicals or by night work responded to lower
concentrations or with higher Incidence of the eye effect. The author
attributed spinner's eye to a neural effect caused by several factors,
Including hydrogen sulflde.
Rubin and Arleff (1945) found no significant Increase In the Incidence
of health effects reported by the subjects, Including general effects on
sleep patterns, disturbances In vision and the digestive system and effect.*
on the eyes, Indicative of hydrogen sulflde exposure or 1n objective neuro-
logical signs (sensory; motor; reflexes Including deep, tendon, pathologi-
cal, superficial and pupillary; decrease In the swinging of arms; tremors of
the fingers or tongue and disturbances In hearing) In workers exposed to
hydrogen sulflde. The workers (100 men) were exposed to an average of
1.0-5.5 ppm hydrogen sulflde. The length of employment ranged from 3 months
to 17 years.
Hlgashl et al. (1983) Investigated the relationship between acute and
chronic hydrogen sulflde exposure of male workers and the Incidence of
effects on the respiratory system and pulmonary function. In the acute
study, changes In pulmonary function were assessed In 30 workers by deter-
mining the forced expiratory flow volume both before and after their 8-hour
shifts. The workers were exposed to an average of 3 ppm hydrogen sulflde
(range of 0.3-7.8 ppm). The exposed workers were employed for an average of
12.3 years. No significant differences In pulmonary function were found
0238d -44- 11/06/89
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between the exposed workers and a comparable group of nonexposed workers (30
men). A questionnaire was administered to 324 male workers divided Into
four categories: 85 exposed smokers (group 1), 30 exposed nonsmokers (group
2), 125 nonexposed smokers (group 3) and 84 nonexposed nonsmokers (group
4). The average length of employment and, therefore, of exposure to
hydrogen sulflde, was 11.7 years In group 1 and 12.6 years In group 2. The
workers were exposed to an average annual concentration of 1.3 ppm hydrogen
sulflde, 4.0 ppm of carbon dlsulflde and <0.1 mg/m3 of sulfurlc acid.
Results of the questionnaire showed significant association of the
prevalence rates of respiratory symptoms with smoking habits, but not with
work history.
Using a self-administered questionnaire, a physical examination, pulmo-
nary function tests and chest radiographs, Chan-Yeung et al. (1980) evalu-
ated 1039 male workers divided Into three groups. Two groups were exposed
to 0.05-0.06 ppm hydrogen sulflde for 14 years: 219 workers exposed primar-
ily to gases and fumes and 325 workers exposed to a mixture of parUculate
matter and vapors. A control group of 496 men was exposed to <0.05 ppm
hydrogen sulflde. No significant differences In respiratory symptoms or
pulmonary function were found between the hydrogen sulfIde-exposed workers
and the controls.
A retrospective study of the mortality patterns of all persons employed
by a Texaco production or pipeline facility for >6 months was performed by
Divine and Barren (1987). The workers were exposed to crude oils with high
but unreported concentrations of hydrogen sulflde. The SMR for the workers
was significantly low for cancer (68), for diseases of the circulatory
system (66) and for all causes of death (63) compared with the U.S. white
male population.
0238d -45- 11/06/89
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6.1.2. Oral Exposure.
6.1.2.1. SUBCHRONIC — The only subchronlc oral data In animals are
from two experiments In a pig feeding study by Hetterau et al. (1964). The
study Is summarized by U.S. EPA (1989), and the dietary data are converted
to dose levels by assuming the pigs weighed 78 kg and consumed 200 g
feed/day. The first experiment suggested digestive disorders In pigs fed
dried green fodder of high hydrogen sulflde content, exposing them to 15
mg/kg/day hydrogen sulflde for 105 days. In the second experiment, In which
the pigs were similarly exposed to three lower doses of hydrogen sulflde,
the digestive effects were not reproduced, and an Intermediate dose of -3.1
mg/kg/day resulted in no changes In body weight gain compared wHh
controls. A LOAEL of 15 mg/kg/day for effects on the gastrointestinal
system and a NOAEL of 3.1 mg/kg/day for effects on body weight gain can be
defined from this study.
6.1.2.2. CHRONIC — Pertinent data regarding the effects of chron.lt_
oral exposure of hydrogen sulflde were not located In the available
literature cited In Appendix A.
6.1.3. Other Relevant Information. The odor of the gas (strong smell of
rotten eggs) Is detectable at concentrations of 0.1-0.2 ppm and offensive at
3-5 ppm. Irritation of the respiratory system and the eyes occurs at 50-200
ppm, with olfactory paralysis developing at 150 ppm. Pulmonary edema Is
found following exposure to 200-250 ppm. At 500-1000 ppm. nervous stimula-
tion occurs, and respiratory paralysis and Immediate death result at concen-
trations of 1000-2000 ppm (Ammann. 1986; Deng and Chang. 1987; VannaUa,
1982).
The danger lies In exposure to concentrations >150 ppm, since the
olfactory cells are paralyzed at this level and odor Is no longer a warning
sign. Pathological observations In cases of fatal poisoning Included
0238d -46- 11/06/89
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greenish discoloration of the blood and viscera, visceral congestion and
pulmonary edema (Poda, 1966; Adelson and Sunshine, 1966).
The third metabolic pathway discussed In Section 5.3., the reaction of
sulfldc v/Uh metallo- and dlsulf1de-conta1nlng proteins, Is the major source
of the toxiclty of hydrogen sulflde (Beauchamp et a!., 1984). This reaction
of hydrogen sulflde Inhibits mitochondria! electron transport at cytochrome
aa_3 (Wever et al., 1975), thus halting oxldatlve phosphorylatlon (Hever et
al., 1975; Nlcholls, 1975; Nlcholls et al., 1976), the body's major energy
source. Tissues of the body requiring the highest levels of energy, such a&
cardiac and nerve tissue, are rapidly and severely affected. The most often
noted results of hydrogen sulflde reactions with such metalloprotelns as
cytochrome aa_ are neurological symptoms (paralysis of the respiratory
center, leading to fatal pulmonary edema) and that cardiac symptoms are
usually secondary to respiratory dysfunction {BUterman et al., 1986).
Hydrogen sulflde also Inhibits other metallo-protelns such as catalase
(Stern, 1932) and succlnlc dehydrogenase.
Ammann (1986) suggested that the toxic effects of hydrogen sulflde are a
result of the Inhibition of cellular respiration, specifically the revers-
ible Inhibition of cytochrome oxldase. A major result of hydrogen sulflde
poisoning Is apnea, which results from effects on the respiratory center 1n
the brain (Haggard et al., 1922; BUterman et al., 1986; Minder and Winder,
1933).
Komblan et al. (1988) Injected rats Intraperltoneal ly with sodium hydro-
sulflde at 10 or 30 mg/kg and demonstrated changes In amlno acid levels In
the bralnstem (the site of the respiratory center In the brain). No changes
In the amlno acid levels were found In the cerebral cortex, the hippocampus
or the strlatum. The authors concluded that, since some of these amlno
acids (glydne, glutamate, glutamlne, gamma-amlnobutyrlc add) act as
0238d -47- 11/06/89
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neurotransmHters In the respiratory center, alteration of their normal
levels may affect respiratory control.
The acute effects of Inhaled hydrogen sulflde have been extensively
studied In animals. Prior et al. (1988) reported LC5Q values of 587 ppm
for a 2-hour exposure, 501 ppm for a 4-hour exposure and 335 ppm for a
6-hour exposure In rats. Tansy et al. (1981) reported an LC~Q value of
444 ppm for a 4-hour exposure In rats. The cause of death In these exposed
animals was severe pulmonary edema (Prior et al., 1988). Production of
edema In the lungs of rats has a definite threshold; once this level Is
attained, edema fluid rapidly leaks Into the lungs and death soon follows
(Lopez et al., 1987, 1989).
Rats exposed to >400 ppm hydrogen sulflde for 4 hours suffered severe
but transient damage to the nasal tissues and pulmonary edema (Lopez et al.,
1987, 1988b). Similarly, exposure to >400 ppm hydrogen sulflde for 4 hours
resulted In lesions In the middle areas of the nasal passages (Lopez et al.,
1988a). No adverse respiratory tract effects (pulmonary edema or nasal
lesions) were found In rats exposed to <200 ppm hydrogen sulflde (Lopez et
al., 1988a,b. 1989).
Lung homogenates from rats treated with aerosols of Staphylococcus
epldermldls after exposure to 45-46 ppm hydrogen sulflde for 4 or 6 hours,
but not 2 hours, had reduced ability to Inactivate viable bacteria (Rogers
and Per In, 1981). The authors concluded that alveolar macrophages had been
adversely affected by the hydrogen sulflde and suggested that Impairment of
alveolar macrophage might be associated with the development of secondary
pneumonia In humans following acute or subacute exposure to hydrogen
sulflde.
Death resulted In guinea pigs, but not dogs following dermal exposure of
approximately half of the body surface to hydrogen sulflde for 45 minutes
0238d -48- 11/06/89
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(Walton and WHherspoon, 1925). Laug and Dralze (1942) observed fatalities
following exposure of 240 era2 areas of the clipped skin of rabbits.
Abrasion of the skin did not decrease the time to death from dermal exposure
to hydrogen sulflde.
6.2. CARCINOGENICITY
6.2.1. Inhalation. Pertinent data regarding the carclnogenlclty of
Inhaled hydrogen sulflde were not located In the available literature cited
In Appendix A.
6.2.2. Oral. Pertinent data regarding the carclnogenlclty of oral
hydrogen sulflde were not located In the available literature cited In
Appendix A.
6.2.3. Other Relevant Information. Pertinent data regarding the carclno-
genlclty of exposure to hydrogen sulflde by other routes were not located In
the available literature cited In Appendix A.
6.3. NUTAGENICITY
Only one study of the mutagenlc potential of hydrogen sulflde was
located In the literature. Hughes et al. (1984) determined that hydrogen
sulflde was not mutagenlc, with or without activation, 1n Salmonella typhl-
mur 1 urn strains TA97, TA98 or TA100 at concentrations of 17-1750 ng/plate.
6.4. DEVELOPMENTAL TOXICITY
The Incidence of spontaneous abortions 1n Finnish women In relation to
the occupation of the women and their husbands was reported by Hemmlnk! and
Nleml (1982). An Increased rate of spontaneous abortions was found In women
employed In rayon textile jobs and In paper products Jobs (p<0.10), and In
women whose husbands were employed In rayon textile Jobs and In chemical
process Jobs. Hydrogen sulflde emissions have been detected In Industries
dealing with paper and rayon. Although not statistically significant, a
0238d -49- 04/02/90
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slightly Increased rate of spontaneous abortions was found In women exposed
to a mean annual concentration of >4 yg/m3 (9.3 abortions/100 pregnan-
cies) compared with those exposed to <4 yg/m3 (7.6 abortions/100
pregnancies). The authors noted that, since the trend was found across all
socloeconomlc groups (namely, employers and higher administrative employees,
lower administrative employees, workers and others), hydrogen sulflde may
affect the rate of spontaneous abortions.
Results of this study are not conclusive because of the many confounding
factors associated with the design of the study.
In this study, data on pregnancies and spontaneous abortions were
obtained from the hospital discharge register. The data on occupations,
places of employment, size of family and places of residence were acquired
from the record of the national population census of 1975. The
concentrations of hydrogen sulflde were obtained from environmental
surveillance data between 1977 and 1979. Pertinent Information such as no
exposure to agents other than hydrogen sulflde, actual duration and level of
exposure, etc., were unavailable In this study.
6.5. OTHER REPRODUCTIVE EFFECTS
Pertinent data regarding other reproductive effects of hydrogen sulflde
were not located 1n the available literature cited In Appendix A.
6.6. SUMMARY
Hydrogen sulflde acts by Inhibiting oxldatlve metabolism; consequently,
the tissues with the greatest oxygen need (such as those of the nervous
system) are most severely affected (Ammann, 1986). Toxic effects resulting
from acute Inhalation exposure Increase In severity with Increasing exposure
levels: at low levels (50-200 ppm), effects such as respiratory and eye
Irritation occur; at higher levels (200-250 ppm). pulmonary edema Is
observed. At concentrations >1000-2000 ppm, respiratory paralysis and death
0238d -50- 04/02/90
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result (Ammann, 1986; Deng and Chang, 1987; Vannatta, 1982). Death In
guinea pigs and rabbits followed dermal exposure to hydrogen sulMde (Walton
and WHherspoon, 1925; Laug and Dralze, 1942). Following subchronlc
(1-year) exposure of an Infant to <0.6 ppm hydrogen sulflde, reversible
neurological damage was found (GaHonde et al.. 1987). In occupationally
exposed workers, eye effects were Induced by 10 ppm (Nesswetha, 1969), and
levels of >20 ppm resulted In unconsciousness, headaches, nausea/vomiting,
disequilibrium and neurophyslcal effects (Arnold et al., 1985). Poda (1966)
reported no adverse effects In workers occupatlonally exposed to up to 10
ppm hydrogen sulflde.
A study Investigating the correlation between the Incidence of sponta-
neous abortions In women with their occupations and those of their husbands
did not conclusively Implicate hydrogen sulflde In developmental toxlclty
(Hemmlnkl and Mem1, 1982), because 1) only an Insignificant Increase In the
Incidence of spontaneous abortions was found In women exposed to >4
ng/m3 hydrogen sulflde and 2) confounding factors (such as exposure to
other agents) could not be ruled out.
Animal studies support the findings that the nervous and respiratory
systems are the targets of hydrogen sulflde administered by the Inhalation
and Intraperltoneal routes (Tox1gen1cs, 1983a,b,c; Lopez et al., 1987,
1986a,b, 1989; Komblan et al., 1988). The Inhalation studies suggest that
rats are more sensitive than mice. Mice showed neurological signs when
Intermittently exposed to 80 but not to 30.5 ppm for 90 days (loxlgenlcs,
1983a). Clinical signs of Irritation and toxlclty were observed In rats In
the same study Intermittently exposed to 10.1 ppm, the lowest concentration
tested. Subchronlc dietary exposure to 15 but not 3.1 mg/kg/day resulted In
digestive disturbances and reduced body weight In pigs (Wetterau et al.,
1964).
0238d -51- 04/02/90
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Only one study on the mutagenlc potential of hydrogen sulflde was
located In the literature. Hughes et al. (1984) determined that hydrogen
sulHde was not mutagenlc. with or without activation, In three strains of
Salmonella typhlmurlum.
0238d -52- 04/02/90
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7. EXISTING GUIDELINES AND STANDARDS
7.1. HUMAN
A verified oral RfD for hydrogen sulflde 1s 0.003 mg/kg/day (U.S. EPA.
1989) based on a NOAEL of 3.1 mg/kg/day for body weight gain In a 105-day
feeding study In pigs (Wetterau et al., 1964).
ACGIH (1988) recommended a TWA-TLV of 10 ppm (14 mg/m3) and a STEL of
15 ppm (21 mg/m3), based on several reports of eye effects seen at concen-
trations <20 ppm (28 mg/m3) Including that of Nesswetha (1969) (ACGIH,
1986)'. The OSHA (1989) final rule was a TWA of 10 ppm and a STEL of 15 ppm,
also based on ocular effects, reduced from the earlier values of 20 and 50
ppm, respectively.
7.2. AQUATIC
The U.S.EPA/OWRS (1986) has recommended a criterion of 2 yg/i of
undlssoclated hydrogen sulflde for freshwater and marine water fish and
other aquatic life.
0238d -53- 04/02/90
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8. RISK ASSESSMENT
8.1. CARCINOGENICITY
8.1.1. Inhalation. No data were available to assess the carcinogenic
potential of hydrogen sulflde from Inhalation.
8.1.2. Oral. No data were available to assess the carcinogenic potential
of hydrogen sulflde from oral exposure.
8.1.3. Other Routes. No data were available to assess the carcinogenic
potential of hydrogen sulflde from other routes.
8.1.4. Weight of Evidence. Pertinent data regarding the carcinogenic
effect of hydrogen sulflde In humans or animals were not located In the
available literature cited In Appendix A. Using the U.S. EPA (1986b) class-
ification scheme, hydrogen sulflde may be assigned to U.S. EPA Group D - not
classifiable as to carclnogenlclty 1n humans.
8.1.5. Quantitative Risk Estimates. Pertinent data from which to
estimate cancer potency for Inhalation or oral exposure to hydrogen sulflde
were not located In the available literature cVted 1n Appendix A.
8.2. SYSTEMIC TOXICITY
8.2.1. Inhalation Exposure.
8.2.1.1. LESS THAN LIFETIME (SUBCHRONIC) -- Several animal subchronlc
Inhalation studies were available for consideration as the.basis for the
subchronlc Inhalation RfD: 90-day Inhalation -studies using mice and two
strains of rats (Toxlgenlcs, 1983a,b,c) (Recs. #6-10, Appendix C) and a
25-week neurotoxlclty study using rats (Gagnalre et al., 1986) (Rec. #5,
Appendix C). In the Toxlgenlcs (1983a,b,c) studies, effects on body weight,
food consumption, neurology and Inflammation of the nasal mucosa were seen
1n the mice exposed to 80 ppm hydrogen sulflde (111 mg/m3). In the rats,
adverse effects on body weights were found In all exposed groups (10.1, 30.5
and 80.0 ppm, or 14, 42.4 and 111 mg/m3) of both strains and signs of
0238d -54- 04/02/90
-------
adverse effects were found, but the exposure level for the appearance of the
clinical effects was not given (Tox1gen1cs, 1983b,c} (Recs. #8-10, Appendix
C). In the neurological study (Gagnalre et al., 1986) (Rec. #5, Appendix
C), only one concentration, 50 ppm (69.5 mg/m3), was tested and no effects
were observed. The exposure levels In all of these studies are more than an
order of magnitude greater than the LOAEL for neurological effects In the
human study described below.
In a human study, neurological effects were reported In a 20-month-old
child exposed to concentrations <0.6 ppm (0.83 mg/m3} hydrogen sulMde for
-1 year (Galtonde et al., 1987) (Rec. #1, Appendix C). The child's family
lived beside a colliery where a burning tip had been emitting hydrogen
sulflde. Upon admission to the hospital, toxic encephalopathy was diag-
nosed. The child was treated and recovered, Indicating the reversible
nature of the effect.
Occupational studies (see Sections 6.1.1.2. and 8.2.2.2.) suggest that
10 ppm may be near the threshold for Irritation and adverse effects In
occupatlonally exposed adults. Although the case report by Galtonde et al.
(1987) Is a very tenuous basis for an RfO because It Involves only one
Infant, the report Is strong evidence that the young may be unusually
sensitive to hydrogen sulf1de-1nduced neurotoxlclty. A provisional RfD for
subchronlc Inhalation exposure, therefore, may be based on the LOAEL of 0.83
mg/m3 In the Galtonde et al. (1987) report. For the purposes of risk
assessment, exposure Is assumed to be continuous. However, this concentra-
tion was a maximum reading, not a TWA. Using an uncertainty factor of 100
(10 for the use of a LOAEL, and 10 for the Inadequacies of the study), an
Inhalation subchronlc RfD of 8 ug/m3 Is derived. A factor to provide
additional protection for more sensitive Individuals Is not applied because
1t 1s assumed that the Infant In the Galtonde et al. (1987) report repre-
0238d -55- 04/02/90
-------
sents the most sensitive population group. Confidence In the key study Is
low because H was a report of only one child, and the reported exposure
concentration Is a maximum, not a TWA. Confidence In the data base Is
medium. Although this Is the only human subchronic Inhalation study avail-
able, a reasonable volume of data exists on acute and occupational exposure
to hydrogen sulflde. However, the absence of teratogenlclty and reproduc-
tive toxlclty data near the LOAEL of 0.83 mg/m3 used here lowers the
confidence In the data base from high to medium. Confidence In the sub-
chronic Inhalation RfD, therefore, Is low.
8.2.1.2. CHRONIC — Chronic Inhalation data are limited to occupa-
tional exposure studies. These studies Indicate that exposure to 10 ppm (15
mg/m3) hydrogen sulflde results In adverse health effects (Nesswetha,
1969), while exposure to <10 ppm (15 mg/m3) does not result In harmful
effects on workers (Poda, 1966). The occupational NOAEL of 10 ppm (15
mg/m3) Is the TLV for occupational exposure (ACGIH, 1988). The case
report by Galtonde et al. (1987) (Rec. #1, Appendix C) strongly Indicated
that Infants are much more sensitive than adults to the effects of hydrogen
sulflde. Adverse neurological effects were reported 1n a child exposed to
0.83 mg/m3 for 1 year. Dividing the occupational NOAEL of 15 mg/m3 by
an uncertainty factor of 10 to account for the most sensitive Individuals
results In a concentration of 1.5 mg/m3, which Is above the LOAEL in the
Galtonde et al. (1987) report and unsuitable as the basis for the RfD for
chronic Inhalation exposure. The necessity of an uncertainty factor to
expand from subchronic to chronic exposure Is debatable, because the period
of Infancy Is a subchronic phenomenon. Therefore, the RFD of 8 pg/m3
for subchronic Inhalation exposure Is adopted as the RfD for chronic
Inhalation exposure. As with the subchronic Inhalation RfD, confidence in
the study, data base and RfD are low, medium and low, respectively.
0238d -56- 04/02/90
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8.2.2. Oral Exposure.
8.2.2.1. LESS THAN LIFETIME (SUBCHRONIC) — The only subchronlc oral
data consist of an 105-day feeding study using pigs (Recs. #1 and 2.
Appendix C) (Wetterau et a!.. 1964), summarized by U.S. EPA (1989). In this
study, gastrointestinal disorders were reported In young (20 kg) pigs fed
hydrogen sulflde 1n the diet at a dose of 15 mg/kg/day for 105 days. The
dose conversion was made by U.S. EPA (1989). In the same study, a dose of
3.1 mg/kg/day In the food of adult pigs (78 kg body weight) had no effect on
body-weight gain. Therefore, a NOAEL of 3.1 mg/kg/day for body weight
changes {Rec. #1, Appendix C) and a LOAEL of 15 mg/kg/day for gastrointes-
tinal effects (Rec. #2. Appendix C) can be derived from this study. A
subchronlc oral RfD of 0.03 mg/kg/day can be derived using an uncertainty
factor of 100 (10 for Interspec.les differences and 10 for Intraspedes
differences). Confidence 1n the key study 1s low because the number of
animals was not reported and because no gross or hlstopathologlcal examina-
tions were performed. Confidence In an oral data base consisting of only
one study Is necessarily low. as Is confidence 1n the subchronlc oral RfD.
8.2.2.2. CHRONIC — No chronic oral studies were available for con-
sideration as the basis for the chronic oral RfD. U.S. EPA (1989} derived
and verified a chronic oral RfO for hydrogen sulflde of 0.003 mg/kg/day by
applying an uncertainty factor of 1000 (10 for Interspecles differences, 10
for Intraspedes differences and 10 to extrapolate from subchronlc exposure)
to the NOAEL of 3.1 mg/kg/day In pigs from the Wetterau et al. (1964) study
(Rec. #1. Appendix C). This chronic oral RfO of 0.003 mg/kg/day Is adopted
because no data were located that would provide a more suitable basis for
the RfD. Confidence In the study, data base and the chronic oral RfD are
low, as discussed In Section 8.2.2.1.
0238d -57- 04/02/90
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9. REPORTABLE QUANTITIES
9.1. BASED ON SYSTEMIC TOXICITY
The U.S. EPA (1983) determined that sufficient data for derivation of an
RQ were not available. Since 1983, new studies, (see Chapter 6) have been
published that provide a basis for derivation of an RQ. Data associating
observed adverse effects with the lowest concentrations or doses producing
them obtained from these studies and two older ones relevant for derivation
of CSs are summarized 1n Table 9-1. Subchronlc studies reporting no
nonartlfactual adverse effects (Gagnalre et al., 1986; Duan, 1959) were not
Included. Since the only chronic toxlclty data available are occupational
exposure studies [most of which are unsuitable for the derivation because
they report only the absence of effects (Hlgash! et al., 1983; Chan-Yeung et
al., 1980; Divine and. Barren. 1987) or supply Inadequate exposure data
(Arnold et al., 1985; Nesswetha, 1969)], Table 9-1 consists of data derived
from the subchronlc studies.
The responses listed In Table 9-1 may be sorted Into categories listed
1n descending severity, as follows: encephalopathy In an Infant (RV =3),
other neurological effects (RV =7), digestive disorders (RV =5), and
e e
body weight effects (RVg=4). The lowest equivalent human dose associated
with each of these effects was selected to construct Table 9-2, In which
composite scores (CS) and reportable quantities (RQ) were computed. An
uncertainty factor was applied to expand from subchronlc to chronic exposure
In all animal studies suitable for Inclusion In Table 9-2. An uncertainty
factor was not used for expansion from subchronlc to chronic exposure for
encephalopathy In an Infant for the reasons stated In Section 8.2.2.2.
RQ values of 100 were derived from Inhalation studies for encephalopathy
In a 20-month-old child (Galtonde et al., 1987) and other neurological
0238d -58- 04/02/90
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TABLE 9-1
i
tn
10
o
4*1
V.
o
to
o
Average Transformed
Route Species/ Sex No. at Height Vehicle Exposure Animal Dose
Strain Start (kg) Ing/kg/day)
Inhalation humans N 1 10° air <0.6 ppm (O.B4 rag/ra») NA
continuously for -12
months
•tee/ N,f 10. 12 0.03<) air BO ppn (111.51 mg/n>) 25.89'
B6C3M 6 hours/day, 5 days/
week for 90 days
rats/F344 N.F IS. IS 0.358 air 10. 1 ppa (14. 08 mg/m») l.bO«
6 hours/day. 5 days/
week for 90 days
humans N NR TO" air 20 ppm (21.68 mg/m»); NA
occupational exposure
Oral pigs NR NR 20* greens 10S days In feed 15. Ok
In food
Equivalent
Human Dose Response
(mg/kg/day)
0.19C Encephalopathy
In a 20-month-old
child; neurolo-
gical effects
l.95f Neuroloytcal
effects In mice
0.27* Body weight loss
In rats
2.84' Neurological
effects In workers
9.88r Digestive dis-
orders In pigs
Reference
Galtonde
el al.. 1967
Toxlgenlcs,
1983a
Toxlgenlcs.
1983b
Ahlborg, 19S1
Wetterau et
al.. 1964
'Purity not reported.
''Reference body weight of a child (U.S. fPA. 1986c)
CA dose of 0.36 mg/kg/day was calculated assuming an Infant body weight of 10 kg and computing an Inhalation rate of 4.26 m'/day from an algorithm
provided by U.S. EPA (1986c). The Human equivalent dose was obtained by multiplying the dose of 0.36 ng/kg/day by the cube root of 10 kg/70 kg to reflect
the greater basal metabolic rate of the Infant than the adult.
dReference mouse body weight (U.S. EPA. 1980)
'Calculated by converting the ppm concentration to mg/m», multiplying by the number of hours/day, number of days/week of exposure, and the animal
Inhalation rate (0.039 mVday for mice and 0.223 mVday for rats (U.S. [PA. 1980)] and dividing by the animal weight
Animal dose Is scaled to the human dose by surface scaling factor (body weight 2/3).
Reference rat body weight (U.S. EPA, 1980)
^Reference body weight of an adult (U.S. EPA. 1980)
Occupational exposure assumed an Inhalation rate of 10 mVday. 5 days/week
jBody weight of pig (Uetlerau et a)., 1964)
Sransformed animal dose (Wetterau et al.. 1964). calculated by U S. EPA (1989)
NA - Not applicable; NR = not reported
-------
0
ftj
to
CO
0.
TABLE 9-2
Composite Scores for Hydrogen Sulflde
Route/
Species
Inhalation/
human
Inhalation/
mice
g Inhalation/
1 rats
Oral/pigs
Chronic
Animal Dose Human MED*
(mg/kg/day) (mg/day)
NA 13.04
25.89 13.66C
1.60 1.92C
15 69.16C
RVd Effect RVe CS°
3.83 Encephalopathy 1n a 8 30.62
20-roonth-old child
3.80 Neurological 7 26.58
effects In mice
5.08 Body weight loss 4 20.30
1n rats
2.74 Digestive disorders 5 13.70
In pigs
RQ Reference
100 Gattonde et
at., 1967
100 Toxlgenlcs,
1983a
1000 Toxlgentcs.
1983b
1000 Uetterau
et al..
1964
Calculated by multiplying the equivalent human dose (Table 9-1) by 70 kg. the reference human body
weight (U.S. EPA. 1980)
^Decimals were not rounded In the chain of computation from reported concentration* or doses to the
composite score; the result was then rounded to two decimal places.
cThe dose was divided by an uncertainly factor of 10 to approximate chronic exposure.
NA = Not applicable
10
O
-------
effects In mice (Toxlgenlcs. 1983d). An RQ of 1000 was derived for body
weight effects 1n F344 rats (Toxlgenlcs, 19B3b) and digestive disorders In
pigs (Wetterman et al.. 1964; U.S. EPA. 1989). The CS of 30.62 for encepha-
lopathy in a human Infant (GaUondo et al., 1987), equivalent to an RQ of
100, Is chosen to represent the chronic (noncancer) toxlclty of hydrogen
sulflde (Table 9-3).
9.2. BASED ON CARCINOGENICITY
As noted In Section 6.1.. no data regarding the carcinogenic effect of
hydrogen sulflde In humans or animals are available. Hydrogen sulflde was
assigned to U.S. EPA (1986b) Group D: not classifiable as to human carctno-
genlclty. Hazard ranking Is not performed for Group D chemicals; therefore,
neither a potency factor nor an RQ was assigned on the basis of carcino-
genic Hy.
0238d -61- 04/02/90
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TABLE 9-3
Hydrogen Sulflde
Minimum Effective Dose (MED) and Reportable Quantity (RQ)
Route: Inhalation
Species/sex: human/male
Dose*: 13.04 rng/day
Duration: -12 months
Effect: encephalopathy In a 20-month-old child
RVd: 3.83
RVe: 8
CS: 30.62
RQ: 100
Reference: Galtonde et al., 1987
'Equivalent adult human dose
0238d -62- 04/02/90
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0238d -68- 04/02/90
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0238d -69- 04/02/90
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0238d -70- 04/02/90
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0238d -72- 04/02/90
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0238d -73- 04/02/90
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0238d -74- 04/02/90
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0238d -76- 04/02/90
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0238d -78- 04/02/90
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Winder, C.V. and H.O. Winder. 1933. The seat of action of sulMde on
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0238d -80- 04/02/90
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APPENDIX A
LITERATURE SEARCHED
This HEED Is based on data Identified by computerized literature
searches of the following:
CHEHLINE
TSCATS
CASR online (U.S. EPA Chemical Activities Status Report)
TOXLINE
TOXLIT
TOXLIT 65
RTECS
OHM TADS
STORE!
SRC Environmental Fate Data Bases
SANSS
AQUIRE
TSCAPP
NTIS
Federal Register
CAS ONLINE (Chemistry and Aquatic)
HSDB
SCISEARCH
Federal Research In Progress
These searches were conducted In May, 1989, and the following secondary
sources were reviewed:
ACGIH (American Conference of Governmental Industrial Hyglenlsts).
1986. Documentation of the Threshold Limit Values and Biological
Exposure Indices, 5th ed. Cincinnati, OH.
ACGIH (American Conference of Governmental Industrial Hyglenlsts).
1987. TLVs: Threshold Limit Values for Chemical Substances 1n the
Work Environment adopted by ACGIH with Intended Changes for
1987-1988. Cincinnati, OH. 114 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed.. Vol. 2A. John Wiley and
Sons, NY. 2878 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed.. Vol. 28. John Wiley and
Sons, NY. p. 2879-3816.
0238d -81- 09/11/89
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Clayton, G.D. and F.E. Clayton, Ed. 1982. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2C. John Wiley and
Sons, NY. p. 3817-5112.
Grayson, M. and 0. Eckroth, Ed. 1978-1984. Klrk-Othmer Encyclo-
pedia of Chemical Technology, 3rd ed. John Wiley and Sons, NY. 23
Volumes.
Hamilton, A. and H.L. Hardy. 1974. Industrial Toxicology, 3rd ed.
Publishing Sciences Group, Inc., Littleton, MA. 575 p.
IARC (International Agency for Research on Cancer). IARC Mono-
graphs on the Evaluation of Carcinogenic Risk of Chemicals to
Humans. IARC, WHO, Lyons, France.
Jaber, H.M., W.R. Habey, A.T. Lieu, T.W. Chou and H.L. Johnson.
1984. Data acquisition for environmental transport and fate
screening for compounds of Interest to the Office of Solid Waste.
EPA 600/6-84-010. NTIS PB84-243906. SRI International, Menlo
Park, CA.
NTP (National Toxicology Program). 1987. Toxicology Research and
Testing Program. Chemicals on Standard Protocol. Management
Status.
Ouellette, R.P. and J.A. King. . 1977. Chemical Week Pesticide
Register. McGraw-Hill Book Co.. NY.
Sax, I.N. 1984. Dangerous Properties of Industrial Materials, 6th
ed. Van Nostrand Relnhold Co., NY.
SRI (Stanford Research Institute). 1987. Directory of Chemical
Producers. Menlo Park, CA.
U.S. EPA. 1986. Report on Status Report In the Special Review
Program, Registration Standards Program and the Data Call In
Programs. Registration Standards and the Data Call In Programs.
Office of Pesticide Programs, Washington, DC.
USITC (U.S. International Trade Commission). 1986. Synthetic
Organic Chemicals. U.S. Production and Sales, 1985, USITC Publ.
1892, Washington. DC.
Verschueren, K. 1983. Handbook of Environmental Data on Organic
Chemicals, 2nd ed. Van Nostrand Relnhold Co., NY.
Wlndholz, M., Ed. 1983. The Merck Index, 10th ed. Merck and Co.,
Inc., Rahway, NJ.
Worthing. C.R. and S.B. Walker, Ed. 1983. The Pesticide Manual.
British Crop Protection Council. 695 p.
0238d -82- 09/11/89
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In addition, approximately 30 compendia of aquatic toxldty data were
reviewed, Including the following:
Battelle's Columbus Laboratories. 1971. Water Quality Criteria
Data Book. Volume 3. Effects of Chemicals on Aquatic Life.
Selected Data from the Literature through 1968. Prepared for the
U.S. EPA under Contract No. 68-01-0007. Washington, DC.
Johnson, W.W. and M.T. Flnley. 1980. Handbook of Acute Toxldty
of Chemicals to Fish and Aquatic Invertebrates. Summaries of
Toxldty Tests Conducted at Columbia National Fisheries Research
Laboratory. 1965-1978. U.S. Dept. Interior, Fish and Wildlife
Serv. Res. Publ. 137, Washington, DC.
McKee, J.E. and H.W. Wolf. 1963. Water Quality Criteria, 2nd ed.
Prepared for the Resources Agency of California, State Water
Quality Control Board. Publ. No. 3-A.
Plmental, 0. 1971. Ecological Effects of Pesticides on Non-Target
Species. Prepared for the U.S. EPA, Washington, DC. PB-269605.
Schneider, B.A. 1979. Toxicology Handbook. Mammalian and Aquatic
Data. Book 1: Toxicology Data. Office of Pesticide Programs, U.S.
EPA. Washington, DC. EPA 540/9-79-003. NTIS PB 80-196876.
0238d -83- 09/11/89
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0
I\J
U>
00
o.
1
oo
4k
1
Species
Inhalation Exposure
Subchronlc human
Chronic human
Carclnogenlclty ID
Oral Exposure
Subchronlc pig
Chronic pig
Carclnogenlclty ID
91 PORTABLE QUANT 1 T 1 E S
Based on chronic toMlclty: 100
Based on Carclnogenlclty: • 10
APPENDIX B
Summary Table for Hydrogen Sulflde
Exposure Effect
0.6 ppm continuously encephalopathy In a
for 12 months 20-month-old child
0.6 ppm continuously encephalopathy In a
for 12 months 20-month-old child
10 ID
3.1 mg/kg/day In feed NOAEL for reduced
body weight gain
3.1 mg/kg/day In feed NOAEL for reduced
body weight gain
ID ID
RfO or qj* Reference
8 wg/rn* Galtonde et al..
1967
B pg/m* Galtonde et al..
1987
ID ID
0.03 mg/kg/day Wetterau et al.,
1964; U.S. EPA,
1989
0.003 mg/kg/day Hetterau et al..
1964; U.S. EPA.
1989
ID ID
Galtonde et al..
1987
10
10 . Insufficient data
CO
10
-------
APPENDIX C
DOSE/DURATION RESPONSE GRAPHS FOR EXPOSURE TO HYDROGEN SULFIDE
C.I. DISCUSSION
Dose-duration response graphs for Inhalation and oral exposure to
hydrogen sulflde generated by the method of Crockett et al. (1985) using the
computer software by Durkin and Meylan (1988) developed under contract to
ECAO-Clncinnati are presented In Figures C-l to C-3. Data used to generate
these graphs are presented In Section C.2. In generation of these figures,
all responses are classified as adverse (FEL, AEL or LOAEL) or nonadverse
(NOEL or NOAEL) for plotting. For Inhalation exposure In Figures C-l and
C-2, the experimental concentration expressed as mg/m3 was multiplied by
the time parameters of the exposure protocol (e.g., hours/day and days/week)
and Is presented as expanded experimental concentration (mg/m3). For oral
exposure, the ordlnate expresses dose as human equivalent dose (Figure C-3).
The animal dose In mg/kg/day Is multiplied by the cube root of the ratio of
the animal:human body weight to adjust for species differences In basal
metabolic rate (Mantel and Schnelderman, 1976). The result Is then
multiplied by 70 kg, the reference human body weight, to express the human
equivalent dose In mg/day for a 70 kg human.
The boundary for adverse effects (solid line) Is drawn to Identify the
lowest adverse effect dose or concentration at the shortest duration of
exposure at which an adverse effect occurred. From this point, an Infinite
line Is extended upward, parallel to the dose axis. The starting point is
then connected to the lowest adverse effect dose or concentration at the
next longer duration of exposure that has an adverse effect dose or concen-
tration equal to or lower than the previous one. This process Is continued
to the lowest adverse effect dose or concentration. From this point, a line
0238d -85- 09/11/89
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1*88
ia
8.1 r
88;
Kev
F .
A .
L •
K .
r •
Sd
FEL
AEi
LOAEL
NCEL
NOAEL
O Line -
Line
Adverse Effects Bounaa'-y
. Nc Aoverse Effects Eounoary
FIGURE C-l
Oose/Ouratlon-Response Graph for Inhalation Exposure to
Hydrogen Sulflde - Envelope Method
0238d
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f
t
fc
C
C
IMS
100 •-
1 T
IT
Ml?
L78
M
LI
1
1
0.01
( 1 n).4 1 « t i or, £xt>l>fur«)
0.M01 8.001 8.01
NUNAN IOUIU DURATION (fr*ctien
CEMSOR£D W»l* HCTNOP
0.1
F
A
L
N
n
FEL
ALL
LOAEl
NOEL
NOAEL
d Line •
Line
Adverse Effects Boundary
. Nc Adverse Effects Boundary
FIGURE C-2
Dose/Duration-Response Graph for Inhalation Exposure to
Hydrogen SulMde - Censored Data Method
0238d
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I
IMC
•
»
•
z
1*8 *•
-•1
18
.81
HUMAN EOUIV »UMT10N (fraction llfrSF4n>
<0r»l Exposure)
L • LOAEL
n . NOAEL
Solid Line .
Dashed Line
Adverse Effects Boundary
. No Adverse Effects Boundary
FIGURE C-3
Dose/Ouratlon-Response Graph for Oral Exposure to
Hydrogen SulMde - Censored Data Method
0238d
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Is extended to the right, parallel to the duration axis. This region of
adverse effects lies above the adverse effects boundary.
Using the envelope method, the boundary for no adverse effects (dashed
line) Is drawn by Identifying the highest no adverse effects dose or concen-
tration. From this point, a line parallel to the duration axis Is extended
to the dose or concentration axis. The starting point Is then connected to
the next lower or equal no adverse effect dose or concentration at a longer
duration of exposure. When this process can no longer be continued, a line
Is dropped parallel to the dose or concentration axis to the duration axis.
The region of no adverse dffects lies below the no adverse effects boundary.
At either ends of the graph between the adverse effects and no adverse
effects boundaries are regions of ambiguity. The area (If any) resulting
from Intersection of the adverse effects and no adverse effects boundaries
Is defined as the region of contradiction.
In the censored data method, all no adverse effect points located 1n the
region of contradiction are dropped from consideration and the no adverse
effect boundary Is redrawn so that It does not Intersect the adverse effects
boundary and no region of contradiction Is generated. This method results
in the most conservative definition of the no adverse effects region.
Figures C-l and C-2 present the dose/duration-response graphs for
Inhalation data using expanded exposure concentrations and generated by the
envelope and censored data methods, respectively. The adverse effects
boundary Is defined by an acute AEL for olfactory paralysis (Rec. #14) and a
LOAEL for eye Injury (Rec. #13) In exposed workers (Ammann, 1986), an acute
LOAEL In rats (Rec. #15) where exposure to hydrogen sulflde compromised the
antibacterial ability of the lungs, and a subchronlc LOAEL In humans for
neurotoxlc effects found In an Infant exposed to hydrogen sulflde for 1 year
0238d -89- 09/11/89
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(GaUonde et al., 1987) (Rec. #1). The Galtonde et al. (1987) study Is the
basis for the chronic and subchronlc Inhalation RfDs.
In the figure generated by the envelope method (Figure C-l), the no
adverse effects boundary Is defined by a NOEL for neurotoxlc effects In rats
(Gagnalre et al., 1986) (Rec. #5). In Figure C-2 (censored data method),
the no adverse effects boundary Is defined by a NOEL for Impaired anti-
bacterial ability of lungs of rats exposed to hydrogen sulflde (Rogers and
Ferln. 1981) (Rec. #16) and NOELs for respiratory system (Hlgashl et al.,
1983) '(Rec. #3) and pulmonary function effects (Chan-Yeung et al., 1980)
(Rec. #2) In occupationally exposed workers.
Using the envelope method, regions of contradiction are defined between
the human equivalent duration (fraction of llfespan) of -0.00004-0.2 In
Figures C-l and C-3. In the censored data method, these regions are
elImlnated.
Figure C-3 presents the dose/duration-response graph for oral data
generated by the envelope method. The data represents the study by Wetterau
et al. (1964) and U.S. EPA (1989) where a LOAEL for gastrointestinal effects
(Rec. #2) and a NOAEL for effects on body weight In pigs (Rec. #1) are
defined. Since no Region of Contradiction Is defined, the censored data
method Is unnecessary. The NOAEL Is the basis for both the chronic and
subchronlc oral RfDs. No other oral studies were available.
C.2. DATA USED TO GENERATE DOSE/DURATION-RESPONSE GRAPHS
C.2.1. Inhalation Exposure.
Chemical Name: Hydrogen Sulflde
CAS Number: 7783-06-4
Document Title: Health and Environmental Effects Document on Hydrogen
Sulflde
Document Number: Pending
Document Date: Pending
Document Type: HEED
0238d -90- 09/11/89
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RECORD #1
Comment:
Citation:
Species:
Sex:
Effect:
Route:
Humans
Male
LOAEL
Inhalation
Dose:
Duration
Duration
Exposure:
Observation:
Number Exposed: 1
Number Responses: 1
Type of Effect: FUND
SHe of Effect: CNS
Severity Effect: 8
Up to 0.6 ppm. No other doses studied.
chronic RfD. 20-month-old child.
reversible.
Galtonde et al.. 1987; U.S. EPA, 1989
O.B36
1.0 years
1.0 years
Bases of subchronlc,
Neurotoxlc effects
RECORD #2:
Species: Humans
Sex: Male
Effect: NOEL
Dose: 0.020
Duration Exposure: 14.0 years
Duration Observation: 14.0 years
Route: Inhalation
Number Exposed:
Number Responses:
Type of Effect:
Site of Effect:
Severity Effect:
NR
0
7
Comment: 0.06 ppm, 8 hours/day, 5 days/week; studied 0.5, 0.6 ppm. No
effects on pulmonary function from hydrogen sulflde exposure.
Citation: Chan-Yeung et al., 1S80
RECORD #3:
Comment:
Citation:
Species:
Sex:
Effect:
Route:
Humans
Male
NOEL
Inhalation
Dose:
Duration Exposure:
Duration Observation:
0.430
12.3 years
12.3 years
Number Exposed: NR
Number Responses: 0
Type of Effect:
Site of Effect:
Severity Effect: 7
1.3 ppm, 8 hours/day, 5 days/week,
effects respiratory system.
Hlgashl et al.. 1983
Occupational study. No
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RECORD #4:
Species:
Sex:
Effect:
Route:
Humans
Male
NOEL
Inhalation
Dose:
Duration
Duration
Exposure:
Observation:
1.800
10.0 years
10.0 years
Number Exposed:
Number Responses
Type of Effect:
Site of Effect:
Severity Effect:
NR
0
Comment:
Citation:
RECORD #5:
5.5 ppm, 8 hours/day, 5
neurological effects.
Rubin and AMeff,
1945
Species: Rats
Sex: Male
Effect: NOEL
Route: Inhalation
Number Exposed:
Number Responses:
Type of Effect:
Site of Effect:
Severity Effect:
NR
0
6
days/week. Occupational study. No
Dose: 49.800
Duration Exposure: 25.0 weeks
Duration Observation: 25.0 weeks
Comment: 50 ppm, 5 days/week; studied one exposure level; no
neurotoxlc effects.
Citation: Gagnalre et al., 1986
RECORD #6:
Comment:
Citation:
Species:
Sex:
Effect:
Route:
Mice
Both
NOEL
Inhalation
Dose: 7.590
Duration Exposure: 90.0 days
Duration Observation: 90.0 days
Number Exposed: 22
Number Responses: 0
Type of Effect:
Site of Effect:
Severity Effect: 4
30.5 ppm. Studied 10.0, 30.5 and 80.0 ppm for 6 hours/day, 5
days/week. No weight effects.
loxlgenlcs, 1983a
0238d
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RECORD #7:
Comment:
Citation:
RECORD #8:
Species: Mice
Sex: Both
Effect: LOAEL
Route: Inhalation
Number Exposed:
Number Responses:
Type of Effect:
SHe of Effect:
Severity Effect:
80 ppm. Studied 10
Toxlgenlcs, 1983a
22
NR
FUND
CMS
7
.1, 30.5,
Species: Rats
Sex: Both
Effect: LOAEL
Route: Inhalation
Number Exposed:
Number Responses:
Type of Effect:
SHe of Effect:
Severity Effect:
30
NR
WGTDC
BODY
4
Dose:
Duration
Duration
22
NR
WG10C
BODY
4
80 ppm, 6
Dose:
Duration
Duration
19.900
Exposure: 90.0 days
Observation: 90.0 days
22
NR
1KRIT
NASAL
4
hours/day, 5 days/week.
2.500
Exposure: 90.0 days
Observation: 90.0 days
Comment:
Citation:
RECORD #9:
10.1 ppm. 6 hours/day,
ppm. Fischer 344 rats
Toxlgenlcs, 1983b
Species: Rats
Sex: Both
Effect: NOAEL
Route: Inhalation
5 days/week. Studied 10.1,
were used.
Dose:
Duration Exposure:
Duration Observation:
30.5, 80.0
7.590
90.0 days
90.0 days
Comment:
Citation:
Number Exposed: 30
Number Responses: 0
Type of Effect:
Site of Effect:
Severity Effect: 4
30.5 ppm, 6 hours/day, 5 days/week. Studied 10.1, 30.5, 80
ppm. No decrease In body weight. Sprague-Oawley rats used.
loxlgenlcs, 1983c
0236d
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RECORD #10:
Comment:
Citation:
Species:
Sex:
Effect:
Route:
Rats
Both
LOAEL
Inhalation
Dose: 19.900
Duration Exposure: 90.0 days
Duration Observation: 90.0 days
Number Exposed: 30
Number Responses: NR
Type of Effect: WGTDC
Site of Effect: BODY
Severity Effect: 4
80 ppm. Protocol In previous record.
Toxlgenlcs, 1983c
Sprague-Dawley,
RECORD #11: Species
Sex:
Effect:
Route:
Number
Number
: Humans
Male
NOEL
Inhalation
Exposed: 30
Responses: 0
Dose:
Duration Exposure:
Duration Observation:
3.620
1 .0 days
1 .0 days
Type of Effect:
Site of Effect:
Severity Effect: 7
Comment: 7.8 ppm, 8 hours. Occupational exposure to 0.3-7.8 ppm.
effect on pulmonary function tests after workshlft.
Citation: Hlgashl et al., 1983
No
RECORD #12:
Comment:
Citation:
Species:
Sex:
Effect:
Route:
Humans
NR
NOEL
Inhalation
Dose: 2.320
Duration Exposure: 1.0 days
Duration Observation: 1.0 days
Number Exposed: NR
Number Responses: 0
Type of Effect:
Site of Effect:
Severity Effect: 7
5 ppm. Reviewed 3-5 ppm, >50, 150-200, 300-500, 500-1000
ppm, 8 hours (assumed). Occupational exposure; offensive
odor. No eye Injury or pulmonary edema.
Ammann, 1986
0238d
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09/11/89
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RECORD #13:
Species:
Sex:
Effect:
Route:
Humans
NR
LOAEL
Inhalation
Number Exposed: NR
Number Responses: NR
lype of Effect: DEGEN
Site of Effect: EYE
Severity Effect: 7
Dose: 23.200
Duration Exposure: 1.0 days
Duration Observation: 1.0 days
NR
NR
EXCRE
LUNG
7
RECORD #14:
Comment:
Citation:
RECORD #15:
Species: Humans Dose: 69.700
Sex: NR Duration Exposure: 1.0 days
Effect: AEL Duration Observation: 1,0 days
Route: Inhalation
Number Exposed:
Number Responses:
Type of Effect:
Site of Effect:
Severity Effect:
150 ppm. Protocols
Ammann, 1986
NR
NR
SENSO
SENSR
9
In previous record. Olfactory paralysis.
Species: Rats Dose: 10.500
Sex: Male Duration Exposure: 1.0 days
Effect: LOAEL Duration Observation: 1.0 days
Route: Inhalation
Number Exposed:
Number Responses:
lype of Effect:
SHe of Effect:
Severity Effect:
3
NR
FUNS
PULMN
3
Comment:
Citation:
45 ppm, 4 hours. Studied 45-46 ppm for
Impaired antibacterial ability of lungs.
Rogers and Ferln, 1981
2, 4 or 6 hours.
0238d
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RECORD #16:
Comment:
Citation:
Species:
Sex:
Effect:
Route:
Rats
Male
NOEL
Inhalation
Dose: 5.340
Duration Exposure: 1.0 days
Duration Observation: 1.0 days
Number Exposed:
Number Responses:
lype of Effect:
Site of Effect:
Severity Effect:
3
0
Comment:
Citation:
RECORD #17:
46 ppm for 2 hours
Rogers and Ferln,
. Protocol
1981
Species: Rats
Sex: Male
Effect: NOEL
Route: Inhalation
Number Exposed:
Number Responses:
12
0
previous record.
Dose:
Duration Exposure:
Duration Observation:
46.500
1 .0 days
1 .0 days
Type of Effect:
Site of Effect:
Severity Effect:
Comment:
Citation:
RECORD #18:
200 ppm, 4
Injury. No
Lopez et al
Species:
Sex:
Effect:
Route:
hours.
pulonary
.. 1987,
Studied
edema .
1988a
Rats
Male
LOAEL
Inhalation
0, 10. 200,
Dose:
Duration
Duration
400 ppm.
Exposure:
Observation:
No nasal
92.
1.0
1.0
900
days
days
--
Number Exposed: 12 12
Number Responses: NR NR
Type of Effect: IRRIT FUNP
Site of Effect: NASAL PULMN
Severity Effect: 5 8
400 ppm. Studied 0, 10, 200, 400 ppm, 4 hours
Injury; pulmonary edema.
Lopes et al., 1987. 1988a
Nasal
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RECORD #19:
Species:
Sex:
Effect:
Route:
Rats
Male
NOEL
Inhalation
Dose: 19.300
Duration Exposure: 1.0 days
Duration Observation: 1.0 days
Number Exposed:
Number Responses:
Type of Effect:
SHe of Effect:
Severity Effect:
12
0
Comment:
Citation:
RECORD #20:
Comment:
Citation:
RECORD #21:
Comment:
Citation:
83 ppm, 4 hours. Studied 83, 439 ppm. No pulmonary edema.
Lopez et al., 1988b
Species: Rats Dose: 102.000
Sex: Male Duration Exposure: 1.0 days
Effect: AEL Duration Observation: 1.0 days
Route: Inhalation
Number Exposed:
Number Responses:
Type of Effect:
Site of Effect:
Severity Effect:
439 ppm. Protocols
Lopez et al., 1988b
12
NR
FUNP
PULMN
8
previous record. Pulmonary edema.
Species: Rats Dose: 103.100
Sex: Both Duration Exposure: 1.0 days
Effect: PEL Duration Observation: 1.0 days
Route: Inhalation
Number Exposed:
Number Responses:
Type of Effect:
Site of Effect:
Severity Effect:
444 ppm, 4 hours. I
lansy et al., 1981
10
NR
DEATH
BODY
10
.CSQ value.
0238d
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RECORD #22:
Comment:
Citation:
RECORD #23:
Comment:
Citation:
RECORD #24:
Comment:
Citation:
Species: Rats Dose: 116.000
Sex: Both Duration Exposure: 1.0 days
Effect: FEL Duration Observation: 1.0 days
Route: Inhalation
Number Exposed: NR
Number Responses: NR
Type of Effect: DEATH
Site of Effect: BODY
Severity Effect: 10
335 ppm, 6 hours. LC5Q value.
Prior et al.. 1988
Species: Rats Dose: 116.000
Sex: Both Duration Exposure: 1.0 days
Effect: FEL Duration Observation: 1.0 days
Route: Inhalation
Number Exposed: NR
Number Responses: NR
Type of Effect: DEATH
Site of Effect: BODY
Severity Effect: 10
501 ppm, 4 hours. LCso value.
Prior et al., 1988
Species: Rats Dose: 68.200
Sex: Both Duration Exposure: 1.0 days
Effect: FEL Duration Observation: 1.0 days
Route: Inhalation
Number Exposed: NR
Number Responses: NR
Type of Effect: DEATH
Site of Effect: BODY
Severity Effect: 10
587 ppm, 2 hours. LCsg value.
Prior et al.. 1988
0238d
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C.2.2. Oral Exposure.
CChemlcal Name: Hydrogen Sulflde
CAS Number:
Document Title:
Document Number
Document Date:
Document Type:
7783-06-4
Health and Environmental Effects Document on Hydrogen
Sulflde
Pending
Pending
HEED
RECORD
Comment:
Citation:
Species:
Sex:
Effect:
Route:
Other/NOS
NR
NOAEL
Food
Dose:
Duration Exposure:
Duration Observation:
3.100
105.0 days
105.0 days
Number Exposed: NR
Number Responses: 0
Type of Effect:
Site of Effect:
Severity Effect: 4
Middle dose of 3, converted from food data by U.S. EPA
(1989). No weight effects. Basis of subchronlc and chronic
oral RfD.
Wetterau et a!., 1964; U.S. EPA, 1989
RECORD #2:
Species:
Sex:
Effect:
Route:
Other/NOS
NR
LOAEL
Food
Dose:
Duration
Duration
Exposure:
Observation:
15.000
105.0 days
105.0 days
Comment:
Citation:
Number Exposed: NR
Number Responses: NR
Type of Effect: IRRIT
SHe of Effect: COLON
Severity Effect: 5
Pigs1 dose levels converted from food data by U.S. EPA
(1989}. Gastrointestinal disturbances.
Wetterau et al., 1964; U.S. EPA, 1989
NR =• Not reported
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