United States
Environmental Protection
Agency
Office of Mobile Source Air Pollution Control
Emission Control Technology Division
2565 Plymouth Road
Ann Arbor, Ml 48105
ePA-A6'j/3-81-028
Air
Hydrogen Sulfide Health Effects
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HYDROGEN SULFIDE HEALTH EFFECTS
with Contributions by
Bonnie L. Carson Harry V. Ellis III
Cecily M. Beall Larry H. Baker
Joy L. McCann
FINAL TASK 4 REPORT
September 15, 1981
Contract No. 68-03-2928
Task Specification No. 4
"Health Effects Support for the Emission Control
Technology Division"
MRI Project No. 4997-T(4)
For
Emission Control Technology Division
Office of Mobile Source Air Pollution Control
U.S. Environmental Protection Agency
2565 Plymouth Road
Ann Arbor, Michigan 48105
Attn: Robert J. Garbe
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PREFACE
This report on health effects of hydrogen sulfide was prepared by Mid-
west Research Institute (MRI) as Task No. 4 under Contract No. 68-03-2928,
"Health Effects Support for the Emission Control Technology Division" for
the U.S. Environmental Protection Agency.
Health effects literature primarily related to inhalation exposures to
hydrogen sulfide has been collected, evaluated, tabulated, and summarized
so that this report can be used to derive a range of concern for human ex-
posure to vehicular atmospheric emissions of hydrogen sulfide.
Task activities were coordinated by the project leader, Mrs. Bonnie L.
Carson, Senior Chemist, and task leader, Ms. Cecily M. Beall, Assistant
Scientist. Documents were rated and summarized by senior pharmacologist
Harry V. Ellis III, of MRI, and epidemiologist Larry H. Baker, M.D. , MRI
consultant, who is an Associate Professor in the Department of Community
Health at the University of Kansas Medical Center. Data were tabulated by
Ms. Beall; Ms. Joy L. McCann, Assistant Scientist; and Ms. Eileen M. Horn,
Junior Chemist. Ms. Beall and Mrs. Carson contributed to the annotated
bibliography. This study was performed under the general supervision of
Dr. Edward W. Lawless, Head, Chemical Impact Assessment Section.
Mr. Robert J. Garbe was the project officer for the Emission Control
Technology Division, U.S. Environmental Protection Agency, and Ms. Colleen
DeMeyer served as Branch Technical Representative.
Approved for:
MIDWEST RESEARCH INSTITUTE
Bruce W. Macy, Directr
Center for Technoeconomic
Analysis
111
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CONTENTS
Preface ii
Figures vi
Tables vi
Summary • • 1
Goals and methods 1
Bioassays • • 2
Animal exposures ...... 2
Human exposure . 5
International recommendations and standards 11
Recommended range of concern 13
Introduction 15
Bioassays ...-..' 19
Experimental Animal Inhalation Exposures 25
Experimental Human Inhalation Exposures 73
Epidemiology 81
Occupational exposures 81
Exposures of the general public 81
Bibliography • • ' • • 89
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FIGURES
Number Page
1-1 Form for Report Rating 16
TABLES
Number Page
S-l Summary of Animal Exposures to H2S 3
S-2 Summary of Human Experimental Exposure to H2S 6
S-3 Summary of Occupational and Epidemiological Exposures
to H2S 8
S-4 Summary of Regulations and Recommendations for Human
H2S Exposure 12
II-l Bioassays 20
III-l Canaries—Acute Experimental Exposure to H2S 26
III-2 Mice—Acute Experimental Exposure to H2S 28
III-3 Mice—Repeated Dose Experimental Exposure to H2S .... 31
III-4 Mice—Chronic Experimental Exposure to H2S 32
III-5 Rats—Acute Experimental Exposure to H2S 33
III-6 Rats—Repeated Dose Experimental Exposure to H2S .... 36
III-7 Rats—Chronic Experimental Exposure to H2S 40
III-8 Guinea Pigs—Acute Experimental Exposure to H2S 43
III-9 Guinea Pigs—Repeated Dose Experimental Exposure to
H2S 44
111-10 Chickens—Acute Experimental Exposure to H2S 47
III-ll Rabbits—Acute Experimental Exposure to H2S. ...... 51
111-12 Rabbits--Repeated Dose Experimental Exposure to H2S. . . 53
vi
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TABLES (continued)
Number
111-13 Rabbits—Chronic Experimental Exposure to H2S 54
111-14 Cats—Acute Experimental Exposure to H2S 55
111-15 Cats—Repeated Dose Experimental Exposure to H2S .... 57
111-16 Monkeys—Acute Experimental Exposure to H2S 58
111-17 Monkeys—Chronic Experimental Exposure to H2S 59
111-18 Dogs—Acute Experimental Exposure to H2S 60
III-19 Dogs—Repeated Dose Experimental Exposure to H2S .... 62
111-20 Pigs—Repeated Dose Experimental Exposure to H2S .... 63
111-21 Goats—Acute Experimental Exposure to H2S 64
111-22 Goats—Repeated Dose Experimental Exposure to H2S. ... 65
111-23 Cows—Repeated Dose Experimental Exposure to H2S .... 66
111-24 Summary of Animal Exposures to H2S . 67
IV-1 Humans—Acute Experimental Inhalation Exposure to H2S. . 74
V-l Studies of Occupational Exposure to H2S 82
V-2 Epidemiological Studies Relevant to H2S Exposure .... 87
Vll
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SUMMARY
This chapter is organized into the following sections: Goals and Meth-
ods, Bioassays, Animal Exposures, Human Exposure, International Recommenda-
tions and Standards, and Recommended Range of Concern.
GOALS AND METHODS
The purpose of this compilation of data on hydrogen sulfide (H2S) in-
halation exposures is to assist the Emission Control Technology Division
(ECTD) of the U.S. Environmental Protection Agency (EPA) to establish the
ranges of exposure conditions that are of concern for H2S in exhausts from
vehicles equipped with catalytic converters, and to be able to advise auto-
mobile manufacturers thereof. The situations of concern are during malfunc-
tions and during exposures in traffic jams, parking and home garages, and
other situations where little dilution of the exhaust is expected before
inhalation. Most of the report is, as directed by ECTD, in the form of
tables based on the literature reviewed. Data from exposures at levels
higher than those of primary concern are included because strictly relevant
information was scarce and these related data might prove helpful in assess-
ing health effects at lower levels.
Documents on inhalation effects of H2S identified from manuals and com-
puterized literature searches were rated in a two-step process by the project
pharmacologist and epidemiologist. First, the document received an A, B,
C, or D rating according to its applicability for deriving a range of concern
for H2S in automobile emissions. Second, if the paper was not a low-rated,
foreign language document,* a theoretical paper, a review, or a nontoxicol-
ogy experimental paper, it received a numerical score based on itemized
features that should be present in an ideal report. For the most part,
only A- and B-rated documents were tabulated; but when any C-rated studies
involved low-level H2S exposures, these were also tabulated. Blanks in the
tables should be construed as denoting missing information in the documents.
Most foreign language articles rated C and D were usually not translated.
Each foreign language document tentatively rated A or B from an English
language abstract or brief examination of the paper was translated in
sufficient degree to judge the experimental design and details. These
papers were numerically scored from the translation.
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BIOASSAYS
Only five studies using cell cultures or tissue sections were found.
They are fully described in Table II-l, and appear to have little informa-
tion directly useful to this task on human exposure to low H2S levels.
Tracheal tissue ciliary activity is one protective mechanism against
infection. The results of Cralley's (1942) study indicate that this ability
is permanently damaged in rabbits by high levels (400-600 ppm) of H2S. This
suggests the possibility of some ciliary inhibition at lower levels. However,
no studies were found that used more pertinent H2S concentrations.
Lung cell phagocytic ability is a second mechanism protecting against
infection. The results of Robinson's (1979 and 1980) studies suggest that,
in rabbits, the complete expression of whatever cellular lesion that is re-
sponsible for a decrease in phagocytic ability following exposure to 50,
60, or 200 ppm H2S is delayed. The effect appears to be dose-dependent, in
terms of both time and concentration. The results of Robinson (1980) indi-
cate that continuous exposure is more detrimental than intermittent exposure
(for the same total exposure time), though some of the data from Robinson
(1979) might suggest the reverse. Considering the lower levels of H2S likely
to be found in automobile exhaust and the short exposure times to even those
levels, extrapolation of these data suggests that there will be little effect
of an individual exposure on phagocytic ability. The effect of the repetition
of these exposures, however, cannot be estimated. The author plans similar
studies at ^ 50 ppm in the future. The low ratings of these studies are at
least partially because only abstracts of the works were available for
evaluation.
The study reported in Husain (1976) and Husain and Zaidi (1977) con-
cerns the effect of H2S (18-500 ppm) on various enzyme activities in rat
lungs. A dose-dependent relationship, not necessarily linear, appears to
exist, suggesting that some slight changes of unknown significance may occur
at lower H2S levels. The authors believe that these enzyme changes could
lead to the deprivation of amino acids needed for protein biosynthesis in
lung tissue.
ANIMAL EXPOSURES
This portion of the report summarizes the data available from animal
studies. The studies are listed in a series of tables, cited below, and
given in Section 3. A summary Table S-l is given in this section for H2S
levels ^28.4 mg/m3 (twice the TLV). Unfortunately, most studies involved
high and even lethal doses, not minimal ones, so there are little data to
aid in determining the lowest range of concern for human exposure.
Studies on acute (< 8 h) exposure to levels £ 1,000 mg H2S/m3 (up to
~ 46,000 mg/m3) have been made by four groups of investigators (Lehmann,
1892; Mitchell and Yant, 1925; Weedon et al., 1940; Klentz and Fedde, 1978)
on a wide range of animals arid the results are summarized as follows: ca-
naries (Table II-l), mice (Table III-2), rats (Table III-5), guinea pigs
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TABLE S-l. SUMMARY OF ANIMAL EXPOSURES TO
Img/nr1)
Time
Species
Effects
28.4
28.4
28.4
28.4
28.4
28.4
22.7
22.7
14.2
14.2
14.2
14
12.1
10
10
4.86-
9.36
0.02
48 h MI'S Decreased food and water intake and rectal
temperature. Weight loss.
90 d MUS Some mortality, survivors showing brain,
liver, and lung abcesses. Survivors lost
weight, had less endurance, and bad in-
stances of bronchopneumonia and hepatitis.
90 d RAT 24% mortality, weight loss, lung pathology,
and significant changes in many blood param-
eters .
1 h/d; GPG Fatigue, somnolence, dizziness, itching, and
11 d eye irritation. Decreased lipids in cerebral
hemisphere and brain stem.
90 d MKY Weight loss. Changes in many blood param-
eters .
21 d COW No effect on feed intake, milk production,
or heart rate. Slight lacrimation.
16 h MUS Slight restlessness. Normal autopsy.
16 h RAT Slight initial restlessness.
5 d MUS Initial decrease in temperature. Decreased
food and water intake, with some recovery by
the end.
41 d RAT Also under cold stress, and showed decreased
weight gain and food utilization. No changes
in blood cells, plasma protein, or weight of
liver and lungs.
4 d GOAT Initial decrease in food and water intake.
7 h/d; DOG Some coughing. Increased water consumption
14 d after each exposure. No change in blood
picture or body weight.
17 d PIG NOEL for body weight gain and respiratory
system.
3 h/d; RAT Weight gain retarded. Changes in motor
3 mo chronaxy. Irritation of mucous membranes
of trachea and bronchi.
6 h/d; RAT Retarded weight gain. Changes in some
4 mo blood parameters (increased hemoglobin).
02 consumption decreased by the end.
Changes in lung and heart enzyme activity.
6 h/d; RAT Decreased liver glycogen and lipid levels,
4 mo blood sugar, and erythrocytes. Increased
blood lipids, hemoglobin, and leukocytes.
12 h/d; RAT Changes in motor chronaxy. No change in
3 mo weight. No pathological changes found in
sacrificed animals.
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(Table III-8), chickens (Table 111-10), rabbits (Table III-ll), cats (Table III-
14), dogs (Table 111-18), and goats (Table 111-21). At the highest levels
there was immediate distress, sometimes death, and usually quick recovery
of the survivors. The exposures were longer at the lower levels, symptoms
developed more slowly, some deaths still occurred, and recovery frequently
was slower. The symptoms imply mucous membrane irritation of the eyes and
respiratory tract, and hypoxia. Acute exposures of the same species to
^ 350 to ~ 700 mg H2S/m3 caused similar effects in somewhat longer time
periods (up to 22 h). The discrepancies between studies on the same species
can probably be attributed to the very low numbers of animals used (gener-
ally 1 to 4), the different strains used, and variations in individual sus-
ceptibility.
In studies of H2S concentrations < 350 mg/m3, the symptoms become less
severe and the exposure times increase. The acute and intermittent exposures
are most directly applicable to this task on human exposure to automobile
exhaust in confined or congested situations. The chronic studies, however,
can be used to confirm the lack of toxicity or to point out possible adverse
effects not considered before.
Hays (1972) found some deaths in mice exposed to even the lowest level
studied, 41.6 mg/m3, with a 16-h exposure (Table III-2). However, 48-h ex-
posure to 28.4 mg/m3 and 120-h exposure to 14.2 mg/m3 (Table III-3) produced
no deaths, although there were toxic effects (on body weight gain and feed
intake). Sandage (1961) exposed mice to 28.4 mg/m3 for 90 d (Table III-4)
and found considerable toxicity: weight loss, increased spontaneous deaths,
lung lesions, and an odd pattern of hematologic effects which may be par-
tially compensated anemia (increased erythrocyte production not quite matching
increased destruction).
In repeated dose studies, Renne and McDonald (1979 and 1980) found no
changes in the major organs of rats exposed to 312.4 mg H2S/m3 for 22 d or
to 142 mg/m3 for 7 d (Table III-6). Sandage (1961) found that rats given
28.4 mg/m3 for 90 d were much like mice: weight loss, increased unscheduled
deaths, and lung pathology. Stolpe et al. (1976) found that the combination
of 14.2 mg H2S/m3 and low temperature (10°C) for 41 d produced additive
toxicity (decreased feed utilization, weight gain).
Chronic studies with rats (Table III-7) show definite toxicity (retarda-
tion of weight gain, and possible slight nerve cell dysfunction) from repeated
exposures (6 h/d for 4 mo) to 10 mg/m3 (Duan, 1959). One study (Elebekova
et al., 1976) reports many changes in hematologic and metabolic parameters
after exposure to 4.86 mg/m3 for 6 h/d for 4 mo.
Most studies (Tables III-8 and III-9) report guinea pigs as responding
similarly to rats to H2S exposure (Mitchell and Yant, 1925; Renne and McDonald,
1979). One study (Renne and McDonald, 1980), however, reports guinea pigs
having an inflammatory response after a 22-d exposure to 312.4 mg/m3, while
rats were unaffected.
In repeated dose studies with rabbits (Table 111-12), Weise (1933) found
little, if any, effects from 20 exposures to 14.2 to 42.6 mg H2S/m3. Chronic
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studies (Table 111-13) reported only slight, temporary effects caused by
exposure to 28.4 to 35.5 mg/m3 for 4 h/d for 150 d (Kuwai, 1960) or to
142 mg/m3 for 30 min/d for 4 mo (Wakatsuki, 1959).
Monkeys may be among the more sensitive species to higher levels of
H2S. Lund and Wieland (1966) found that less than half an hour of 710 mg/m3
was lethal to rhesus monkeys, with significant individual variability
(Table 111-16). However, in one of the more useful studies, Sandage (1961)
exposed monkeys to 28.4 mg/m3 for 90 d (Table 111-17). He found signficant
weight loss but no major specific toxic effects, compared to more severe
reactions by mice and rats to the same exposure.
The lowest dose (146.3 mg/m3) tested by Mitchell and Yant (1925) was
lethal to dogs in 16 h (Table 111-18). However, Moser (1940) exposed dogs
to 130 to 150 mg/m3 7 h/d for ~ 8 wk, and found acute signs implying irrita-
tion (coughing, thirst, tearing, conjunctivitis). Exposure to 14 mg/m3 for
7 h/d had no major toxic effects, with complete recovery before the next
day's exposure (Table 111-19).
Only slight effects were found in larger mammals repeatedly exposed to
lower H2S levels. Curtis et al. (1975) found pigs unaffected by 17 d at
12.1 mg H2S/m3 or 19 d at 2.84 mg H2S/m3 plus 36 mg NH3/m3 (Table 111-20).
Hays (1972) found several indications of stress in goats exposed to 71 or
142 mg/m3 for 4 d. He also reported minimal toxic effects (decreased feed
and water intake) the first day goats were exposed to 14.2 mg/m3, but re-
covery by the end of the 4-d study (Table 111-22). Cows were unaffected by
21 d of 28.4 mg H2S/m3 (Hays, 1972; Table 111-23).
Overall, there are few studies in the area of uncertainty for adverse
health effects (^ TLV). Most studies involve high and even lethal doses.
Specific toxic signs imply that the primary effects of H2S are irritation
of mucous membranes and hypoxia via the well-known subcellular effects.
There is limited evidence that large animals are less susceptible and that
some tolerance develops. From these animal data, the upper limit of the
range of concern should be about 15 mg/m3, which is the TLV (ACGIH, 1978).
There are no animal data for defining a lower limit.
HUMAN EXPOSURE
This section of the report summarizes the data available from human
experimental and human environmental (occupational and epidemiological)
studies. The most significant studies are cited below, and all studies are
described in Sections 4 and 5. Summary Tables S-2 and S-3 are given in
this section. A discussion of confounding factors in human environmental
studies is included.
Human Experimental Studies
Human studies are relatively limited. Lehmann (1892) did a large number
of high dose short-term experiments (see Table IV-1). His basic finding
was irritation of mucous membranes (eyes, respiratory tract).
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TABLE S-2. SUMMARY OF HUMAN EXPERIMENTAL EXPOSURE TO H2S
Level
(mg/m3)
Exposure Table
Effects
3,499-
8,165
Acute
IV-1
1,420-
4,700
994-
1,988
284-
568
0.20-
0.96
0.08-
0.50
0.27
0.15
0.1
0.031-
0.09
0.012-
0.03
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
Acute
IV-1
IV-1
IV-1
IV-1
Eye, nose, and mouth irritations, leading
to congestion and secretion. Higher ex-
posures also caused dizziness, trembling,
numbness, and heart palpitations. After-
wards, swollen and light-sensitive eyes,
headache, fatigue, diarrhea, and bladder
tenesmus lasting from several hours to a
day.
Irritation of eyes, nose, throat, and
trachea, leading to tearing, swelling, and
catarrh. Symptoms increased with increas-
ing time and concentration. Sometimes irri-
tation and headache continued for several
hours after exposure stopped.
Weak irritation of the eyes and throat at
the lower levels. At the highest level,
bronchitis, rhinitis, and heavy conjunc-
tivitis lasted up to 4 d.
No signs of irritation, as determined by
cursory observation and subjective reaction.
All people in the test group detected the
odor.
IV-1 Range of odor thresholds within a group.
IV-1 Range of odor thresholds within a group.
IV-1 Threshold of objectionability (not odor).
IV-1 Most people in the test group detected the
odor.
IV-1 Some of the people in the test group de-
tected the odor.
IV-1 Range of odor thresholds within a group.
(continued)
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TABLE S-2. (concluded)
Level
(mg/m3)
Exposure Table
Effects
0.012
0.026
0.012-
0.013
(2 studies)
0.010
(2 studies)
0.005-
0.009
0.008
0.00067
Acute IV-1 Odor was not detected.
Acute IV-1 Increased light sensitivity-related eye
responses.
Acute IV-1 One study found significantly increased
light sensitivity-related eye responses.
The other study did not.
Acute IV-1 Range of "calculated" odor thresholds
within several groups.
Acute IV-1 No effect on the ability of the eye to
adapt to darkness.
Acute IV-1 Lowest concentration at which all subjects
recognized the odor.
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TABLE S-3. SUMMARY OF OCCUPATIONAL AND EPIDEMIOLOGICAL EXPOSURES TO H2S
Level Exposure
(mg/m3) time Table
Effects
^ 28.4-
> 852
(and low
concns. of
HCN, S02,
CS2, hydro-
carbons)
326.6
40-185
142
Acute" V-l
13.7-
36.6
15-35
28.4
(often ex-
ceeded)
7.1-14.2
(and S02 and
lower ali-
phatic com-
pounds)
7.1-14.2
(and S02)
< 14.2
20 min V-l
Acute,
repeated
"Acute"
5-15 y
V-l
V-l
V-l
V-l
V-l
V-l
V-l
V-l
Fatigue, dizziness, unconsciousness with or
without respiratory failure. Rapid recovery
(0.5 h) except for some nervous symptoms
possibly lasting up to 1.5 mo.
Unconsciousness, cramping, slow and shallow
breathing, and low blood pressure. Fully
recovered in 6 mo.
Within several hours, many signs of eye,
nose, and throat irriation. Wide variation
in individual responses.
Within several hours, many signs of eye
irritation. A wide variation in individual
response, light cases recovering in a few
hours, and severe cases in a week.
Eye irritation of varying severity, lasting
from several hours to days- Some individuals
had repeated episodes.
Nausea, weakness, and pain in the chest.
Complete recovery within a week, no sequelae.
Fatigue, loss of appetite, irritability,
headache, loss of memory, itching, and irri-
tation of the eyes and respiratory tract.
Respiratory, gastroenteric, eye, and skin
irritation.
Dermal symptoms suggestive of an allergic-
type response. Some lung damage.
Weakness, nausea, dizziness, headache,
nervousness, and occasional unconsciousness.
(continued)
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TABLE S-3.. (concluded)
Level
(mg/m3)
Exposure
time
Table
Effects
0-9.94 3d V-l Occasional slight and irregular changes in
serum Fe and transferrin levels and in
fractions of urinary sulfates.
•\, 0.03- 29 d . V-2 Mild symptoms of nausea, vomiting, headache,
•v Q.43 shortness of breath, burning eyes, respira-
tory tract irritation, gastrointestinal
complaints, and disturbed sleep.
0.005- Chronic V-2 Headache, weakness, nausea, vision problems,
0.300 and higher general morbidity rates in those
households with ^ 0.05 mg H2S/m3.
0.028- Chronic V-2 Babies were poorly developed, underweight,
0.055 listless, anemic, dyspeptic, and more sus-
ceptible to infectious diseases.
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Other effects such as headache, fatigue, anorexia, and light sensitivity
may have been the result of the stress of the irritation. At his lowest
level (284 to 568 mg/m3 for an hour), there was no apparent irritation.
All other relevant papers involved fractions of a mg/m3. The greater
number involve estimation of odor thresholds. These varied from 0.00067 mg/m3
(Leonardos et al., 1969) up to 0.27 mg/m3 (Williams et al., 1977). In addi-
tion, Tonzetich and Ng (1976) noted an "objectionability threshold" of
0.15 mg/m3.
A few experiments have looked for the effects of very low levels of
H2S on sensitivity to light (dark adaptivity). The threshold is about 0.01
mg/m3 (Baikov, 1963; Duan, 1959).
Human Environmental Studies
These are divided into two groups. Occupational exposures (refinery
workers, tunnelers and miners, etc.) are listed in Table V-l. General public
exposures are listed as epidemiological studies in Table V-2. In general,
these studies are confounded by other noxious exposures and complicated by
varying H2S exposures. Some are also confounded by dubiously matching con-
trol groups. Their exposure is greater than a few hours, unlike all the
experimental studies above.
The occupational studies (Table V-l) are not useful, except to confirm
experimental observations that the major sites for H2S effects are the eyes
and respiratory tract. There are also several occupational studies describing
similar H2S effects, but not giving atmospheric H2S levels (Demaret and
Fialaire, 1974; Aves, 1929; Ahlborg, 1951; Burnett et al., 1977; Chertok,
1968). There is very dubious evidence for a threshold in the range-of 1 to
10 mg/m3 (cf. TLV of 15 mg/m3). One study of babies chronically exposed to
0.028 to 0.055 mg H2S/m3 from their mothers' clothing reported anemia and
unde rdevelopment.
The epidemiological studies (Table V-2) are even less useful. A review
of several epidemiological studies in the U.S.S.R. (as well as some experi-
mental data) concluded that chronic exposure to tenths and hundredths of a
mg/m3 can lead to general debility, headaches, vertigo, nausea, and other
subjective sensations (Gurinov, 1952).
Confounding Factors
Cigarette smoking is a frequent confounding factor in studies of human
exposure to H2S both because of the respiratory tract effects of the whole
smoke and the presence of H2S in the smoke. Estimates of H2S levels in cig-
arette smoke vary with the type of tobacco, type of filter, and the investi-
gator: 81 to 87 pg/nonfilter cigarette and 25 to 89 |Jg/filter cigarette
(Horton and Guerin, 1974), 30 to 49 [Jg/nonfilter cigarette and 18.7 to
41.5 |Jg/filter cigarette (Morie, 1971), 3.4 |Jg/40 ml unfiltered puff and
3.1 pg/40 mL filtered puff (Newsome et al., 1965), and 4.3 (Jg/puff (nonfilter
cigarette; Mattina, 1972). From the latter data it can be estimated that
10
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after each puff of a nonfilter cigarette containing 4.3 [Jg H2S, tne lun§
will be exposed momentarily to air containing ~ 6.1 mg H2S/m3 (4.3 pg/0.7 L
tidal lung volume). This is ^ 40% of the TLV (15 mg/m3).
Reviews of human exposure to H2S frequently include the many studies
of employees of the viscose rayon industry. These studies were not in-
cluded in the tables of this task report because of the confounding presence
of CS2 (which causes symptoms similar to those of H2S) and H2S04 (which is
also toxic). The main symptoms reported are fatigue, nerve effects, and
eye irritation (Masure, 1950; Rubin and Arieff, 1945; Kranenberg and Kessener,
1925; Barthelemy, 1939), although other effects have been mentioned (Kriz
et al., 1976; Vasil'eva, 1973). Animal (Wakatsuki, 1959; Kuwai, 1960; Masure,
1950; Misiakiewicz et al. , 1972) and human (Baikov, 1963) studies indicate
at least additive and possibly synergistic effects between H2S and CS2 in a
mixture. Two of the studies on viscose workers (Barthelemy, 1939; Kranenberg
and Kessener, 1925) state that the presence of CS2 and H2S04 probably plays
a part in the formation of eye lesions by increasing sensitivity.
INTERNATIONAL RECOMMENDATIONS AND STANDARDS
Many countries have regulations concerning the levels of H2S in dif-
ferent situations. Studies have also been done giving recommendations for
possible regulations. A summary of such information is given in Table S-4
and in the following paragraphs.
The American Conference of Governmental Industrial Hygienists suggests
14.0 mg H2S/m3 as the time-weighted-average threshold limit value and 21 mg/m3
as the short-term-exposure limit (ACGIH, 1980). The Occupational Safety
and Health Administration standard for H2S exposure is 30 mg/m3 for a ceiling
level. The Maximum Allowable Concentrations (MAC) in air in the U.S.S.R.
for 1972 were 10 mg H2S/m3 in the workplace, and 0.008 mg/m3 as both the
one-time and average limit in populated places (U.S.S.R., 1972). In 1968,
the workplace MAC's for six other countries ranged from 10 to 30 mg H2S/m3
(ILO/WHO, 1970).
Several studies have been done by trade or professional associations
and, while having no regulatory authority, make recommendations for allow-
able H2S concentrations in different situations. The VDI Committee on Air
Purification in West Germany recommended atmospheric Permissible Imission
Concentrations (PIC) of 0.15 mg/m3 (half-hour mean value) and 0.3 mg/m3 (3
x day half-hour mean value). The recommended work-station concentration
was 30 mg/m3 (Verein Deutscher Ingenieure, 1970). In the United States, a
study by the Illinois Institute for Environmental Quality (Booras, 1974)
recommended an environmental standard for gaseous H2S of 0.015 mg/m3 based
on 8-h average sample. Two major studies were done in the U.S.S.R. Loginova
(1957) recommended 0.03 mg/m3 for pure H2S and 0.015 mg/m3 for H2S as a con-
stituent of natural gas as the limits in the atmosphere. Gurinov (1952)
recommended 0.05 mg/m3 as the maximum single limit of allowable H2S in com-
munity air and 0.015 mg/m3 as the maximum average concentration.
11
-------
TABLE S-4. SUMMARY OF REGULATIONS AND RECOMMENDATIONS
FOR HUMAN H2S EXPOSURE
H2S level
(mg/m3)
30
21
14
10
0.3
0.15
0.05
0.005-
0.05
0.03
0.015
Recommendation/Regulation
Recommended work-station concentration
Short-term-exposure limit in the United States
Time-weighted-average TLV in the United States
Maximum Allowable Concentration in Workplaces
in the U.S.S.R
3 x day half-hour mean value, atmospheric PIC
Half -hour mean value, atmospheric PIC
Maximum allowable single limit in community
air
Range of concern for automobile emissions
Limit of pure H2S in the atmosphere
Maximum allowable average concentration in
Source
VDI (1970)
ACGIH (1980)
ACGIH (1980)
USSR (1972)
VDI (1970)
VDI (1970)
Gurinov (1952)
This study
Loginova (1957)
Gurinov (1952)
community air
0.015 Atmospheric limit of H2S as a constituent of
natural gas
0.015 Environmental standard based on 8-h average
sample
0.008 One-time and average limit in populated places
in the U.S.S.R
Loginova (1957)
Booras (1974)
USSR (1972)
12
-------
RECOMMENDED RANGE OF CONCERN
There is little human evidence for defining a range of concern. The
EPA Task 4 Work Directive suggested a preliminary region of uncertainty with
regard to the health effects of H2S of 0.15 to 15 mg/m3. The TLV is 15 mg/ni3;
this seems to be much too high (Booras, 1974). The TLV applies to a self-
selected body of healthy workers exposed 8 h/d, 40 h/wk. This is not the
situation of concern for automobile emissions.
The human experimental data (Table IV-1) contains a large gap from
~ 300 mg/m3 to ^ 1 mg/m3, including most of the area of uncertainty. Health
effects information is scarce, and most human experimental data concerns
odor perception. The best known property of H2S is its rotten egg odor.
The odor threshold could be used as the upper level of the range of concern.
However, estimates range from 0.005 to 0.27 mg/m3 (54-fold) because of in-
dividual variability, and the perception of a toxic substance's odor may
diminish with the time of exposure so people would cease to be annoyed.
The minimum odor threshold detected was 0.005 mg/m3 (Adams et al., 1968).
The level not affecting eye sensitivity to light was 0.008 to 0.01 mg/m3
(Duan, 1959; Baikov, 1963). Light sensitivity-related eye responses were
seen at 0.012 to 0.013 mg/m3 (Duan, 1959; Baikov, 1963). Babies were anemic
and underdeveloped following chronic exposure to 0.028 to 0.055 mg/m3 (Glebova,
1950). In an epidemiological study, Loginova (1957) reported nervous and
gastrointestinal disturbances during chronic exposure to ^ 0.05 mg H2S/m3.
In conclusion, we suggest 0.005 mg/m3 as the lower level of the range
of concern as a first estimate. Suggested estimates for the upper level of
the range of concern are 0.03 mg H2S/m3 for babies (a more susceptible group)
and 0.05 mg H2S/m3 for adults.
13
-------
SECTION I
INTRODUCTION
This report was compiled as the fourth of several tasks under Contract
No. 68-03-2928, "Health Effects Support for the Emission Control Technology
Division (U.S. Environmental Protection Agency, Ann Arbor, Michigan)." The
goal of the project is to evaluate health effects literature on specific
compounds emitted from automobiles equipped with emission-control devices
(specifically catalytic converters), not for the purpose of creating a cri-
teria document but to identify a range of concern or a no-observable-effect
level for each compound to serve as guidance to automobile manufacturers in
their development of future emission-control devices.
The present report was meant to be largely a series of charts or tables
of pertinent data with the tests logically ordered according to exposure
levels. The narrative summary was not meant to describe again each paper
in detail. There are admittedly some disadvantages in not doing so; e.g.,
some of the gradations in effect that the authors of a particular paper
observed may be diluted or lost when the details are spread throughout an
exceptionally large table, or between several tables. Papers described in
a largely narrative fashion, however, often are difficult to compare. Re-
sults that appear within their source paper to be quite definitive may ap-
pear less so or even anomalous when juxtaposed in tabular format with other
results from similar studies. Hence, the present format was designed to
facilitate comparisons.
Literature related to health effects of inhaled H2S was collected mainly
by computer search of TOXLINE and TOXBACK and manual search through the NRC
Subcommittee report on hydrogen sulfide. Approximately 350 papers and other
documents were evaluated, but only about 40 contained original data suitable
for tabulation.
Experimental animal and human exposure studies were evaluated and sum-
marized by a senior Ph.D. pharmacologist. Occupational exposures were rated
by an epidemiologist with an M.D. degree. Figure 1-1 is the form used for
rating documents by the project pharmacologist and epidemiologist. Each
document was rated in a two-step procedure according to the applicability
of its subject matter and to the quality of the experimental methodology.
The letter assigned in rating the document A, B, C, or D was derived from
the corresponding lower case letters under item 7 in Figure 1-1. Thus, a
study was rated A if it directly applies to or assists in establishing a
level of concern for exposure to ^S. The second part of the rating is the
15
-------
Article No. 4997-4-
CHECK WHERE APPROPRIATE :
1. Do they state/limit the problem?
2. Adequacy of sample
j
3. Replicability
4. Controls /control procedures
5. Completeness and comprehensibility
of results
6. Validity of conclusions, inter-
pretation of data
PAPER
DEFECTIVE
0
PAPER IS
SUB-
STANDARD
1
STANDARD
QUALITY
SUPERIOR
PAPER
3
7. Applicability to health effects of H2S as guidance for establishing a range
of concern for H2S in automobile exhaust.
.(circle one)
a.
b.
Clearly, directly applies/assists in establishing a range of concern
(Chronic human studies; acute exposure of humans if minimal effects.)
Research requires major inferences; potentially applicable.
(Chronic animal studies; acute human, maximal effect; acute animal,
minimal effects.)
c. Useful hints or suggestions; tentatively applicable.
(Acute animal, lethal effects; studies in above categories but effects
reported not appropriate.)
d. Not directly applicable (peripheral useful information).
Figure 1-1 - Form for Report Rating
16
-------
methodology score. The document reviewer checked off which score should be
given for each of the first six items in Figure 1-1, and the total was writ-
ten at the top of the page along with the letter that rated the paper's ap-
plicability. In some cases, such as reviews, theoretical papers, and low-
rated foreign language documents, a paper may have received an applicability
rating (generally C or D) but none on methodology.
Data, including the MRI-assigned rating, from the A-, B-, and some C-
rated papers were tabulated by mid-level scientists. Information for each
topic heading was carefully sought; so if blanks appear in the table, the
reader can generally assume the data were not given. Information which was
unclear in the original document but needed for tabulation is preceded in
the tables by a qualifying word such as "apparently." Sometimes a group
published several papers that described the same tests. To avoid redundancy,
all pertinent papers were cited and the test was described as well as pos-
sible from all the papers' descriptions.
The final written summary of the tabulated data was also performed by
a senior pharmacologist. This summary attempts to reflect objectively the
scientific community's thought as a whole and does not reflect the tabular
material be weight. The tables reflect the amount of data generated, and
the summary puts the evaluated data in perspective with the overall scien-
tific community's opinions.
The references are cited in an annotated bibliography that includes
not only each document's rating but also a brief comment on its pertinence
(or lack of same) to the study. English titles are given for foreign lan-
guage documents, and an abbreviation of the language is given in parentheses
at the end of the citation.
The report is organized into the following chapters: 2. Bioassay
Tests, 3. Experimental Animal Inhalation Exposures, 4. Experimental
Human Inhalation Exposures, and 5. Epidemiology. The Summary precedes the
entire report and the Annotated Bibliography follows it.
17
-------
SECTION II
BIOASSAYS
Only five in vitro studies were found in the literature. The results,
described in Table II-l, appear to have little information directly useful
to this task on determining a range of concern for human exposure to H2S in
automobile exhaust. The data are discussed in the Summary.
19
-------
TABLE II-l. BIOASSAYS
Compound and
Concentration in
mg/m3 (ppm)
H2S 568-1,136
(400-800)
Temperature
and
Humidity
29-31°C,
> 95%
H2S 712.8
(502)
ro
o
H2S 359.3
(253)
H2S 284
(200)
Preparation
Exposed
Fresh (< 2.5 h)
excised rabbit
tracheal tissue
Rat (albino, ITRC
colony) lung
homogenate
Rat (albino, ITRC
colony) lung
homogenate.
Alveolar macrophages
obtained by lavage
of the lungs of
New Zealand White
rabbits of either
sex.
Description of Tests
and Duration
A 2 x 4 mm section was placed
in a tissue chamber, and the ir-
ritant gas added at a flow rate
similar to that in a living
rabbit for 5-10 min. Cilia were
observed through a microscope.
Time to cessation of activity
and then recovery in air or
Ringer's solution was deter-
mined.
< 5 ml of H2S gas was injected
from a glass syringe into a
pre-evacuated glass vial con-
taining 5 ml of the homogenate.
The exposed supernatant was
kept in the cold for 1 h, then
enzyme levels were measured.
< 5 ml of H2S gas was injected
from a glass syringe into a
pre-evacuated glass vial con-
taining 5 ml of the homogenate.
The exposed supernatant was
kept in the cold for 1 h,
then enzyme levels were
measured.
Cell cultures were exposed to
H2S for 48 h in the airstream
of a flow-through incubator.
Phagocytic ability (as mea-
sured by the uptake of poly-
vinyltoluene beads) and
viability (as measured by
Trypan Blue and neutral red
stains) were immediately
determined.
Results
Exposure to 800 ppm for 5 min
did not prevent recovery in
Ringer's solution. There was
cessation of ciliary beating
without recovery in air in 5 min
at 600 ppm and in 10 min at 400
ppm.
Inhibited:
Acid phosphatase 49.0%
Alkaline phosphatase 43.8%
GPT (glutamic-pyruvic- 52.5%
transaminase)
GOT (glutamic oxalo- 14.0%
acetic-transaminase)
ATPase (adenosine 41.0%
triphosphatase)
Stimulated: Arginase 57.5%
No effect: Aldolase
Inhibited:
Acid phosphatase 62,0%
Alkaline phosphatase 34.0%
GPT 42.3%
GOT 17.2%
ATPase 37.2%
Stimulated: arginase 51.7%
No effect: aldolase
Relative to controls:
Phagocytic ability 2-7%
Viability 9-23%
Reference and
Rating
Cralley (1941)
D-6
Husain (1976)
D-6
Husain and Zaidi
(1977)
D-ll
Hasain (1976)
D-6
Husain and Zaidi
(1977)
D-ll
Robinson (1979)
C-6
-------
TABLE II-l. (continued)
Compound and
Concentration in
mg/cn3 (ppm)
H2S 284
(200)
Temperature
and
Humidity
Preparation
Exposed
Alveolar macrophages
obtained by lavage
from the lungs of
New Zealand White
rabbits of either
sex.
Description of Tests
and Duration
Cell cultures were exposed to HZS
for 8 h in the airstream of a flow-
through incubator. Following 16 h
of recovery, there was another
8-h exposure period. Following
another 16-h recovery period,
there was an additional 8-h exposure
Phagocytic ability was immediately
measured.
Results
There was a 32% decrease
in phagocytic ability relative
to the controls.
Retcrence and
Rating
Robinson (1979)
C-6
H2S 284
(200)
H2S 284
(200)
H2S 153.4
(108)
Alveolar macrophages
obtained by lavage
from the lungs of
New Zealand White
rabbits of either
Alveolar macrophages
obtained by lavage
from the lungs of
New Zealand White
rabbits of either
Rat (albino, ITRC
colony) lung
homogenate.
Cell cultures were exposed to
H2S for 8-h in the airstream
of a flow-through incubator.
After 16 h of recovery,
cultures were again exposed
for 8 h. Phagocytic ability
was determined immediately.
Cell cultures were exposed to
H2S for 24 h in the air-
stream of a flow-through in-
cubator. Phagocytic ability
and viability were measured
immediately and 24 h after
recovery.
< 5 ml of H2S gas was injected
from a glass syringe into a
pre-evacuated glass vial
containing 5 ml of the
homogenate. The exposed
supernatant was kept in
the cold for 1 h, then en-
zyme levels were measured.
65% decrease in phagocytic
ability relative to the
controls.
Immediately after exposure,
relative to controls:
Phagocytic ability 69-77%
Viability 90-95%
After 24-h recovery, further
decreases in ability were observed
relative to controls:
Phagocytic ability 7-15%
Viability 37-50%
Inhibited:
Acid phosphatase 38.5%
Alkaline phosphatase 35.0%
CPT 38.2%
GOT 16.5%
ATPase 32.0%
Stimulated: arginase 33.0%
No effect: aldolase
Robinson (1979)
C-6
Robinson (1979)
C-6
Husain (1976)
D-6
Husain and Zaidi
(1977)
D-ll
-------
TABLE II-l. (continued)
Compound and
Concentration in
mg/m3 (ppm)
H2S 85.2
(60)
Temperature
and
Humidity
H2S avg. 76.5
(avg. 53.9)
ho
H2S 71
(50)
HZS 56.8
(45.6)
Preparation
Exposed
Alveolar macrophages
obtained by lavage
of the lungs of male
New Zealand White
rabbits.
Alveolar macrophages
obtained by lavage
of the lungs of male
New Zealand White
rabbits.
Alveolar macrophages
obtained by lavage
from the lungs of
New Zealand White
rabbits of either
sex.
Rat (albino, ITRC
colony) lung
homogenate.
Description of Tests
and Duration
Cell cultures were exposed to
H2S for 24 or 48 h in the air-
stream of a flow-through in-
cubator. Those exposed for
24 h were then given 24-h
recovery time. Phagocytic
ability was measured at 48 h.
Two types of culture methods
were used.
Cell cultures were exposed to
H2S in the airstream of a flow-
through incubator for one of
several different regimens:
8 h; 8 h -I- 16 h delay + 8 h;
8 h + 16 h delay + 8 h +
16 h delay + 8 h; 16 h; or
24 h. Phagocytic ability was
measured 24 h after the last
exposure (presummably of each
regimen).
Cell cultures were exposed to
H2S for 20 h in the airstream
of a flow-through incubator.
After 24-h recovery,
phagocytic ability and
viability of the cells were
determined.
< 5 ml of HjS gas was injected
from a glass syringe into a
pre-evacuated glass vial con-
taining 5 ml of the homogenate.
The exposed supernatant was
kept in the cold for 1 h,
then enzyme levels were
measured.
Results
Only exposure for 48 h (no re-
covery time) had an effect on
phagocytic ability (~ 20%
decrease) of cells cultured on
gas-impermeable flasks. Cells
cultured on gas-permeable mem-
branes (more similar to in vivo
exposure) showed — 95% inhibition
of phagocytic ability after 24-h
exposure with 24-h recovery and
after 48-h exposure.
Exposure for 8 h had no effect
on phagocytic ability. Inter-
mittent exposures caused a
definite decrease, and con-
tinuous exposure caused even
greater reductions (0-11%
of the controls).
Relative to controls:
Phagocytic ability 88%
Viability 88-94%
Inhibited:
Acid phosphatase 33.0%
Alkaline phosphatase 19.5%
GPT 27.9%
GOT 19.5%
ATPase 24.0%
Stimulated: arginase 23.8%
No effect: aldolase
Reference and
Rating
Robinson (1980)
C--
Robinson (1980)
C--
Robinson (1979)
C-6
Husain (1976)
D-6
Husain and Zaidi
(1977)
D-ll
-------
TABLE II-l. (continued)
Compound and
Concentration in
mg/m* (ppm)
H2S 25.8
(18.2)
Temperature
and
Humidity
Preparation
Exposed
Rat (albino, ITRC
colony) lung
homogenate.
Description of Tests
and Duration
< 5 ml of HjS gas was
injected from a glass
syringe into a pre-
evacuated glass vial con-
taining 5 ml of the
homogenate. The exposed
supernatant was kept in
the cold for 1 h, then
enzyme levels were measured.
Results
Inhibited:
Acid phosphatase 16.8%
Alkaline phosphatase 11-0%
OPT 25.9%
GOT 15.9%
ATPase 13.3%
Stimulated: arginase 22.0%
No effect: aldolase
Reference and
Rating
Husain (1976)
D-6
Husain and Zaidi
(1977)
D-ll
-------
SECTION III
EXPERIMENTAL ANIMAL INHALATION EXPOSURES
The essential parameters of numerous animal inhalation exposure experi-
ments are tabulated in this section. The primary organization of data is
by .species, in order of increasing weight (canaries to cows in this case).
Within a species, studies are divided by dosing duration: acute exposure
(^ 24 h), repeated exposure, and chronic exposure (^ 90 d). Within a single
table, reported results are listed in order of decreasing exposure level.
The tables have been arranged in the aforesaid manner for the following
reasons: (a) there were about 125 separate tests tabulated; (b) there are
distinct differences in lung anatomy among the laboratory species used, and
the differences seen in their relative responses may have been largely due
to these anatomical differences; and (c) by putting the highest concentra-
tions and worst effects first, one can more readily understand the signif-
icance of minor or less-severe changes occurring at lower levels. However,
a condensation of the data by H2S concentration is in Table 111-24.
In the animal exposure tables in this section, the column headed Total
Length of Expt. includes not only the total length of exposure to H2S but
also any recovery time observed in the study. This recovery time was in-
cluded to note the endurance or reversibility.of the toxic effects.
25
-------
TABLE III-l. CANARIES—ACUTE EXPERIMENTAL EXPOSURE TO H2S
Compound(s) and
Concentration(s)
in
H2S
H2S
H2S
H2S
H2S
H2S
mg/m3 (ppm)
1,036.6
(730)
880.4
(620)
738.4
(520)
624.8
(440)
397.6-440.2
(280-310)
269.8-298.2
(190-210)
Humidity Mode Species/ No. of Duration and Total
and of Strain/ Test No. of Frequency Length
Temperature Exposure Age/Weight Animals Controls of Exposure of Expt .
Not given Exposure Canaries Not given None < 2 min,
chamber once
Not given Exposure Canaries 2 None < 2 min,
chamber once
.Not given Exposure Canaries 1 None < 2 min,
chamber once
Not given Exposure Canaries 4 None < 2 min,
chamber once
Not given Exposure Canaries 3 None < 30 min,
chamber once
Not given Exposure Canaries 4 None 1 h, once
chamber
Effects
Falls off perch, unconscious.
Dead in 18-20 s. No recov-
ery.
Falls off perch, unconscious
14-20 s. Quick recovery.
•Edema and falls off perch, un-
consciousness; quick recovery.
Forced respiration, dizziness,
edema, 13-20 s unconscious-
ness. Quick recovery.
Excitement, partial collapse
for a short period, then
fairly rapid recovery. Edema,
forced breathing, unconscious-
ness, and death. Quick re-
covery of survivors.
In less than 2 min the birds
partially collapsed then re-
covered and were excited.
Through the first 0.5 h, there
was occasional gasping, edema,
forced respiration, dizziness
and weakness, and unconscious-
ness. Some deaths occurred by
the end of the hour and the
survivors recovered slowly.
Reference
and Rating
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
-------
TABLE III-l. (continued)
Compound(s) and
Concentration(s)
in me/")3 (ppm)
H2S 198.8
(140)
Humidity
and
Temperature
Not given
Exposure
chamber
Species/
Strain/
Age/Weight
Canaries
No. of
Test
Animals
No. of
Controls
None
Duration and Total
Frequency Length
of Exposure of ExpL.
8 h, once
44 h
H2S 99.4-142
(70-100)
Not given
Exposure
chamber
Canaries
None
8 h, once
44 h
H2S 49.7-92.3
(35-65)
Not given
Exposure
chamber
Canaries
None
18 h, once
Effects
Reference
and Rating
Mitchell
and Yant
(1925)
B-10
Subjects exhibited excitement
and one slight case of edema
from 30 min-1 h. From 1-4 h
forced breathing, dizziness,
and weakness were prominent.
At 4-8 h very forced breath-
ing, unconsciousness, and death
occurred. All the birds that
lived through the exposure pe-
riod died 12-36 h later.
Between 30 min and 1 h, one
case of slight edema and one
case of panting were recorded.
At 1-4 h, edema, dizziness,
general stupidity, and forced
breathing through the mouth
were noted. From 4-8 h, very
forced respiration, edema,
dizziness, unconsciousness,
and death occurred. Those
surviving the actual expo-
sure died in the following
12-36 h.
At 4-8 h, stupid, heavy Mitchell
breathing, edema. At 8-18 h, and Yant
weakness - inability to perch; (1925)
death. B-10
Mitchell
and Yant
(1925)
B-10
-------
TABLE II1-2.
MICE—ACUTE EXPERIMENTAL EXPOSURE TO H2S
Compound(s) and
Concentration(s)
in mg/ro3 (ppm)
H2S 1,420
(1,000)
Humidity
and
Temperature
74.6
73.3
8.8%,
3.3°F
Continuous
flow in-
halation
chamber
Species/
Strain/
Age/Weieht
Mice
No. of
Test
Animals
No. of
Controls
None
Duration and
Frequency
of Exposure
< 1 h, once
Total
Length
of Expt.
< 1 h
Effects
50% mortality after 18 min.
Animals active during first
few minutes. There was
marked lacrimation, and all
were dead in 20 min.
Reference
and Rating
Weedon
et al.
(1940)
B-8
H2S 344
(250)
74.6 + 8.8%,
73.3 + 3.3°F
Continuous
flow in-
halation
chamber
Mice
Animals were found to have
well-collapsed lungs with small
hemorrhages, congested livers
and kidneys, and distended stom-
achs.
None < 8 h, once 8 h 50% mortality after 410 min. Weedon
At end of 2 h, animals were et al.
gasping moderately and their (1940)
abdomens were distended. All B-8
were dead in 8 h.
oo
H2S 142
-(110)
25 °C
Inhalation Mice,
chamber Swiss-
Webster
8 F 8 controls 8 h, once
treated
same, 8
mice de-
prived of
food and
water
(controls
acciden-
tally ex-
posed to
20-30 ppm;
see 30 ppm
entry)
Animals were found to have
slightly congested brains, mas-
sive hemorrhages of all lung
lobes, pale and enlarged livers,
moderately distended stomachs
with rare minute hemorrhages,
and pale kidneys.
8 h Modified lethal concentration Hays
duration 50 was 7.5 h. Three (1972)
mice died and rest were hypo- B-13
thermic. Erythrocyte carbonic
anhydrase activity (an enzyme
involved in the handling of
COg, and so reflects the non-
oxygen side of respiration)
not inhibited. Mice did not
eat or drink available food
or water.
-------
TABLE III-2. (continued)
Compound(s) and
Concentratioo(s)
in mg/in3 (ppm)
H2S 89.5
(63)
Humidity
and
Temperature
74.6 + 8.8%,
73,3 + 3.3°F
Continuous
flow in-
halation
chamber
Species/
Strain/
Age/Weight
Mice
No. of
Test
Animals
H2S 71
(50)
25°C
Inhalation Mice,
chamber Swiss-
Webster
8 F
10
VO
H2S 41.6
(30)
25°C
Inhalation Mice,
chamber Swiss-
Webster
8 F
No. of
Controls
None
Duration and
Frequency
of Exposure
16 h, once
Total
Length
of Expt.
16 h
16 h
8 controls 16 h, once
treated
sane, 8 de-
prived of
food and
water
(Controls
acciden-
tally ex-
posed to
20-30 ppm;
see 30 ppm
entry.)
8 controls 24 h, once 13 d
treated the
same, and 8
mice de-
prived of
food and
water (Both
groups ac-
cidentally
exposed to
20-30 ppm
H2S)
Effects
50% mortality after 804 min.
One survived the test but
died 23 h later.
Animals were found to have.
congested brains, massive
lung hemorrhages, pale and
enlarged livers, distended
stomachs with few moderate-
sized hemorrhages, and pale
kidneys.
Modified lethal concentration
duration 50 was 15 h. Animals
were hypothermic. Erythrocyte
carbonic anhydrase activity
not inhibited. Food and water
intake reduced 70% during ex-
posure.
Keference
and Rating
Weedon
et al.
(1940)
B-8
Hays
(1972)
B-13
The modified lethal concentra- Hays
tion duration 50 was 18.5 h. (1972)
Three mice died and the rest B-13
were hypothermic. Two mice
died at 42 h. By day 4 rectal
temperatures had increased to
pre-exposure level. Food and
water intake decreased and mice
lost weight. By day 13 weight
had returned to normal.
Control and fasted groups re-
sponded similarly, they lost
weight and were hypothermic.
At 47 h one of fasted mice
died. All had recovered by day
13.
-------
TABLE III-2. (continued)
Cooipound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 22.7
(16)
Humidity
and
Temperature
74.6 + 8.8%
73.3 + 3.3°F
Continuous
flow in-
halation
chamber
Species/
Strain/
Age/Weight
Mice
No. of
Test
Animals
No. of
Controls
None
Duration and
Frequency
of Exposure
16 h, once
Total
Length
of Expt.
16 h
Effects
No abnormal reactions other
than an initial slight rest-
lessness which quickly dis-
appeared. Autopsy normal.
Reference
and Rating
Weedon
et al.
(1940)
B-8
-------
TABLE III-3. MICE—REPEATED DOSE EXPERIMENTAL EXPOSURE TO H2S
Compound (s) and
Concent ration(s)
in ng/ra3 (ppm)
H2S 28.4
(20)
Humidity
and
Temperature
25°C
Mode
of
Exposure
Inhalation
chamber
Species/
Strain/
Age/Weight
Mice,
Swiss-
Webster
No. of
Test No. of
Animals Controls
7 M 7 controls
treated
same, 7
mice de-
prived of
food and
water
Duration and
Frequency
of Exposure
48 h, once
Total
Length
of Expt
48 h
H2S 14.2
(10)
25°C.
Inhalation Mice,
chamber Swiss-
Webster
6 F
6 F
5 d, once
5 d
Effects
Food and water intake de-
creased 20%, rectal' temper-
atures decreased 3.7°C, and
animals lost weight. Sleep
time as induced by pento-
barbital not different from
control except deprived group
slept longer.
No deaths. Body temperature
dropped significantly after
48-h exposure but was not sig-
nificantly different from con-
trols during rest of study.
Erythrocyte carbonic anhydrase
activity not inhibited. Food
and water intake dropped 60%
during first 24 h but was in-
hibited only 28% by day 5 as
compared to controls.
Reference
and Rating
Hays
(1972)
B-13
Hays
(1972)
B-13
-------
TABLE III-4. MICE—CHRONIC EXPERIMENTAL EXPOSURE TO H2S
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 28.4
(20)
Humidity
and
Temperature
50 + 10%,
70 + 5°
(Control
room up
to 86°F)
Mode Species/
of Strain/
Exposure Age/Weight
Exposure
chamber
Mice, avg.
wt. 25 g
No. of
Test
Animals
100 M
No. of
Controls
100 M
Duration and
Frequency
of Exposure
90 d,
continuous
Total
Length
of Expt.
90 d
OJ
to
Effects
Mortality 26% versus 16% in
controls. Statistically sig-
nificant weight loss after
90 d and decrease in swimming
endurance compared to controls.
Lung pathology present in 33%
of animals autopsied compared
to 17% in controls.
Statistically significant
changes in blood parameters at
90-d exposure over pre-exposure
levels: leukocytes, hematocrit,
hemoglobin, MCV, MCHb, in-
creased; erythrocytes de-
creased. Compared with con-
trols at 90 d: leukocytes,
reticulocytes, hematocrit,
hemoglobin, MCV (mean corpuscular
volume), MCHb (mean corpuscular
hemoglobin), increased; platelets
decreased.
Reference
and Rating
Sandage
(1961)
B-10
Mice that died during test pe-
riod exhibited abcesses of the
brain, liver, and lung. Sacri-
ficed animals exhibited in-
stances of bronchopneumonia and
hepatitis.
-------
TABLE III-5. RATS—ACUTE EXPERIMENTAL EXPOSURE TO
CO
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
HjjS 1,420
(1,000)
Humidity
and
Temperature
74.6 + 8.8%,
73.3 + 3.3°F
H2S 1,122-1,278 Not given
(790-900)
H2S 880.A
(620)
Not given
H2S 738.4-752.6 Not given
(520-530)
Species/
Strain/
Age/Weight
Continuous Rats
flow in-
halation
chamber
No. of
Test
Animals
8
No. of
Controls
None
Exposure Rats
chamber
40
Exposure Rats
chamber
Duration and Total
Frequency Length
of Exposure of Expt.
< 1 h, once
< 1 h
Not given £ 1 h, once ~ 1 h
Not given £ 1 h, once ~ 1 h
Exposure Rats
chamber
Not given < 4 h, once
Effects
Reference
and Rating
Weedon
et al.
(1940)
B-8
50% mortality after 14 min.
Animals were active during
the first 5 min, prostrated
in 11 min, and all were dead
in 37 min.
Animals were found to have
slightly congested brains, well-
collapsed lungs with small hem-
orrhages, congested livers,
distended stomachs, and con-
gested kidneys.
0-2 min: unconscious in a few Mitchell
seconds; respiration ceased. and Yant
A few rats had clonic and (1925)
tetanic spasms. B-10
2-30 min: respiration
stopped.
30 min-1 h: death or rapid
recovery after exposure.
0-2 min: great excitement, Mitchell
escape from cages. and Yant
2-30 min: stands up in cor- (1925)
ner, falls over, unconscious- B-10
ness, clonic spasms.
30 min-1 h: unconsciousness
and death or fairly rapid re-
covery.
0-2 min: excitement and pant- Mitchell
ing. and Yant
2-30 min: forced breathing, (1925)
eyes closed, weakness, edema. B-10
30 min-1 h: very sick and
weak, distressed.
1-4 h: unable to stand, very
labored breathing, eyes closed,
mouth open, high excitement, and
death or slow recovery.
-------
TABLE III-5. (continued)
U)
-IS
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 639
(450)
H2S 440.2-497
(310-350)
H2S 355
(250)
Humidity Mode Species/ No. of Duration and Total
and of Strain/ Test No. of Frequency Length
Temperature Exposure Age/Weight Animals Controls .of Exposure of Expt.
Not given Exposure Rats 2 Not given < 4 h, once
chamber
Not given Exposure Rats . 13 Not given < 8 h, once
chamber
74.6 + 8.8% Continuous Rats 8 Not given 22 h, once 22 h
73.3 * 3.3°F flow in-
halation
chamber
Effects
0-2 min: excitement, evidence
of distress.
2-30 min: standing up in cor-
ner of cage with nose high,
edema .
30 min-1 h: inability to
stand, eyes closed, very forced
respiration.
1-4 h: semiconsciousness, un-
consciousness, great activity,
and death or slow recovery.
0-2 min: washed face.
2-30 min: washed face, eyes
closed, standing up in corner
of cage.
30 min-1 h: eyes closed,
coughs; forced and rapid res-
piration; weakness.
1-4 h: very forced respira-
tion; evidence of great dis-
tress, spasms, and some deaths.
4-8 h: semiconsciousness,
unconsciousness, and death or
very slow recovery.
50% mortality not reached.
Animals were restless during
the first 25 min, then quieted
down. First death occurred
during the 17 h, 3 were dead
at end of 23 h.
Reference
and Rating
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
Weedon
et al.
(1940)
B-8
Animals that died were found
to have congested brains, dis-
tended and extremely hemor-
rhagic lungs, distended hearts,
congested livers, distended
stomachs and intestines, and
congested kidneys.
-------
TABLE III-5. (continued)
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
II2S 269.8-340.8
(190-240)
H2S 89.5
(63)
CO
H2S 22.7
(16)
Humidity
and
Temperature
Not given
74.6 + 8.8%
73.3 + 3.3°F
Exposure
chamber
Species/
Strain/
Age/Weight
Rats
Continuous
flow in-
halation
chamber
74.6 + 8.8% Continuous
73.3 + 3.3°F flow in-
halation
chamber
No. of
Test
Animals
17
No. of
Controls
Rats
None
Rats
None
Duration and
Frequency
of Exposure
Total
Length
of Expt.
Not given < 18 h, once
16 h, once
16 h
16 h, once
16 h
Effects
2-30 min: quiet, standing
in corner, head high, washes
face.
30 min-1 h: standing up,
quiet, in corner
1-4 h: little panting.
4-8 h: forced breathing.
8-18 h: forced breathing
and death or very slow recov-
ery after exposure.
50% mortality not reached.
Animals unaffected at first
but by 16 h they were leth-
argic and breathing heavily.
One rat died, and it had con-
gested brain, half of lung
collapsed, moderately dark red
liver and kidneys, distended
stomach and caecum.
No abnormal reactions other
than a slight initial rest-
lessness.
Reference
and Rating
Mitchell
and' Kant
(1925)
B-10
Weedon
et al.
(1940)
B-8
Weedon
et al.
(1940)
B-8
-------
TABLE III-6. RATS--REPEATED DOSE EXPERIMENTAL EXPOSURE TO
H2S 312.4
(220)
H2S 312.4
(220)
Humidity
and
Temperature
Not given
Not given
Not given
Mode Species/
of Strain/
Exposure Age/Weight
Inhalation Rats
Inhalation Wistar
rats
(Charles
River Lab. )
pregnant
females
Inhalation Wistar
rats,
14 wk;
after ex-
posure,
mated to
6-9-wk-old
virgin fe-
males
No. of Duration and Total
Tpst No. of Frequency Length
Animals Controls of Exposure of Expt.
Not Not given 22 d 22 d
given
Not Not given 3 h/d; 21 d
given 5 d/wk;
For 14 d
through
gestation,
or for 5 d
during a
portion of
major
organogenesis
10 M Not given 3 h/d, 7d ~ 13.5 wk
H2S 312.4
(220)
N1I3 180
(250)
Not given
Inhalation Rats
Not
given
Not given 22 d
22 d
No evidence of effect on
respiratory tract, kidnoy,
liver, adrenal, heart, gas-
trointestinal tract, lira in,
spleen, or eye tissues,
examined microscopically.
No evidence of maternal tox-
icity. Fertility equivalent
to the controls. No evidence
of embryotoxicity (prenatal
mortality or decrease in mean
litter weight). Some rib de-
formities occurred, which were
also seen in the controls, al-
though at lower rates.
Nondominant lethal effects
found in uteri and fetuses of
female rats sacrificed 18 d
after cohabitation. Fertility
(90^), preimplantation loss,
avg. no. of corpora lutea, im-
plants, postimplantation loss,
and no. of resorptions were aLl
similar to control values.
No evidence of exposure effect
seen in respiratory tract,
kidney, liver, adrenal, heart,
gastrointestinal tract, brain,
spleen, or eye tissues, exam-
ined microscopically.
Reference
and Rating
Renne and
McDonald
(1980)
C--
Andrew
et at .
(1979)
Andrew
et al.
(.1979)
D-9
Renne and
McDonald
(1980)
C--
-------
TABLE III-6. (continued)
Compound(s) and
Concentration(s)
in mg/ni3 (ppm)
H2S 284
(200)
Humidity
and
Temperature
Not given
Inhalation
chamber
Species/
Strain/
Age/Weight
Rats
No. of
Test
Animals.
No. of
Controls
Duration and
Frequency
of Exposure
24 h
Total
Length
of Expt.
48 h
H2S 142-198.8
(100-140)
Not given Exposure Rats
chamber
19 • Not given < 48 h, once
H2S 142
(100)
Not given Inhalation Rats
Not
given
Not given 7 d
7 d
Effects
Reference
and Rating
Robinson
et al.
(1979)
C-6
Free cells lavaged from the
lungs after 24-h recovery
showed increases in the no. of
free cells and percent of
polymorphonuclear neutrophils
(PUN), and decreases in the
percent of lymphocytes and
macrophages. Changes are
indicative of an inflammatory
response. Phagocytic ability
of the free cells was de-
creased. Viability was rela-
tively unaffected.
1-4 h: indication of irrita- Mitchell
tion to the nose by continual and Yant
washing of face. (1925)
4-8 h: irritation of nose and B-10
eyes.
8-18 h: forced breathing.
18-48 h: death or very slow re-
covery following exposure.
No significant histopathologic Renne and
lesions or clinicopathologic McDonald
alterations. (1979)
C—
H2S 142
(100)
NH3 180
(250)
Not given Inhalation Rats
Not
given
Not given 7 d
7 d No significant histopathologic Renne and
lesions or clinicopathologic McDonald
alterations. (1979)
C—
H2S 49.7-92.3
(35-65)
Not given Exposure Rats
chamber
Not given 100 h, once 100 h
1-4 h: showed irritation to Mitchell
nose by continued washing of and Yant
face. (1925)
4-8 h: irritation of nose and B-10 .
eyes.
8-18 h:
18-48 h:
quiet.
pus in eyes and nose,
hair rough. No worse after
100 h continuous exposure.
-------
TABLE III-6. (continued)
Compound(s) and Humidity
Concentration(s) and
in mg/m3 (ppro) Temperature
H2S 28.4
(20)
50 + 10%,
75 + 5°F
(Control
room up
to 86°F)
Mode Species/ No. of
of Strain/ Test No. of
Exposure Age/Weight Animals Controls
Inhalation Rats, 50 M 50 M
chamber Sprague~
Dawley ,
general pur-
pose strain,
avg. wt. 175 g
Duration and Total
Frequency Length
of Exposure of Expt
90 d, 90 d
continuous
u>
00
H2S 14.2
(10)
H2S lit.2 (10)
NH3 71 (50)
50-70%
10°C
Inhalation Rats
13
50-70%
10°C
Inhalation Rats
12
15
(2 control
groups,
one held
under op-
timal tem-
perature,
other at
108C)
20
(2 control
groups,
one held
under op-
timal tem-
perature,
other at
10°C)
41 d
41 d
50 d
50 d
Effects
Reference
and Rating
Mortality 24% versus 4% in Sandage
controls. Significant weight (1961)
loss after 90 d. B-10
Lung pathology present in 33%
and kidney pathology in 6% of
animals autopsied.
Statistically significant
changes in blood parameters at
90-d exposure over pre-exposure
levels: platelets, reticulo-
cytes, hematocrit, hemoglobin,
MCV, MCHb, increased. Compared
with controls at 90 d: leuco-
cytes and reticulocytes, in-
creased; platelets, decreased.
After 7 wk, significantly less Stolpe
wt. gain, 81% for the test et al.
group versus 92% for controls (1976)
under cold conditions, both B-10
compared to controls at an op-
timal temperature. Food util-
ization reduced, 132% versus
122% for controls under cold
conditions. No differences in
blood cells, plasma protein, or
wt. of liver and lungs.
Significantly less wt. gain, Stolpe
81% versus 92% for controls et al.
under cold conditions. Food (1976)
utilization reduced, 148% B-10
versus 122% for controls under
cold conditions. No differ-
erences in blood cells, plasma
protein, or wt. of liver and
lungs.
-------
TABLE III-6. (continued)
u>
vo
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 7.1 (5)
m3 42.6 (30)
Humidity
and
Temperature
50-70%
10°C
Mode Species/
of Strain/
Exposure- Age/Weight
Inhalation Rats
No. of
Test
Animals
12
Duration and
No. of Frequency
Controls of Exposure
13 Continuous
(2 control 53 d
groups,
one held
at optimal
temperature,
one at 10°C)
Total
Length
of Expt
S3 d
H2S 7.1 (5)
HH3 42.6 (30)
Oust 42.34 + 14.07
50-70%
10°C
Inhalation Rats
15
15
(2 control
groups,
one held
under op-
timal tem-
perature,
other at
10°C, both
exposed to
dust same
as test
rats)
44 d, exposed 44
to dust for
1 h, 2 times/d,
5 d/wk
Effects
Reference
and Rating
Stolpe
et al.
(1976)
B-10
No differences in wt. gain
from the cold control, both
92% of rats at optimal tem-
perature. Food utilization
reduced, 148% versus 122%
for cold conditions. No
differences in blood cells,
plasma protein, or wt. of
liver and lungs.
Less wt. gain than cold con- Stolpe
trols, 87% versus 92%. Food et al.
utilization reduced, 130% (1976)
versus 122% for controls under B-10
cold conditions.
No differences in blood cells,
plasma protein, or wt. of liver
and lungs.
-------
TABLE III-7. RATS—CHRONIC EXPERIMENTAL EXPOSURE TO
Compound(s) and
Concentrat ion(s)
in cng/m3 (ppm)
H2S 50
CO 300
Humidity
and
Temperature
Not given
Mode Species/
of Strain/
Exposure Age/Weight
Inhalation Rats, albino
chamber
No. of
Test
Animals
Not
given
No. of
Controls
Duration and
Frequency
of Exposure
Not given 4 h/d, 6 mo
Total
Length
of Expt.
6 mo
H2S 10
Not given
Inhalation Rats, albino,
chamber 60-90 g
10 H
10 M
12 h/d, "ex-
cept days off,
for 3 mo
17 wk
Effects
02 consumption lowered 17%.
Erythrocyte content increased
117%, Hb content not signifi-
cantly changed.
Summation - threshold index
down 83% at 2 wk (controls down
93%) but later increased to
120% of original value (con-
trols .were 104% of original
value) .'
Increased respiration in heart
and lung tissue, no change in
kidneys. Significant increase
in percent of active neutro-
phils. Increased permeability
of vessels.
Wt. retarded compared to con-
trols.
Change in the motor chronaxy
(a measure of nerve cell func-
tion) of rats. In controls
chronaxy of straightening is
consistently above the chron-
axy of flexing. After 2-wk
exposure the two reversed and
remained that way through 6 wk;
over the next 3 wk the two re-
turned to normal positions, re-
versed again, and finally moved
back toward a normal relation-
ship.
In the 2 rats killed for study,
there was slight irritation of
mucous membranes of trachea and
bronchi. Changes in appearance
of some dendrites in brain cor-
tex.
Reference
and Rating
Mel'nichenko
(1968)
B-7
Duan
(1959)
B-10
-------
TABLE III-7. (continued)
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 10
(Concentration re-
ported as MAC, no
value given.
This value taken
from 1972 MAC in
U.S.S.R, 1972)
Humidity
and
Temperature
Not given
Species/
Strain/
Age/Weight
No. of
Test
Animals
Inhalation Rats, albino ~ 26
chamber
No. of
Controls
~ 26
Duration and
Frequency
of Exposure
6 h/d
Total
Length
of Expt.
H2S 9.36 + 0.51 Not given
Inhalation Rats, white, 24
chamber 80-200 g
6 h/d, daily
except Sunday,
4 mo
ft mo
H2S 4.86 + 0.08 Not given
Inhalation Rats, white, 22 14
chamber 80-200 g
6 h/d, daily
except Sunday,
4 mo
4 mo
Effects
Retardation of wt. gain. No
significant changes io number
of erythrocytes. Hb content
of blood significantly in-
creased. Number of leukocytes
fluctuated up and down over 4
mo, was higher than controls
at end. 02 consumption in-
creased slightly at beginning,
then decreased to 21.4% less
than controls. No significant
change in succinate dehydrog-
enase (SDG) activity in lungs
or kidneys, 16.7% decrease of
SDG activity in heart. Activ-
ity of cytochrome oxidase in
lungs increased 19.0%.
Reduced level of glycogen in
liver (91.9%), lower blood
sugar (69.1%), increased
lipids in blood (202.6%),
and lower.lipids in liver
(27.9%). Expressed lipemia
present. Lowering of eryth-
rocytes, significant increase
of hemoglobin and leukocytes,
and slight leukocytosis.
Reduced level of glycogen in
liver (68%), lower blood sugar
(50.2%), lower lipids in liver
(38.8%), and increased lipids
in blood (98.6%). Expressed
lipemia present. Increase in
erythrocytes, hemoglobin,
slight increase in eosinophils
and segmented neutrophils,
slight reticulocytosis, ex-
pressed leukopenia, and sharp
lowering of monocytes and
lymphocytes.
Reference
and Rating
Aitbaev
et al.
(1976)
B-9
Elebekova
et al.
(1976)
B-ll
Elebekova
et al.
(1976)
B-ll
-------
TABLE III-7. (continued)
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 0.02
Humidity
and
Temperature
Not given
Mode
of
Exposure
Inhalation
chamber
Species/ No. of
Strain/ Test No. of
Age/Weight Animals Controls
Rats,
60-90
albino, 10 H 10 H
g
Duration and
Frequency
of Exposure
12 h/d, "ex-
cept days off,"
Total
Length
of Expt
17 uk
-P-
ro
Effects
No change in wt.
controls.
compared to
Reference
and Ratine
Duan
(1959)
B-10
Change in the motor chronaxy
of rats. In controls chron-
axy of straightening is con-
sistently above the chronaxy
of flexing. After 2-wk expo-
sure the two were converging
and stayed near the same
through 7 wk. During the 7th
wk chronaxy of flexing ex-
ceeded chronaxy of straight-
ening, then the two moved back
toward normal.
No pathological changes noted
in 2 of the rats killed and ex-
amined.
-------
TABLE III-8. GUINEA PIGS—ACUTE EXPERIMENTAL EXPOSURE TO H2S
Compound(s) and Humidity
Concentration(s) and
in
H2S
II2S
H2S
H2S
mg/m3 (ppm) Temperature
2, 130 Not given
(1,500)
1,420-1,562 Not given
(1,000-1,100)
1 , 164 .4 Not given
(820)
340.8 Not given
(240)
Mode Species/ No. of Duration and Total
of Strain/ Test No. of Frequency Length
Exposure Age/Weight Animals Controls of Exposure of Expt.
Exposure Guinea pigs 2 Not given < 30 min, once
chamber
Exposure Guinea pigs 10 Not given < 30 min, once
chamber
Exposure Guinea pigs 5 Not given < 30 min, once
chamber
Exposure Guinea pigs 3 Not given < 18 h, once
chamber
Effects
0-2 min: spasms, convulsions,
unconsciousness, and cessation
of respiration.
2-30 min: death for one,
quick recovery for the other.
0-2 min: unconsciousness,
spasms, convulsions.
2-30 min: cessation of res-
piration, spasms, death.
2-30 min: increased respira-
tion.
8-18 h: 2 died, the other had
forced respiration and cough
with slow recovery following
Reference
and Rating
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
exposure.
B-10
-------
TABLE III-9. GUINEA PIGS—REPEATED DOSE EXPERIMENTAL EXPOSURE TO H2S
Compound(s) and
Concent ration(s)
in rag/tn3 (ppm)
H2S A97
(350)
Humidity
and
Temperature
Not given
Mode
of
Exposure
Exposure
chamber
Species/
Strain/
Age/Weight
Guinea pigs
No. of
Test
Animals
3
No. of
Controls
Not given
Duration and
Frequency
of Exposure
< 54 h, once
Total
Length
of Expt
H2S 312.4
(220)
H2S 312.4
(220)
Not given
Inhalation Guinea pigs Not Not given 22 d
given
Not given
H2S 312.4
(220)
NH3 180
(250)
Not given
Inhalation Guinea pigs, Not
previously given
exposed to
100 ppm H2S
for 7 d
Inhalation Guinea pigs Not
given
Not given 7 d
Not given 22 d
Reference
Effects and Rating
4-8 h: forced respiration. Mitchell
8-18 h: forced respiration, and Yant
weakness, 2 died, other one (1925)
very weak and sick. Third B-10
guinea pig removed from expo-
sure after 54 h but died 4 d
later.
22 d Mild, acute, suppurative, in- Renne and
flammatory infiltrate in the McDonald
lungs and trachea. No effect (1980)
on kidney, liver, adrenal, C—
heart, gastrointestinal tract,
brain, spleen, or eye tissues.
7 d Mild increase in the incidence Renne and
of acute inflammatory lesions McDonald
of the respiratory tract. 40% (1979)
incidence of mild interstitial C--
pneumonitis. Mild acute sup-
purative tracheit'is and lar-
yngitis. Mild chronic
nephritis in some.
22 d Mild, acute, suppurative, Renne and
inflammatory infiltrate in McDonald
the lungs and trachea. Mild, (1980)
acute, suppurative rhinitis C--
and laryngitis. Slight in-
crease in the incidence and
severity of intralurainal
calcification of renal corti-
cal tubules. No effect on
liver, adrenal, heart, gastro-
intestinal tract, brain, spleen,
or eyes.
-------
TABLE III-9. (continued)
Compound(s) and Humidity Mode Species/ No. of Duration and Total
Concentration(s) and • of Strain/ Test No. of Frequency Length
in mg/m3 (ppm) Temperature Exposure Age/Weight Animals Controls of Exposure of Expt
H2S 312.4
(220)
NH3 180
(250)
Not given Inhalation Guinea pigs, Not Not given 7 d
previously given
exposed .to
100 ppm H2S
and 250 ppm
NH3 for 7 d
7 d
H2S 284
(200)
Not given
Inhalation Guinea pigs
chamber
II2S 146.3
(103)
H2S 142
(100)
II2S 142
(100)
NH3 180
(250)
24 h
48 h
Not given Exposure Guinea pigs 2
chamber
Not given Inhalation Guinea pigs Not
given
Not given Inhalation Guinea pigs Not
given
Not given < 48 h, once
Not given 7 d
Not given 7 d
7 d
7 d
Effects
Mild increase 'in the incidence
of acute inflammatory lesions
of the respiratory tract. 70%
incidence of mild interstitial
pneumonitis. 40% incidence of
mild suppurative bronchiolitis.
Mild acute suppurative trache-
itis and laryngitis. 100% in-
cidence of mild chronic
nephritis.
Free cells lavaged from the
lungs after 24-h recovery
showed increases in the no.
of free cells and percent
of polymorphonuclear
neutrophils (PUN), and de-
creases in the percent of
macrophages and lymphocytes.
Changes are indicative of an
inflammatory response.
Phagocytic ability was
slightly decreased.
Viability was unaffected.
8-18 h: labored and forced
breathing.
18-48 h: death in one case
with slow recovery for the
other.
Reference
and Rating
Renne and
McDonald
(1979)
C--
Robinson
et al.
(1979)
C-6
Mitchell
and Yant
(1925)
B-10
No significant histopathologic Renne and
lesions or clinicopathologic McDonald
alterations. (1979)
C--
No significant histopathologic. Renne and
lesions or clinicopathologic McDonald
alterations. (1979)
C--
-------
TABLE III-9. (continued)
Compound(s) and
Concentration(s)
in mg/ra3 (ppm)
H2S 49.7-92.3
(35-65)
Humidity
and
Temperature
Not given
Mode
of
Exposure
Exposure
chamber
Species/
Strain/
Age/Weight
Guinea pigs
No. of
Test
Animals
2
No. of
Controls
Not given
Duration and
Frequency
of Exposure
< 100 h, once
Total
Length
of Expt
II2S 28.4
(20)
40%
30 ± 4°C
Inhalation Guinea pigs,
chamber 400-500 g
6 M
6 M
1 h/d, 11 d
11 d
Effects
8-18 h: hair rough.
18-48 h: hair rough, pus in
eyes and nostrils, cough. No
worse after 100 h continued
exposure; all recovered.
Fatigue, somnolence, dizzi-
ness, itching, and eye irri-
tation were observed. Sig-
nificant lowering of total
lipids and phospholipids
in the cerebral hemisphere
and brain stem, but no change
in the levels in the cerebellum.
No change in cholesterol level
in any of these regions. In-
creased" lipid peroxidation in
the cerebral hemisphere.
Reference
and Rating
Mitchell
and Yant
(1925)
B-10
Haider
et al.
(1980)
D-ll
-------
TABLE 111-10. CHICKENS—ACUTE EXPERIMENTAL EXPOSURE TO H2S
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 5,680
H2S 4,260
H2S 2,840
Humidity Mode
and of
Temperature Exposure
"Ambient tern- Spontan-
perature and eous
pressure" breathing
through
tracheo-
storay and
closed
ventila-
tory sys-
tem
"Ambient tern- Spontan-
perature and eous
pressure" breathing
through
tracheos-
tomy and
closed
ventila-
tory sys-
tem
"Ambient tern- Spontan-
perature and eous
pressure" breathing
through
tracheos-
tomy and
closed
ventila-
tory sys-
tem
Species/ No. of
Strain/ Test
Age/Weight Animals
White Leg- 5 M
horn chick-
ens (Callus
domesticus) ,
Babcock
strain ,
2.1 kg
(anesthe-
tized with
sodium pheno-
barbital to a
light plane)
White Leg- 5 M
horn chick-
ens (Callus
domesticus) ,
Babcock
strain,
2.1 kg
(anesthe-
tized with
sodium
phenobar-
bital to a
light plane)
White Leg- 10 M
horn chick-
ens (Callus
domesticus) ,
Babcock
strain,
2.1 kg
(anesthe-
tized with
sodium
phenobar-
bital to a
light plane)
Duration and Total
No. o£ Frequency Length
Controls of Exposure of Expt.
Each < 30 min, once 30 min
served as
its own
control;
10 M used
for compar-
ison to
anesthesia
time, and
experi-
mental pro-
cedures .
Each 30 min, once 30 min
served as
its own
control ;
10 M used
for compar-
ison to
anesthesia
time, and
experi-
mental pro-
cedures .
Each 30 min, once 30 min
served as
its own
control ;
10 M used
for compar-
ison to
anesthesia
time, and
experi-
mental pro-
cedures .
Effects
Exhibited struggling, gasping,
apnea , and intermittent bursts
of irregular breaths at vari-
ous tiroes during the exposure.
Death within 15 min for all
subjects. Cardiac arrest used
as death indicator. Variance
was significantly different
from control group.
Exhibition of what appeared
to be concentration-related
alterations in respiration,
with increase in variables
within 1 min. Increased res-
piration continued throughout
the first 5 min of exposure
then returned to normal during
remainder of exposure.
Exhibition of what appeared to
be concentration-related alter-
ations in respiration, with in-
crease in variables within 1
min. Increased respiration
continued throughout the first
5 min of exposure then returned
to normal during the remainder
of exposure.
Reference
and Rating
Klentz
and Fedde
(1978)
B-12
Klentz
and Fedde
(1978)
B-12
Klentz
and Fedde
(1978)
B-12
-------
TABLE 111-10. (continued)
oo
Compound (s) and
Concentration(s)
in mg/m3 (ppm)
H2S 1,420
H2S 781
H2S 738.4
Humidity
and
Temperature
Body temper-
ature main-
tained at
40°C, and
ambient
pressure
Body temper-
ature main-
tained at
40°C, and
ambient
pressure
Body temper-
ature main-
tained at
40°C, and
ambient
pressure
Mode
of
Exposure
Unidirec-
tional
artificial
ventila-
tion
Unidirec-
tional
ventila-
tion
Unidirec-
tional
ventila-
tion
Species/ No. of Duration and Total
Strain/ Test No. of Frequency Length
Age/Weight Animals Controls of Exposure of Expt
Adult White 2 H Served as < 5 min, once 30 min
Leghorn own con-
chickens, trols
Babcock
strain
(anesthe-
tized with
sodium
phenobar-
bital and
secured in
dorsal re-
cumbancy)
Adult White 1 M Served as 30 min, once 30 min
Leghorn own con-
chicken, trol
Babcock
strain
(anesthe-
tized with
sodium
phcnobar-
bital and
secured in
dorsal re- .
cumbancy)
Adult White 1 M Served as 30 min, once 30 min
Leghorn . own con-
chicken, trol
Babcock
strain
(anesthe-
tized with
sodium
phenobar-
bital and
secured in
dorsal re-
cumbancy)
Effects
Decreased respiratory fre-
quency, increased sternal
movements after 30 s. Intra-
pulmonary C02 receptor dis-
charges increased in frequency
peaking at 40-80 s. Both
birds died within 5 min.
Reference
and Rating
Klentz
and Fedde
(1978)
B-12
Decreased respiratory fre- Klentz
quency, increased sternal and Fedde
movements after 30 s, sternal (1978)
movements ceased within 4 min. B-12
Intrapulmonary C02 receptor
discharges increased in fre-
quency.
Decreased respiratory fre- Klentz
quency, increased sternal and Fedde
movements after 30 s, sternal (1978)
movements ceased within A min. B-12
Intrapulmonary C02 receptor
discharges increased in fre-
quency, peaking at 40 s.
-------
TABLE 111-10. (continued)
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 710
H2S 710
H2S 639
Humidity
and
Temperature
."Ambient
temperature
and pressure"
Body temper-
ature main-
tained at
40°C, and
ambient
pressure
Body temper-
ature main-
tained at
40°C, and
ambient
pressure
Node
of
Exposure
Spontan-
eous
breathing
through
tracheos-
tomy and
closed
ventila-
tory sys-
tem
Unidirec-
tional
artifi-
cial
ventila-
tion
Unidirec-
tional
artificial
ventila-
tion
Species/ No. of
Strain/ Test
Age/Weight Animals
White Leg- 10 M
horn chick-
ens, (Callus
domesticus) ,
Babcock
strain,
2.1 kg
(anesthe-
tized with
sodium
phenobar-
bital to a
light plane)
Adult White 1
Leghorn
chicken,
Babcock
strain
(anesthe-
tized with
sodium
phenobar-
bital and
secured in
dorsal re-
cumbancy)
Adult White 1 M
Leghorn
chicken,
Babcock
strain
(anesthe-
tized with
sodium
phenobar-
bital and
secured in
dorsal re-
cumbancy)
Duration and Total
No. of Frequency Length
Controls of Exposure of Expt.
Each 30 min, once 30 min
served as
its own
control;
10 M for
compar-
ison to
anesthesia
time, and
experi-
mental pro-
cedures.
Served as 30 min, once 30 min
own con-
trol
Served as 30 min, once 30 min
own con-
trol
Effects
Respiration not significantly
affected. No significant dif-
ferences in variability com-
compared to controls.
Increased amplitude of sternal
movement, decreased respira-
tory frequency, respiration
ceased after 200 s. Intra-
pulmonary C02 receptor dis-
charges increased in frequency,
peaking at 70 s.
Decreased respiratory fre-
quency, increased sternal
movements after 30 s, sternal
movements ceased after 10 min.
Intrapulmonary C02 receptor
discharges increased in fre-
quency, peaking at 20 s. .
Reference
and Rating
Klentz
and Fedde
(1978)
B-12
Klentz
and Fedde
(1978)
B-12
Klentz
and Fedde
(1978)
B-12
-------
TABLE 111-10. (continued)
Compound (s) and
Concentration(s)
in mg/m3 (ppm)
H2S 497
Humidity
and
Temperature
Body temper-
ature main-
tained at
40°C, and
ambient
pressure
Mode
of
Exposure
Unidirec-
tional
ventila-
tion
Species/ No. of
Strain/ Test
Age/Weight Animals
Adult White 1 M
Leghorn
chicken,
Babcock
strain
(anesthe-
tized with
sodium
phenobar-
bital and
secured in
dorsal re-
cumbancy)
Duration and Total.
No. of Frequency Length
Controls of Exposure of Expt
Served as 30 min, once 30 min
own con-
trol
Effects
Decreased respiratory fre-
quency, increased sternal
movements after 30 s, sternal
movements ceased within 4 min.
Intrapulmonary C02 receptor
discharges increased in fre-
quency, peaking at 100 s.
Reference
and Rating
Klentz
and Fedde
(1978)
B-12
-------
TABLE III-ll. RABBITS—ACUTE EXPERIMENTAL EXPOSURE TO
Compound(s) and Humidity
Concentration(s) and
in mg/m3 (ppm) Temperature
H2S 46, 150 Not given
(32,500)
H2S 18,460 Not given
(13,000)
H2S 11,644 Not given
(8,200)
Mode Species/
of Strain/
Exposure Age/Weight
Inhalation Rabbit,
chamber "big and
strong"
Inhalation Rabbit,
"rather
weak"
Inhalation Rabbit
chamber
No. of
Test No. of
Animals Controls
1 , None
exposed
to 1,846
rag H2S/m3
for 8 h,
1 wk be-
fore
1 None
1 , None
exposed
in the
previous
week to
6,150,
5,112, and
1 ,846 mg
H2S/m3 for
2 min,
3.5 h, and
8 h, re-
spectively
Duration and Total
Frequency Length
of Exposure of Expt. Effects
2.5 min 12.5 min Immediate collapse, lying on
its side, dyspnea, and body
muscle spasms. When exposure
stopped, was completely para-
lyzed, but attempted to walk
3 min later, and was "rather
normal" 10 min later.
3 min 18 min Staggering, shaky movements,
fell on its side, rolled over
several times, and stretched
rear legs. Strained respira-
tion, rate increasing to 27
from 22 (for 0.5 min). Quick
recovery.
10 min "Few In 2 min, fell on its side,
hours" rolled over, nystagmus (rapid,
involuntary eye movement,
implying CNS problems), and
stretching of extremities.
After 5 min, began clonic
and tonic convulsions of all
paws, and series of strong
roll-overs. Respiration in-
creased to 42 (for 0.5 min) by
10 min. When removed, could
not stand; began crawling in
4 min; recovered fairly fast in
the next hours.
Reference
and Rating
Lehmann
(1892)
B-9
Lehmann
(1892)
B-9
Lehmann
(1892)
B-9
H2S 5,112-8,236;
avg. 6,958
(3,600-5,800;
avg. 4,900)
Not given
Inhalation Rabbit
chamber
None
1 h at 5,112; ~ 32 h After 24 h: increasingly rest- Lehmann
1 h 40 min at less, then tonic extending (1892)
8,236 mg H2S/m3 movements of the legs, then B-9
collapsed on its side, with
head twisted; increasing
dyspnea; eyes still and half-
closed; muscle spasms; mucous
membranes red.
By the end: spasms in all legs,
tonic and tetanic extensions in
the neck muscles, clearly nys-
tagmus, dilated pupils, and
slightly opaline corneas. 30 h
after exposure stopped, head
leaning to the right, rolling
movements with nystagmus, respir-
ation 30, and would not eat.
-------
TABLE III-ll. (continued)
Compound(s) and
Conccntration(s)
in rog/m3 (ppm)
H2S It, 544-6, 674;
avg. 5,112
(3,200-4,700;
avg. 3,600)
Humidity
and
Temperature
Mot given
Mode
of
Exposure
Inhalation
chamber
Species/
Strain/
Age/WeiRht
Rabbit,
"very big
and strong"
No. of
Test No. of
Animals Controls
1 , None
exposed
to 1,300
ppm for
8 h, 2 wk
before
Duration and
Frequency
of Exposure
1 h at 6,674;
then 2.5 h at
4,544
Total
Length
of Expt
3.5 h
H2S 2,982-3,124;
avg. ->. 3,124
(2,100-2,200;
avg. -v. 2,200)
Hot given
H2S 1,846-2,414;
avg. 2,130
(1,300-1,700;
avg. 1,500)
H2S 1,846
(1,300)
Not given
Not given
Inhalation Rabbit,
chamber "thin"
Inhalation Rabbit
chamber
Inhalation Rabbit,
chamber "big and
strong"
1,
exposed
for 3 min
to 13,000
ppm the
day before
None 1 h 40 min 8 h
at 2,982; 6 h
at 3,124;
then 20 min at
2,982 mg H2S/m3
None 8 h at 1,846; 10 h
then 2 h at
2,414 mg
H2S/m3
None 8 h 8 h
Effects
Respiration decreased from 63
to 14 (for 0.5 min) after
1.25 h, then increased to 26.
No obvious symptoms.
Few symptoms. Respiration de-
creased in first 4 h, 21-10
(for 0.5 min). After 5 h,
increasing dyspnea, 25-40.
Sat quietly after exposure
stopped.
Quiet, lethargic. Respiration
increased from 16-12 to 38
(for 0.5 rain) in 4 h, then
decreased slightly. At 8 h,
muzzle slightly opened and
strained breathing. By 10 h,
occasional coughing.
Quiet. No signs of irritation
for the first hour. Respira-
tion 46-41 (for 0.5 min), de-
creased for next 2.5 h, then
increased for 2 h, frequently
to 55-65. Strained breathing
towards the end. Fine after
exposure stopped.
Reference
and Rating
Lehmann
(1892)
B-9
Lehmann
(1892)
B-9
Lehmann
(1892)
B-9
Lehmann
(1892)
B-9
-------
TABLE 111-12. RABBITS—REPEATED DOSE EXPERIMENTAL EXPOSURE TO
Compound(s) and
Concentrat ion(s)
in mg/m3 (ppm)
H2S 1,420
(1,000)
Humidity
and
Temperature
Mode Species/
of Strain/
Exposure Age/Weight
Inhalation Rabbits
chamber
H2S 142
(100)
Inhalation Rabbits
chamber
to
H2S 50-100
(35.2-70.4)
H2S 14.2-42.6
(10-30)
90%,
20°C
Inhalation Albino
chamber rabbits,
1.5-2.0 kg
Inhalation Rabbits
chamber
No. of
Test
Animals
3 H
No. of
Controls
3 M
None
Duration and
Frequency
of Exposure
?/wk,
18 d
?/wk,
15 d
Not Not given 5 d
given
2 H None ?/d,
?/wk,
20 d
Total
Length
of Expt.
18 d
15 d
5 d
20 d
Effects
Reference
and Rating
Weise
(1933)
B-9
No obvious disturbances for
3 d. Then increasing irrita-
tion of the connective mem-
branes, leading to erosion of
the eye membranes. One animal
lost weight. Intermittent
heavy breathing, but no distinct
changes in respiration rate he-
fore and after each exposure.
No findings on autopsy except
slight changes in the stomach
or small intestines of 2 ani-
mals .
Temporarily increased eye Weise
secretion. Quiet, moderately (1933)
exhausted-looking at the end. B-9
Slight decrease in respiratory
frequency at the end of expt.
No weight loss. 2/3 showed,
on autopsy and microscopic
examination, evidence of in-
creased blood circulation in
the gastrointestinal tract
(including hyperemia and loss
of the villus epithelium in
the small intestine).
No evidence of any eye lesions Masure
was seen. (1950)
B-10
No effect on respiration rate,
white and red blood cell
counts, hemoglobin levels, or
appetite. Slight weight de-
crease. On autopsy, no
changes. Some changes in
microscopic exam, of the small
intestines of one animal.
Weise
(1933)
B-9
-------
TABLE 111-13. RABBITS—CHRONIC EXPERIMENTAL EXPOSURE TO
Compound(s) and Humidity Mode Species/ No. of Duration and Total
Concentration(s) and of Strain/ Test No. of Frequency Length
_in rag/m (ppm) Temperature Exposure Age/Weight Animals Controls of Exposure of Exot
H2S 142
(100)
Not given Inhalation Rabbits, 44 30 min/d, It rao
chamber domestic, daily, 4 mo
avg. wt.
20 kg
Ui
H2S 28.4-35.5 Not given Inhalation Rabbits,
(20-25) chamber domestic,
avg. wt.
20 kg
5 M
5 M
h/d, 150 d 210 d
Effects
Reference
and Rating
Wakatsuki
(1959)
C-8
No measurable abnormal find-
ings in the general condition,
body weight, number of eryth-
ocytes, serum calcium, total
serum protein, and serum pro-
tein fraction. There was de-
cline in specific gravity of
blood. Some slight changes
such as oligochromemia, reti-
culocytosis, leucopenia, and
relative lymphocytes is, which
quickly returned to normal
after exposure stopped.
No change in general state and Kuwai
specific gravity of blood. (1960)
There was an initial increase B-10
in free cholesterol and fall
in ester ratio that returned
to normal levels after a short
period.
-------
TABLE 111-14. CATS—ACUTE EXPERIMENTAL EXPOSURE TO
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 10,082-11,644;
avg. 10,792
(7,100-8,200;
avg. 7,600)
Humidity
and
Temperature
Not given
Species/
Strain/
Age/Weight
No. of
Test
Animals
Inhalation Cat, "young 1
chamber and strong"
No. of
Controls
None
In
Ui
H2S 9,656-10,224;
avg. 10,082
(6,800-7,200;
avg. 7,100)
Not given
Inhalation
chamber
Cats
and
, "young
strong"
2,
1 exposed
to 7,600
ppm for
•». 2 h,
3 d before
None
H2S 5,112-8,236;
avg. 6,958
(3,600-5,800;
avg. 4,900)
Not given
Inhalation Cats
chamber
2,
1 exposed
in the
previous
wk to 3,200
and 7,100
and 7,600
ppm for
2-8 h each
None
II2S 7,952
(5,600)
Not given
"Box"
Cat, •>• 3 kg
None
Duration and
Frequency
of Exposure
1 h at 11,644;
then 49 min at
10,082 mg/m3
Total
Length
of Expt.
1 h at 9,656;
7 h at 10,224
mg/n3
1 h at 5,112;
1 h 40 min
at 8.236
"a few
hours"
41 min
41 min
Effects
Reference
and Rating
For first y 1.5 h, alternating Lehmann
restlessness and lying in (1892)
sleep position, occasional B-9
mewing and sneezing, eyes
closed, no salivation, and
respiration increasing from
13 to 24 (for 0.5 min) then
deepening and decreasing to
8. After 100 min,•restless,
staggering, dilated pupils,
urinates and defecates, and
increasing dyspnea with respir-
ation at 130 by the end. Some
recovery 1 h after exposure
stopped; complete recovery "in
the following hours."
Previously exposed cat after Lehmann
3 h: could not stand up, eyes (1892)
closed with small pupils, B-9
continuous secretion of thick
saliva, nose dry.
Removed after 4 h 16 min: No
response to stimulus, irregu-
lar respiration, no perceived
heartbeat. Slow recovery, fine
the next day. The other cat
died after 8 h 9 min.
Previously exposed cat was im- Lehmann
mediately in the sleeping (1892)
position, eyes closed, sali- B-9
vated. Respiration 6-10 (for
0.5 min). The other cat was
in the sleeping position after
15 min, respiration 13-23.
After 2 h: bloody feces, vomit-
ing, and salivation. Both re-
covered after several hours.
Quiet and slightly sleepy.
No other symptoms.
Lehmann
(1892)
B-9
-------
TABLE 111-14. (continued)
Compound (s) and
Concent ration (s)
in mg/m3 (ppm)
II2S 4,544-6,674;
avg. 5,112
(3,200-4,700;
avg. 3,600)
Humidity
and
Temperature
Not given
Node
of
Exposure
Inhalation
chamber
Species/
Strain/
Age/Weight
Cat
No. of
Test No. of
Animals Controls
1, None
exposed
to 1,400
ppm for
10 h, 1 wk
before ,
and 1,300
ppm for
8 h, 2 wk
before
Duration and
Frnquenry
of Exposure
1 h at 6,674;
2.5 h at
4,544 mg/m3
Total
Length
of Expt
3.5 h
H2S 5,396
(3,800)
Not given
H2S 2,982-3,124; Not given
avg. •*• 3,124
(2,100-2,200;
avg. •>. 2,200)
H2S 1,846-2,414; Not given
avg. 2,130
(1,300-1,700;
avg. 1,500)
H2S 1,846
(1,300)
Not given
"Box" Cat, 3 kg
Inhalation Cats,
chamber "young,
strong"
Inhalation Cat
chamber
Inhalation Cat
chamber
2,
1 exposed
to 7,100-
7,600 ppm
for 10 h,
3 or 6 d
before
1,
with
10-h ex-
posure
to 1,500
ppm, 2 d
before
None
None
None
None
65 min
1 h 40 min at
2,982; 6 h at
3,124; 0.5 h
at 2,982 mg/m3
8 h at 1,846;
2 h at 2,414
mg/m3
8 h
65 min
8 h
10 h
8 h
Effects
Rrt i-rrm•<•
.iiid R.i I i ng
Immediately lay on its stomach. Lclimann
Respiration decreased from 16 (1892)
to 8 (0.5 min). Eyes closed, B-9
half asleep. Weak continuous
secretion of thick saliva after
12 min.
Lehmann
(1892)
R-9
Lehmann
(1B92)
B-9
No symptoms.
Previously exposed cat lay on
its side, respiration •*• 14
(for 0.5 min), strong pulse
(51). At end, was half nar-
cotized, had weak reaction
to stimulus, could barely
walk, occasional salivation,
and had red ears.
Other animal: no symptoms
for 3 h, then lay on its side.
No clear signs of illness. Lehmann
Quiet, lying on floor. Respir- (1892)
ation 10-17 (for 0.5 min). B-9
Towards the end, nose slightly
wet, occasional coughing.
Fine after exposure stopped.
Quiet, lying down. Respira- Lehmann
tion 8-12 (for 0.5 min), (1892)
changing after 2 h. Salivary B-9
secretions for "* 4.5 h. Re-
covered quickly.
-------
TABLE 111-15. CATS—REPEATED DOSE EXPERIMENTAL EXPOSURE TO
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 1,420
(1,000).
Humidity
and
Temperature
Not given
Species/
Strain/
AgeVWeight
No. of
Test
Animals
Inhalation Cats
chamber
No. of
Controls
None
Duration and
Frequency
of Exposure
12 h/d,
?/wk,
18 d
Total
Length
of Expt.
18 d
Effects
Moderate hoarseness the only
sign of illness. No changes
in the gastrointestinal tract
except increased mucous mem-
brane secretion in one cat.
The other cat had severe
edema of the lung.
Reference
and Rating
Weise
(1933)
B-9
-------
TABLE 111-16.
MONKEYS—ACUTE EXPERIMENTAL EXPOSURE TO H2S
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 710
(500)
Humidity
and
Temperature
Not given
Species/
Strain/
Age/Weight
No. of
Test
Animals
Inhalation
chamber
Rhesus monkey 1
No. of
Controls
None
Duration and
Frequency
of Exposure
H2S 710
(500)
Not given
Inhalation Rhesus monkey 1
chamber
None
Total
Length
of Expt.
35 min, once < 1 h
25 min, 3 d
later another
17-min exposure
8 d
CO
Effects
Reference
and Rating
Rubbing of eyes, intense gasp- I.und and
ing decreasing in intensity Wetland
until heart and respiration (1966)
stopped. Died after 35 min, B-8
blood sugar level at time of
death 640 mg%.
No discernible pathological
changes in any area of brain,
nor in kidneys or heart.
Frequent rubbing of eyes, Lund and
gasping, and sudden uncon- Wieland
sciousness. After 25 min (1966)
respiration stopped, animal B-8
revived and was exposed again
on 3rd d. In second exposure
animal became unconscious after
17 min and died 5 d later.
Blood sugar was 200 rog% day
of death.
H2S
710
(500)
Not given
Inhalation Rhesus monkey 1
chamber
None
22 min, once 10 d
Pathological changes in main
ganglia of brain characterized
by spot-like cellular reactions
and vascular changes. Exten-
sive changes in cerebral cortex
including cellular and vascular
changes.
Frequent rubbing of eyes, Lund and
gasping, and sudden uncon- Wieland
sciousness after 22 min. (1966)
Exposure ended, it regained B-8
consciousness after 140 min,
but was somnolent, moved little,
was disoriented, and had little
appetite. It improved only
slightly before being killed at
10 d.
Pathological changes in brain,
very extended cortex losses in
the middle cortex strata in the
region of the parietal brain
and occipital brain. No vis-
ibl.e pathological changes in
main ganglia of brain, kidney,
heart, and liver.
-------
TABLE 111-17. MONKEYS—CHRONIC EXPERIMENTAL EXPOSURE TO H2S
Compound(s) and
Concent rat ion (s)
in mg/m3 (ppm)
H2S 28. A
(20)
Humidity
and
Temperature
50 + 10%,
57 + 5°
(Control
room up
to 86°F)
Mode
of
Exposure
Inhalation
chamber
Species/
Strain/
Age/Weight
Rhesus
monkeys ,
avg. wt.
1-7 kg
No. of
Test
Animals
10 H
No. of
Controls
10 H
Duration and
Frequency
of Exposure
90 d
Total
Length
of Expt.
90 d
Effects
No deaths. Statistically
significant weight loss after
90 d.
Statistically significant
Reference
and Ratini
Sandage
(1961)
B-10
changes in blood parameters
at 90 d exposure over pre-
exposure levels: erythrocytes
and araylase increased, and MCHb
and HCHbC (mean corpuscular
hemoglobin concentration) de-
creased. Compared with con-
trols at 90 d: HCHbC decreased,
and urine alkaline phosphatase
increased.
Ln
-------
TABLE III-18,
DOGS—ACUTE EXPERIMENTAL EXPOSURE TO H2S
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 48,280
(34,000)
Humidity
and
Temperature
Not given
"Box"
H2S 7,952
(5,600)
Not given "Box"
H2S 5,396
(3,800)
Not given "Box"
H2S 2,130-2,272 Not given
(1,500-1,600)
H2S 1,817.6
(1,280)
Not given
Exposure
chamber
Exposure
chamber
Species/
Strain/
Age/Weight
Oog,
•v fi.6 kg
No. of
Test No. or
Animals Controls
Dog,
•>• 6.6 kg
Dog,
6.6 kg
Dogs
Dogs
1
None
Duration and
Frequency
of Exposure
•>• 2 min
Total
Length
of Expt.
~ 4.5 h
None
41 min
None
65 min
65 min
Not given < 30 min, once
Not given < 30 min, once
Effects
Re IrrciHT
and Rat ing
Alternating clonic ami tonic
convulsions, tlion moribund hut
with strong heartbeat. After-
wards, needed artific.il "re-
animation." 8 min Later, deep
respiration, cramps, attempted
to get up, urinated and defe-
cated. By 4.5 h, passably re-
covered - eating, and no in-
flammation symptoms of mucous
membranes.
After 2 min, was moribund,
with stretching spasms, di-
lated pupils, and slow, very
deep respiration. Some re-
covery, but with epileptic
attacks interrupted by eu-
phoric periods. After 20
min of recovery, was ahle to
walk waveringly. The next
day had injected conjunctiva
and walked stiffly. Even-
tually recovered.
Restless, sneezing, blinking,
slightly twitching legs, and
yawning in the first 10 min.
By 15 min, slight gasping
and choking, with pounding
carotids. Then itching nose,
"flabby standing," and "de-
creased intelligence." Ira-
proving by 30 min, and no
disturbance at the end.
0-2 min: spasms, respira-
tion stops.
2-30 min: death.
0-2 min:
stops.
2-30 min:
spasms, respiration
death.
I.Himaun
(1RQ2)
R-'l
Lehmann
(1892)
B-9
Lehmann
(1892)
B-9
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-IO
-------
TABLE 111-18. (continued)
Compotind(s) and Humidity Mode Species/
Concentration(s) and of Strain/
in mB/m3 (ppm). Temperature Exposure Age/Weight
H2S 1,420-1,618.8 Not given Exposure Dogs
(1,000-1,140) chamber
H2S 1,207-1,263.8 Not given Exposure Dogs
(850-890) chamber
H2S 1,079.2-1,136 Not given Exposure Dogs
(760-800) chamber
H2S 497
(350)
H2S 340.8
(240)
H2S 146.3
(103)
Not given Exposure Dogs
chamber
Not given
Not given
Exposure
chamber
Exposure
chamber
Dogs
Dogs
No. of Duration and Total
Test No. of Frequency Length
Animals Controls of Exposure of Expt.
8 Not given < 30 rain, once
Not given < 30 min, once
Not given £ 1 h, once
Effects
Not given < 16 h, once
Not given < 16 h, once
Not given < 16 h, once
0-2 ain: falls over uncon-
scious, spasms, convulsions,
respiration stops.
2-30 rain: death.
0-2 min: falls over uncon-
scious, spasms, convulsions.
2-30 min: respiration stops,
death.
0-2 min: falls over uncon-
scious; spasms, convulsions.
2-30 min: respiration stops,
spasms.
30 min-1 h: respiration
stopped and 1 animal died;
other taken out and recovered.
2-30 min: lacrimation and
nervousness.
30 min-1 h: depression.
1-4 h: depression to stupor.
4-8 h: labored breathing,
hemorrhage, and death.
1-4 h: depression.
4-8 h: forced respiration,
lacrimation.
8-16 h: both died.
4-8 h: lacrimation and de-
pression.
8-16 h: pus in eyes, death
intense.
Reference
and Rating
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
-------
TABLE 111-19.
DOGS—REPEATED DOSE EXPERIMENTAL EXPOSURE TO H S
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 130-150
Humidity
and
Temperature
Mot given
Inhalation
chamber
Species/
Strain/
Age/Weight
Dogs
H2S 14
Not given
Inhalation
chamber
Dogs
NJ
No. of
Test
Animals
4 (2 ex-
posed to
14 mg
H2S/ra3
for 2 wk
prior to
this ex-
posure)
No. of
Controls
Apparently
none
Duration and
Frequency
of Exposure
Total
Length
of Expt.
7 h/d, ~ 8 wk ~ 8 wk
Apparently
none
7 h/d, 14 d
14 d
Effects
Reference
and Rating
Moser
(1940)
B-ll
(No effect on 2 dogs during 2
wk at lower exposure, except
increased drinking.) At
higher concentration, dogs
were less lively, nauseous,
ate less, and drank more. All
dogs coughed and had increased
secretion of tear ducts and one
developed moderately strong con-
junctival infection. Nausea
and breathing difficulties dis-
appeared shortly after removal
from exposure chamber each day.
No significant blood changes.
Occasional coughing. In- Moser
creased liquid consumption and (1940)
reluctance to eat shortly after B-ll
each poisoning.
Very lively on returning to
chamber the next day,.with no
signs of poisoning. No change
in blood picture or body weight.
-------
TABLE 111-20. PIGS—REPEATED DOSE EXPERIMENTAL EXPOSURE TO H2S
Compound(s) and
Concert trat ion (s)
in niR/m3 (ppm)
H2S 12.1
(8.5)
H2S 2.84 (2)
HH3 36 (50)
Humidity
and
Temperature
17-19°C
17-19°C
Mode
of
Exposure
Inhalation
chamber
Inhalation
chamber
Species/
Strain/
Age/Weight
Pigs,
crossbred,
13.2 kg
Pigs,
crossbred,
13.2 kg
No. of
Test No. of
Animals Controls
3 3
(All of the same
sex, unspecified)
3 3
(All of the same
sex, unspecified)
Duration and Total
Frequency Length
of Exposure of Expt.
17 d
19 d
Effects
No effect on body wt. gain.
No pathological changes in
respiratory system.
No effect on body wt. gain.
No pathological changes in
respiratory tract.
Reference
and Rating
Curtis
et al.
(1975)
C-10
Curtis
et al.
(1975)
C-10
-------
TABLE 111-21.
GOATS—ACUTE EXPERIMENTAL EXPOSURE TO H S
Compound (s) and
Concentration(s)
in mg/ra3 (ppm)
H2S 1,817.6-
1,888.6
(1,280-1,330)
H2S 1,420-1,562
(1,000-1,100)
H2S 1,164.4
(820)
Humidity
and
Temperature
Not given
Not given
Not given
Mode
of
Exposure
Exposure
chamber
Exposure
chamber
Exposure
chamber
Species/
Strain/
Age/Weight
Goats
Goats
Goat
No. of Duration and Total
Test No. of Frequency Length
Animals Controls of Exposure of Expt.
4 Not given < 30 min, once
4 Not given < 30 min, once
1 Not given < 30 min, once
Effects
0-2 min: falls over uncon-
scious, spasms, and cessation
of respiration.
2-30 min: death.
0-2 min: distress and excite-
ment, bleats.
2-30 min: falls over uncon-
scious, spasms, convulsions,
and cessation of respiration,
death.
2-30 min: increased respira-
tion.
Reference
and Rating
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
Mitchell
and Yant
(1925)
B-10
-------
TABLE 111-22. GOATS—REPEATED DOSE EXPERIMENTAL EXPOSURE TO
Ln
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 142
(100)
Humidity
and
Temperature
17°C
H2S 71
(50)
17°C
H,S
14.2
(10)
17°C
Species/
Strain/
Age/Weight
Inhalation Goats, mixed
chamber breed, 3-4 y,
35-75 kg
Inhalation Goats, mixed
chamber breed, 3-4 y,
35-75 kg
Inhalation Goats, mixed
chamber breed, 3-4 y,
35-75 kg
No. of
Test
Animals
6 F
4 F
4 F
No. of
Controls
Served as
own con-
trols
Served as
own con-
trols
Served as
own con-
trols
Duration and
Frequency
of Exposure
4 d, once
Total
Length
of Expt.
4 d
4 d, once
4 d
4 d, once
4 d
Effects
Reference
and Rating
Hays
(1972)
B-13
Respiration frequency de-
creased, rectal temperature
increased 0.7°C, returning to
near normal after 4 d. Food
and water intake decreased
37 and 25%, respectively, dur-
ing first 2 d, regaining near
normal levels after 4 d.
Plasma cortisol increased but
returned to normal levels
after 4 d of exposure.
Plasma cortisol increased Hays
(possibly indicating stress) (1972)
and rectal temperature in- B-13
creased 0.7°C, but both re-
turned to near normal after
4 d of exposure. Food and
water intake decreased by 64%
during the 2nd d, but increased
some after 4 d.
Food and water intake de- Hays
creased by 20 and 63% re- (1972)
spectively on first day, but B-13
returned to near normal levels
thereafter.
-------
TABLE 111-23. COWS—REPEATED DOSE EXPERIMENTAL EXPOSURE TO
Compound (s) and
Concentration(s)
in
H2S
mg/mj (ppra)
28.4
(20)
Humidity Mode
and of
Temperature Exposure
50%, 20°C Inhalation
through
exposure
hood over
cow's head
Species/
Strain/
Age/Weight
Cows (lac-
tating),
Holstein,
avg. wt.
499 kg
No. of Duration and Total
Test No. of Frequency Length
Animals Controls of Exposure . of Expt.
3 Served as 21 d, once 71 d
own con-
trols
prior to
exposure
Effects
No effect on feed intake, milk
production, or heart rate.
Slight lacrimation.
Reference
and Rating
Hays
(1972)
B-13
-------
TABLE 111-24. SUMMARY OF ANIMAL EXPOSURES TO H,S
Level
(mg/m3)
7,952-
48,280
5,112-
46,150
5,112-
11,644
1,846-
7,952
2,840-
4,260
1,079-
2,272
1,420-
2,130
Time
2-40
min
2 min-
~ 3 h
~ 2 h-
~ 8 h
40 min-
10 h
30 min
30 min-
1 h
30 min
Species
DOG
RBT
CAT
CAT
1,846-
6,674
5,680
5,396
2-10 h
30 min
65 min
RBT
CKN
DOG
CKN
DOG
GPG
Effects
Cramping, spasms, convulsions, slow and deep
respiration, epileptic-type attacks. Very slow
recovery.
Weakness, staggering, collapse, spasms, dyspnea,
mucous membrane irritation. Fairly rapid recov-
ery.
Restlessness, weakness, eye and nose irritation,
changes in respiration. One died, the rest recov-
ered in several hours.
Few symptoms: quiet, slight respiration changes,
occasional coughing, salivary secretions. Fine
after exposure. One previously exposed cat had
more severe reactions.
Increased respiration, lethargy, occasional
coughing. Fine after exposure stopped.
Gasping, apnea, cardiac arrest, and death.
Signs of irritation, gasping and choking, and
weakness for 30 min. Then apparent habituation
(Lehmann, 1892).
Increased respiration for 5 min, then normal.
Spasms, convulsions, unconsciousness, respira-
tion stops, then death (Mitchell and Yant, 1925).
Spasms, convulsions, unconsciousness, and death.
67
-------
TABLE 111-24. (continued)
Level
(mg/m3)
Time
1,888.6 30 rain
1,420
1,420
440-
1,420
18 d
12 h/d;
18 d
20 min
1-8 h
Species
GOAT
RBT
CAT
MUS
RAT
1,164.4
6,248-
1,036.6
710
710
30 min
30 min
2 min
30 min
22-35
GPG
GOAT
CAN
CKN
MKY
mm
Effects
Unconsciousness, spasms, convulsions, respiration
stops, and death.
Increased irritation of mucous membranes, inter-
mittent heavy breathing, slight intestinal changes
found on autopsy.
One had increased mucous membrane secretions, and
one had severe edema.
Marked lacrimation, all died. Lung, liver, kid-
ney, and stomach damage.
Excitement, forced breathing, weakness, spasms,
unconsciousness, and sometimes death. Survivors
recovered more quickly after short, high exposures
than after longer, low exposures. Damage to all
major organs.
Increased respiration.
Increased respiration.
Edema, dizziness, unconsciousness. Quick recov-
ery.
No effect on respiration.
Eye irritation, gasping, unconsciousness, and
death. Pathological changes in the brain, but
not in the kidney, heart, or liver.
68
-------
TABLE 111-24. (continued)
Level
(mg/m3)
340.8-
497
146.3-
497
49.7-
440.2
269.8-
355
312.4
312.4
312.4
146.3
142
142
Time
54 h
16 h
3 h/d;
5-14 d
22 d
48 h
15 d
Species
GPG
DOG
30 min- CAN
18 h
16-22 h RAT
RAT
RAT
14 d and GPG
22 d
284
130-
150
24 h
7 h/d;
8 wk
RAT
GPG
DOG
GPG
RBT
30 min/d; RBT
4 mo
Effects
Forced breathing, weakness, immediate or delayed
death in some, slow recovery of survivors.
Lacrimation, nervousness, forced breathing,
death.
At higher levels, immediate partial collapse
followed by some recovery. Then for all levels:
gasping, forced breathing, edema, weakness, un-
consciousness, and immediate or delayed death.
Quiet, forced breathing, signs of irritation,
< 50% mortality, and slow recovery of survivors.
Damage to lungs, heart, liver, stomach, kidneys,
and intestines.
No dominant lethal effects induced during spermato-
genesis in male rats. No embryotoxicity following
exposure of pregnant females.
NOEL for major organs.
Mild acute inflammatory lesions of the respira-
tory tract. NOEL for other major organs.
Changes in lavaged lung cell composition indicat-
ing inflammatory response.
Quiet, nausea, coughing, moderate conjunctival ir-
ritation, breathing difficulties at the end of
each day. No significant blood changes.
Forced breathing, some death, slow recovery of
survivors.
Some initial eye irritation. Quite, exhausted-
looking, slight decrease in respiratory frequency.
No change in general condition. Some slight
changes in blood parameters.
69
-------
TABLE 111-24. (continued)
Level
(mg/m3)
142
71-
142
41.6-
142
14.2-
42.6
28.4
28.4
Time
7 d
4 d
8-24 h
20 d
4 h/d;
150 d
48 h
90 d
Species
RAT
GPG
GOAT
MUS
50-100
49.7-
92.3
50
5 d
16 h
100 h
100 h
6 h/d;
6 mo
RBT
; RAT
RAT
GPG
RAT
RBT
RBT
MUS
MUS
Effects
No histopathologic lesions or clinicopathologic
changes.
Increased rectal temperature, decreased food and
water intake, and increased plasma cortisol lev-
els . All returned to normal by the end.
Hypothermia, decreased food and water intake,
weight loss, ~ 50% mortality. Pathological
changes in the major organs. Survivors recov-
ered their weight in ~ 2 wk.
No eye lesions.
Lethargy and heavy breathing by the end. Exten-
sive organ damage in the one that died.
Eye and nose irritation, rough hair. Recovered.
Nose and eye irritation, rough hair. Recovered.
Decreased 02 consumption. Increased erythrocyte
and active neutrophil content, permeability of
vessels, and respiration in heart and lung tissue.
No change in respiration rate, WBC, RBC, hemo-
globin, and autopsy findings. Slight weight de-
crease.
No change in general condition. Slight initial
increase in free cholesterol.
Decreased food and water intake and rectal tem-
perature. Weight loss.
Some mortality, survivors showing brain, liver,
and lung abscesses. Survivors lost weight, had
less endurance, and had instances of broncho-
pneumonia and hepatitis.
70
-------
TABLE 111-24. (continued)
Level
(mg/m3) Time Species Effects
28.4 90 d RAT 24% mortality, weight loss, lung pathology, and
significant changes in many blood parameters.
28.4 1 h/d; GPG Fatigue, somnolence, dizziness, itching, and eye
11 d irritation. Decreased lipids in cerebral hemi-
sphere and brain stem.
28.4 90 d MKY Weight loss. Changes in many blood parameters.
28.4 21 d COW No effect on feed intake, milk production, or
heart rate. Slight lacrimation.
22.7 16 h MUS Slight restlessness. Normal autopsy.
16 h RAT Slight initial restlessness.
14.2 5 d MUS Initial decrease in temperature. Decreased food
and water intake, with some recovery by the end.
14.2 41 d RAT Also under cold stress, and showed decreased
weight gain and food utilization. No changes in
blood cells, plasma protein, or weight of liver
and lungs.
14.2 4 d GOAT Initial decrease in food and water intake.
14 7 h/d; DOG Some coughing. Increased water consumption after
14 d each exposure. No change in blood picture or
body weight.
12.1 17 d PIG NOEL for body weight gain and respiratory system.
10 3 h/d; RAT Weight gain retarded. Changes in motor chronaxy.
3 mo Irritation of mucous membranes of trachea and
bronchi.
10 6 h/d; RAT Retarded weight gain. Changes in some blood param-
4 mo eters (increased hemoglobin). 02 consumption de-
creased by the end. Changes in lung and heart en-
zyme activity
71
-------
TABLE 111-24. (continued)
Level
(mg/m3)
4.86-
9.36
0.02
Time
6 h/d;
4 mo
Species
RAT
12.h/d; RAT
3 mo
Effects
Decreased liver glycogen and lipid levels, blood
sugar, and erythrocytes. Increased blood lipids,
hemoglobin, and leukocytes.
Changes in motor chronaxy. No change in weight.
No pathological changes found in sacrificed
animals.
72
-------
SECTION IV
EXPERIMENTAL HUMAN INHALATION EXPOSURES
Table IV-1 describes acute laboratory human exposures to hydrogen sulfide.
In the Summary, Table S-2 condenses all the information regarding experimental
human exposure, from about 8,000 mg/m3 to 0.008 mg/m3. The American Conference
of Governmental Industrial Hygienists gives 14.0 mg/m3 as the time-weighted-
average threshold limit value and 21 mg/m3 as the short-term-exposure limit
(ACGIH, 1980).
73
-------
TABLE IV-1. HUMANS—ACUTE EXPERIMENTAL INHALATION EXPOSURE TO
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 8,165
(5,750)
Inhalation
chamber
H2S 7,554
(5,320)
Inhalation
chamber
H2S 7,540
(5,310)
Inhalation
chamber
H2S 5,297-7,001
(3,730-4,930)
Inhalation
chamber
Ho. of
Test
Subjects
1 M, with
3 prior
exposures
to 1,420-
4,700 mg/m3
for several
hours each
1 M, with
3 previous
exposures
to high
levels
No. of
Controls
None
1 H, with
7 previous
exposures
to 1,420-
8,165 mg/m3
for several
hours each
1 M, with
1 previous
exposure
to 3,124
mg/m3
Duration and
Frequency of
Exposures
3 h 19 rain
Total
Length of
Expt.
3 h 19 min
None
30 min
2 h
None
40 min
40 min
None
1 h 35 min
2 h
Effects
Pain in the nose, then eyes, then
heavy continuous catarrh of both.
Slight headache towards the end.
Pale, trembling, and numbness.
Afterwards, increased eye pain and
catarrh, and roseola-type exanthe-
mata (rose-colored rash) on 2 fingers.
Increasing irritation of the eyes and
nose. Forced to leave the chamber
for 2 min, after 20-min exposure,
then returned. By the end: strong
cough, heart palpitations, difficulty
in breathing, violent pain in the
eyes, dizziness, trembling, extreme
fatigue, and in 10 min feeling of bi-
lateral intracranial pressure. After
exposure stopped, eye pains, heart
palpitations, and pulse decreased.
Fatigue, cranial pressure, diarrhea,
bladder tenesmus, and lower body pains
lasted until the next day.
Irritation of the trachea, painful
eyes, catarrh of nose and eyes,
and a headache by the end which
increased slightly after the ex-
posure stopped.
Difficulty breathing, coughing, and
irritation of the eyes, mouth,
and nose. After exposure stopped,
eyes were light-sensitive, painful,
watering, and closed, with swollen
eyelids and red conjunctiva, within
3 min. Pain in the eyes gone after
30 min. Fatigue, anorexia, light
sensitivity, diarrhea, and bladder
tenesmus continued until the next day.
Reference
and
Rating
Lehmann (1892)
B-9
Lehmann (1892)
B-9
Lehmann (1892)
B-9
Lehmann (1892)
B-9
-------
TABLE IV-1. (continued)
Ul
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
H2S 3,499-5,832
(2,464-4,107)
H2S 4,700
(3,310)
H2S 4,629
(3,260)
H2S 2,982-3,976
(2,100-2,800)
H2S 3,706
(2,610)
Mode of
Exposure
Inhalation
chamber
Inhalation
chamber
Inhalation
chamber
Inhalation
chamber
Inhalation
chamber
1 M, with
2 previous
exposures
to high
levels
1 M, with
a previous
exposure
to 1,420-
2,130 mg/m3
for 1 h
1 M, with
4 previous
exposures
to 1,420-
8,165 mg/m3
for several
hours each
3 M,
1 with 9
previous
exposures
to high
levels
1 M, with
2 previous
exposures
to 1,420
and 4,700
mg/m3 for
several
hours each
No. of
Controls
None
Duration and
Frequency of
Exposures
1 h 50 min
Total
Length of
Expt.
•>. 4 h
None
53 min
63 min
None
2 h 25 min
2 h 25 min
None
0.5 h
0.5 h
None
46 min
46 min
Effects
Eye irritation, varying in intensity.
Nasal catarrh. Difficulty breath-
ing after 1 h 21 min. Considerable
conjunctival congestion at the end.
After exposure stopped, viblent eye
pains for 2 h, continuing through the
night along with diarrhea, bladder
tenesmus, fatigue, and bronchial
catarrh.
Increasing irritation of the nose,
throat, trachea, and eyes. Head-
ache 10 min after exposure stopped.
After 45 min, tickling in throat and
trachea. After 1 h 45 min, intense
headache in the forehead and pain-
ful pressure in the eyes. No
symptoms after exposure stopped.
Painful irritation of the nose and
throat in 5-7 rain. Very disagree-
able by the end. Eye irritation.
The 3 were about equally sensitive.
Irritation of trachea and nose.
Painful and watering eyes. No
symptoms after exposure stopped.
Reference
and
Rating
Lehmann (1892)
B-9
Lehmann (1892)
B-9
Lehmann (1892)
B-9
Lehroann (1892)
B-9
Lehmann (1892)
B-9
-------
TABLE IV-1. (continued)
Compound (s) and
Concentration (s)
in mg/m3 (ppm)
H2S 3,550
(2,500)
H2S 2,982-3,266
(2,100-2,300)
Mode of
Exposure
Inhalation
chamber
Inhalation
chamber
No. of
Test
Subjects
1 M, with
8 previous
exposures
to 1,420-
8,165
mg/m3 for
several
hours each
1 M, 27 y,
strong
and very
healthy
No. of
Controls
None
None
H2S 2,982
(2,100)
Inhalation
chamber
H2S 2,982
(2,100)
Inhalation
chamber
Duration and Total
Frequency of Length of
Exposures Expt.
1 M, with
9 previous
exposures
to 1,420-
8,165
mg/m3 for
several
hours each,
1 immedi-
ately, be-
fore this
expt.
1 M, with
6 previous
exposures
to 1,420-
8,165
mg/m3 for
several
hours each
3 h 4 min
•>• 5.5 h
52 min
3 h
None
2 h 38 min
4 d
None
1 h
Several
hours
Effects
Headache. Irritation of mucous mem-
branes, leading to conjunctivitis.
Symptoms disappeared in 2.5 h after
exposure stopped. '
Immediate but temporary difficulty in
breathing. Increasing irritation
of the eyes (tearing, swelling,
and secretions) and nose (secre-
tions). Only slight nose catarrh
20 min after exposure stopped.
Bladder tenesmus 2 h later, and
diarrhea that night.
"Damp" headache, pains in the eyes and
nose. By the end, strong headache
and heavy tearing. These symptoms
plus fatigue and sleeplessness con-
tinued for 2 d, decreased on the 3rd
day. Subject recovered on the 4th day
except for paleness, moodiness, and
pain in the supraclavicular region.
After 5 min: irritation of throat.
After 26-35 min: irritation of
nose, larynx, and conjuctiva. After
1 h: headache on left side.
Symptoms lasted several hours after
the end of exposure.
Reference
and
Rating
Lehmann (1892)
B-9
Lehmann (1892)
B-9
Lehmann (1892)
B-9
Lehmann (1892)
B-9
-------
TABLE IV-1. (continued)
Compound(s) and
Concentration(s)
in mg/m3 (ppm)
II2S 1,761-2,783
(1,240-1,960)
Inhalation
chamber
No. of
Test
Subjects
1 M, with
It previous
exposures
to high
levels
No. of
Controls
None
H2S 1,988-2,130
(1,400-1,500)
H2S 1,420-2,130
(1,000-1,500)
H2S 2,059
(1,«0)
H2S 1,420-1,988
(1,000-1,400)
Inhalation 3 M,
chamber 1 with 9
previous
exposures
to high
levels
Inhalation 1 M,
chamber young,
strong,
over-
weight
Inhalation 1 M, with
chamber 5 previous
exposures
to 1,420-
8,165
mg/m3 for
several
hours each
Inhalation 1 M, with
chamber 5 previous
exposures
to high
levels ,
1 just he-
fore this
expt.
Duration and
Frequency of
Exposures
3 li
Total
Length of
F.xpt.
•>• (S.5 h
None
1 h?
1 h?
None
None
1 h
3 h 56 min
6 h
None
3 h
->• 4 d
Effects
Increasing irritation of the eyrs,
mouth, and trachea, with coughing,
for "~ 1 h. Eye irritation and
sensitivity to light disappeared
from 1.5 to 2 h, then returned along
with difficulty in breathing. By the
end, no complaints other than a small
cough. Afterwards, a slight headache
for 30 min, with fatigue, rhinitis, and
bronchitis lasting for several hours.
Slight irritation of throat and eyes.
Re f'r rrnre
and
Raj. ing
I.ehniaim ( I R92)
n-9
Increasing irritation of the mucous
membranes of the nose, throat,
larynx, and conjuctiva. At the
end, coughing. Symptoms continued
"for a while" after exposure stopped.
Headache after a few minutes. Irrita-
tion of the bifurcation of the tra-
chea at the end of the exposure.
Afterwards: conjunctivitis, strong
nasal catarrh, and headache. Symptoms
cleared in ~ 2 h, with tearing and
headaches recurring later in the day
Increasing irritation of eyes and
trachea, with burning pains, heavy
salivation and mucous secretion,
difficulty in breathing, and cough-
ing for 1 h 45 min. By 1 h 55 min
only nasal secretion remained, and
was "absolutely well" hy 2 h 15 min.
Some recurrence of irritation at 2 h
37 min. Afterwards, painful, liglit-
sensitive eyes and lipadachr for 7 h,
and some pain the next day. Bronchitis,
rhinitis, and heavy conjunctivitis were
diagnosed. Rye irritation remained
after 4 d.
Lehmann (1892)
B-9
Lehmann (1892)
B-9
I.ehmann (1892)
B-9
Lehmann (1892)
B-9
-------
TABLE IV-1. (continued)
00
Compound (s) and
Concentration^ )
in mg/m3 (ppn)
H2S 1,420-1,846
(1,000-1,300)
H2S 1,704-1,804
(1,200-1,300)
H2S 994-1,278
(700-900)
H2S 284-568
(200-400)
H2S 0.012-0.96
H2S 0.08-0.5
H2S 0.27
(0.19)
Mode of
Exposure
Inhalation
chamber .
Inhalation
chamber
Inhalation
chamber
Inhalation
chamber
Inhalation
Inhalation
Olfactometer
with sniff-
ing tubes
No. of
Test No. of
Subjects Controls
1 M, with None
6 previous
exposures
to high
levels
3 H, None
1 with 9
previous
exposures
to high
levels
3 M, None
1 with 9
previous
exposures to
high levels
3 M, None
1 with 9
previous
exposures
to high
levels
11, Served
16-55 y as own
controls
14, 18-
30 y,
"practi-
cally
healthy"
10
Duration and Total
Frequency of Length of
Exposures Expt.
1 h 23 min 1 h 23 min
1 h? 1 h?
1 h? 1 h?
1 h 1 h
Exposures at
each level
repeated
several times
for unknown
length of
time
Not given,
1 test/d,
daily for
3-4 d
Not given
Effects
Weak irritation of nasal mucous mem-
branes.
Clearly disagreeable irritation of
the eyes and throat.
Slight irritation of the throat and
eyes.
No signs of irritation.
Odor not perceptible at 0.012-0.026
mg HgS/m3. Varying odor perception
at 0.031-0.090 mg/m3. Most perceived
the odor at 0.10, and all did at 0.20-
0.96 mg/m3. Taking into account in-
dividual sensitivity, authors give the
odor threshold of H2S as 0.040 mg/m3.
Range of odor thresholds.
Odor threshold.
Reference
and
Rating
Lehmann (1892)
B-9
Lehmann (1892)
B-9
Lehmann (1892)
B-9
Lehmann (1892)
B-9
Loginova (1957)
A-10
Baikov (1963)
A-9
Williams et al.
(1977)
A-13
-------
TABLE IV-L. (continued)
--J
\D
Compound(s) and
Concent rat ion(s)
in mg/m3 (ppm)
H2S 0.15
II2S 0.012-0.030
H2S 0.013
H2S 0.012
M2S 0.010
H2S 0.010
H2S 0.005-0.009
(3.39-6.44 ppb)
H2S 0.008
H2S 0.00067
(0.00047)
Mode of
Exposure
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
Inhalation
chamber with
face expo-
sure only
Inhalation
Odor test
room
No. of
Test No. of
Subjects Controls
8,
20-30 y
12
3 Served as
own con-
trols
prior to
exposure
3, Served as
18-28 y own con-
trols
prior to
exposure
3 Served as
own con-
trols
prior to
exposure
3, Served as
18-28 y own con-
trols
prior to
exposure
998
M & F,
•>• 20 y
3 Served as
own con-
trols
prior to
exposure
4 Served as
trained own con-
Duralion and Total
Frequency of Length of
Exposures Expt.
Not given
20-35
"observations"
5 min, once, 60 min
during min
15-20 of the
expt .
5 min, during 180 min
min 15-20
of a 60-min
expt. , re-
peated on
3 days
5 min, once, 60 min
during min
15-20 of the
expt.
5 min, during 180 min
min 15-20
of a 60-min
expt. , re-
peated on 3
days
15 s, once
5 min, once, 60 min
during min
15-20 of
the expt.
Effects
odor trols
ana Iysts
Threshold of odor object i onabi 1 i ty
(not odor detection).
Range of minimum concentrations at
which the odor of 1I2S was smclled.
Light sensi t i vi ty-re 1 a ted eye re-
sponses increased slightly more
than at the 0.010 mg/m3 exposure
level, for the 40 min following
exposure.
Statistically significant increase in
light sensitivity of the eye in the
40 min following exposure.
Statistically significant increase
in the light sensitivity-related
eye responses by the 20th min, and
for the following 40 min.
No effect on light sensitivity of the
eye.
Range of means of calculated odor
thresholds from four test groups.
Ability of eye to adapt to darkness
not affected.
Lowest concentration at which all
the subjects positively rrcognizr
Lhr oflo r .
* t p r
Tonzetitli nml Ng
(1976)
B-9
Dunn (1959)
R-10
Duan (19r>9)
B-10
Raikov (1963)
A-9
Duan (1959)
B-10
Baikov (1963)
A-9
Adams eta).
(1968)
B-ll
Duan (1959)
B-10
Lrona nlos
e t a I .
(1969)
A-ll
-------
SECTION V
EPIDEMIOLOGY
The Summary contains a discussion of the epidemiological studies and
condenses the data into one table, Table S-3.
OCCUPATIONAL EXPOSURES
Data for occupational exposures to hydrogen sulfide are given in Table V-l
These studies are not particularly useful in establishing a range of concern
for H2S in automobile emissions because of the high levels in some, the prob-
able presence of confounding factors in many (especially the petroleum and
shale oil industry reports), and the possible inadequacies of the H2S sam-
pling and analysis procedures in others.
EXPOSURES OF THE GENERAL PUBLIC
Data from the two epidemiological studies of exposure of the general
public are given in Table V-2. Weaknesses in study design considerably
lessen the value of these reports in helping to determine a range of con-
cern for H2S.
81
-------
TABLE V-l. STUDIES OF OCCUPATIONAL EXPOSURE TO H S
oo
NJ
Compound(s)
Concentrations)
mg/ra3 (ppm)
Duration
H2S < 28.4-> 852
(< 20-> 600)
Air levels varied
with location
Also small amounts of
CS2, HCN, S02, and
hydrocarbons
Population Croup
Description Exposed
Shale oil plant workers
Controls
None
H2S 326.6
(230)
Exposure lasted
~ 20 min
Worker in shale oil
plant
1 M,
30 y
None
Effects
Symptoms included: a sudden
feeling of fatigue, espe-
cially in the legs; dizzi-
ness; and intense anxiety
followed by unconsciousness
with or without respiratory
failure. Pains in back of
head, dizziness, and some-
times nausea followed re-
gaining consciousness.
Symptoms subsided in half
an hour except in some
cases nystagmus (involun-
tary rapid eye movement)
and Romberg's sign. Re-
flexes, coordination, eye
movements, visual acuity,
lungs, heart, blood, and
blood pressure were normal.
Found unconscious, froth
about mouth, cramps in right
arm, slow, shallow breath-
ing, low blood pressure.
He fully recovered in 6 d
with no recurrence of
symptoms over 2 y.
Remarks
Reference and
Rating
Descriptive case study of Ahlborg (1951)
clinical findings follow- B-9
ing relatively brief high
concentrations of H2S mixed
with a variety of "gasoline
vapors." As a group, expo-
sures were poorly defined,
but 7 case reports give expo-
sure in great detail. Rates
of symptoms and morbidity are
not given for this group, al-
though they would have been
available. Therefore, the
"risk" of unconsciousness, etc.,
is difficult to quantify from
these data. There is some con-
fusion between "acute," "subacute,"
and "chronic" exposures vs.
effects. Subacute exposure,
p. 260, is defined as extremely
intense, but brief. This is
in fact a mild acute exposure
with subacute effects or symp-
toms. Acute effects may fol-
low chronic exposure and vice
versa.
Ahlborg (1951)
B-9
-------
TABLE V-l. (continued)
oo
Compound(s)
Concentration(s)
mg/m3 (ppm)
Duration
H2S •«• 40-185 (from
5 single grab
samples)
Description
Workers building a
tunnel
Population Group
Controls
50
H2S * 142
(~ 100)
Apparently a one-time
measurement for a
problem which lasted
several years
Coal miners
120
Effects
In 9 mo, 163 instances of
eye irritation were seen
half an hour to several
hours after descending into
the tunnel: burning, grainy
sensation, and haloes seen
around lights. The symp-
toms were not pronounced
while in the tunnel, but
increased when workers
came out: photophobia,
lacrimation, broken blood
vessels and tiny blisters
oo the cornea, and occasion-
ally a light cough, irrita-
tion of the nose and pharynx,
and nausea. The most exposed
developed conjunctivitis and
blepharitis. Large vari-
ability between individual
responses.
Symptoms of eye irritation
occurred after several
hours of exposure. Wide
variability in severity
of response. The light
cases exhibited burning,
conjunctival congestion,
and lacrimation; symptoms
disappearing in several
hours. Severe cases ex-
hibited intense burning,
gritty sensation, conjunc-
tival congestion, photo-
phobia, blepharospasm,
abundant lacrimation, and
violent headaches lasting
up to a week. No habitua-
tion was found, and possibly
evidence of sensitization.
Remarks
Is exposure to H2S reliable?
No other gases were tested
for. Workers in a similar
tunnel, but with no H2S
detected, had no eye irrita-
tions. Reasonable descriptive
information (intermittent ex-
posure of 50 people), relevant
to H2S, but the issue of
repeated and intermittent ex-
posure is not discussed. Are
the same persons equally at
risk, are some repeatedly more
sensitive than others, etc.?
The one h^S measurement done
used an imprecise method,.
so the value is doubtful.
From the range of clinical
symptoms, it is evident that
considerable variation in ex-
posure levels occurred, which
are essentially not measured.
Without dose/duration measure-
ment, it is difficult to see
the value of this descriptive
report to this project.
Reference and
Rating
Larsen (1944)
A-9
Deveze (1956)
B-8
-------
TABLE V-l. (continued)
oo
•p-
Compound(s)
Concentration(s)
rog/ra3 (ppm)
Duration
H2S 13.7-36.6
H2S 15-35 (levels
measured 4.3 h
after exposure)
Description
Workers in a sugar
beet processing
plant
Accidental exposure of
workers in a viscose
plant while repairing
a tank heater
Population Group
Controls
Not given
9 M
H2S 28.4
(20)
Daily exposure
level often
exceeding this
Shale oil plant workers.
Controls from the shale
quarry
459 M
384 H
Effects
Eye complaints were seen,
generally at the higher
H2S levels: pains, light
sensitivity, tears, and
headaches. Problems lasted
several hours to days, and
some workers had repeated
eye pain.
4/9 complained of nausea,
weakness, and pain in the
chest, and were hospital-
ized. After 1 wk, no
symptoms were found on in-
ternal, eye, neurological,
and psychiatric examina-
tion and EKG. 5/9 were
only briefly affected. All
were examined 2 y later,
and no after-effects were
found.
Frequency of nonoccupational
disease the same in both
groups. Plant workers re-
ported 20% more fatigue, 5%
more loss of appetite, and
increased irritability.
Slightly more headaches, loss
of memory, and itching. 50%
more complaints from conjunc-
tivitis and 25% more from
respiratory tract. Frequency
of reported fatigue increased
with length of employment and
degree of exposure.
Remarks
No controls or comparison
group. Apparently no
other gases or compounds
tested for.
Reference and
Rating
Kranenburg and
Kessener (1925)
B-9
Prouza (1970)
B-5
Attempt at non-concurrent Ahlborg (1951)
prospective evaluation B-9
that falls down because of
limited information on dur-
ation of exposure. Rates of
symptoms are determined regard-
less of exposure duration and then
stratified by those employed
> or < 2 y. Since dramatic
differences are present be-
tween these 2 groups, it would
have been imperative to calcu-
late person-month or person-
year exposure to determine ac-
curately differences in symptom
frequency. The marked dif-
ference in fatigue, greater in
Group I (exposed to H2S) with
light work load, suggests pos-
sibility of (1) interviewer bias
or (2) drift of less pliysically
fit worker to Group I. These
potential biases are not discussed.
-------
TABLE V-l. (continued)
c»
Ul
Compound(s)
Concentratioo(s)
"Dg/rn3 (ppm)
Duration
H2S 7.1-14.2
(5-10)
S02 not given
"lower aliphatic
compounds"
Probably for at
least several
years
H2S 7.1-14.2
(5-10)
S02 not given
5-15 y (at least
one worker had only
intermittent ex-
posure)
Description
Gasoline desulfuriza-
tion plant workers
Population Croup
20
Controls
20
workers
of the
same age
from an-
other
dept. of
the plant
Gasoline desulfuriza-
tion plant workers
30
H2S < 14.2
(< 10)
Actual measurements
weren't made; an
alarm set for this
level never went
off
Workers in a
water plant
heavy
Not
given
Effects
There were 93 possible symp-
toms of irritation in ex-
posed workers versus 23 for
controls: 34 vs. 7,
respiratory; 20 vs. 8,
gastroenteritis; 30 vs.
3, eye; and 9 vs. 3, skin.
Nine workers showed dermal
affectations, 4 with papulo-
pruritis and erythe-
matous-wheal-like lesions
(possibly indicating an
allergic response), and 1
presented a syndrome of cut-
anea invelerata, pannicolo-
patia of the Besnier-Boek-
Schaumann type and a miliary
sarcoidosis of the lung of re-
cent insurgence. Two of above
5 were sensitive to solution of
H2S in water as a patch test.
In 7 y, 123 cases of over-
exposure were seen: weak-
ness, nausea, dizziness,
headache, and nervousness.
Includes several reports
of apparently higher ex-
posures, resulting in more
severe symptoms and uncon-
sciousness. A perforated
eardrum and alcohol con-
consumption both seem to
increase the toxicity of
H2S.
Remarks
A survey of 40 workers
in a petrol desulfurization
plant, 20 of whom were
at risk of toxicity
to both H2S and S02. Com-
parability of the 2 groups
is not determined. Data
suggests that low-level expo-
sure to 5-10 ppm may have
respiratory and mucous membrane
effects. Duration of exposure
needs to be determined.
A descriptive survey of 30
workers, with no control
or comparison groups.
Reference and
Rating
Benin! and
Colamuss i
(1969)
B-8
Benini and
Colamussi
(1969)
B-8
This is a descriptive uncon-
trolled study in which
there is no correlation
of duration of exposure
(e.g. distance from source,
length of employment) and
subsequent symptoms. Largely
anecdotal account of the
relationship of alcohol and
H2S, and the problem with
perforated eardrums.
Poda (1966)
B-4
-------
TABLE V-l. (continued)
oo
Compound(s)
Cbncentration(s)
mg/m3 (ppm)
Duration
H2S 0-9.94
(0-7)
3 d, with at least
the preceding 3 mo
without H2S expo-
sure, before the
plant started de-
dulfurization
H2S 0.028-
0.055
Population Group
Description
Workers in a gasoline 13,
desulfurizing plant 30-55 y
Controls
Breast-fed babies (1 mo- Unknown
3 y) in a factory nurs- no. out
ery whose mothers of 90
worked in the viscose babies
spinning shop studied
Unknown
no. out
of 90
babies
studied
Effects
Slight and irregular
changes were seen in the
serum Fe and transferrin
levels, and the elimination
of the various fractions
of urinary sulfates, in
only some of the workers.
Analysis was made of the air
at the baby's nose while nurs-
ing. H2S (and no CS2) was
found, emanating from the
mothers' clothing. The bab-
ies were poorly developed,
underweight, listless,
anemic, pale, dyspeptic, and
susceptible to more frequent
and severe infectious
diseases. They frequently
vomited after feeding, and
began walking and teething
late. Babies with mothers
in other shops were normal.
When mothers were moved out
of the viscose shops, the
babies' development improved.
Reference and
Remarks Rating
Its main use is the attempt Benini and
at physiologic measurements Colamussi
to correlate with health (1970)
outcomes. Only 13 persons B-6
were evaluated, therefore
variable results and dubious
conclusions. No dose-response
relationship seen. .
The hard data are limited, but Glebova
this is a solid study. The (1960)
observed correlation of B-8
spinning shop (but not other
workshops) employment of the
mothers with symptoms in
the babies rules out most
other likely causes.
-------
TABLE V-2. EPIDEMIOLOGICAL STUDIES RELEVANT TO H2S EXPOSURE
oo
• Compound(s)
Concentration(s)
mg/m3 (ppm)
H2S levels ranged
from ~0.03-~0.43
(0.020->0.300),
with levels of
0.020-0.125 ppm
for 7 h one day,
and >0.300 ppm for
1 h another day
Population Croup
Description
Residents of affected
areas of Terre Haute,
Ind., May 18-June 15,
1964.
Controls
(41
health/
odor
complaints
received,
20 people
interviewed
by phone)
H2S 0.005-0.300
Hydrocarbons
Residents of 113 apart-
ments using unpurified
natural gas for heat-
ing
Not
given
Not
given,
resi-
dents
in same
city,
but
without
gas
heat
Effects
Numerous citizen complaints
of nausea and vomiting,
respiratory tract -irrita-
tion, headaches, gastro-
intestinal complaints,
shortness of breath, burn-
ing eyes, and disturbed
sleep. Few were serious
enough to warrant seeking
medical treatment.
Those in households with
^0.05 mg/m3 complained
of headaches, weakness,
nausea, and vision prob-
blems. Reactions of sampl-
ing crew indicate that the
odor threshold for H2S in
natural petrolic gas was
0.01-0.03, and for free H2S
was 0.04. For a period of
2 y, the morbidity per 1,000
residents was * 50% higher
in the exposed group.
Morbidity rates were higher
in the test group for the
< 3, 20-49, and 50-59 y age
groups.
Remarks
Reference and
Rating
Weak cross-sectional study. U.S.P.H.S.
Exposure data poorly defined (1964)
with an almost a priori as- A-6
sumption of H2S as the agent
(what about S02, particulates,
etc.). Only the 20 individuals
who originally complained were
interviewed, without any con-
trols or appropriate comparison
group. Standard epidemiologic
measures were not used. Ab-
sentee rates were derived from
hospitals; what of susceptible
individuals (i.e., children,
school rates, etc.)? Infor-
mation is suggestive but sampling
is inadequate, controls are ab-
sent, and this must cast some
doubt on the conclusions.
The study is fascinating, but
raises serious questions of
the comparability between
the two regions. Although
the sex distribution is simi-
lar and age-specific rates are
considered (note that the sum-
mary difference - 52% - is not
age-adjusted), no comparability
of socioeconomic status is
present. In view of the 40%
increase in infectious disease
in the exposed group, this
difference is a significant
one, and perhaps the major
explanation for the difference
in morbidity rates. It is not
uncommon to see a 40% increase
among the poor or disadvantaged
(i.e., those without gas heat?).
Also note the varying widths of
the age ranges used, particularly
the wide 20-49 y group, where
most of the morbidity was
found.
Loginova (1957)
"B-10
-------
BIBLIOGRAPHY-
4-127 ACGIH, American Conference of Governmental Industrial Hygienists
Committee on TLVs. 1971. Documentation of Threshold Limit Values
for Substances in Workroom Air, ed. 3. ACGIH. Cincinnati, Ohio.
pp. 11-12.
B--. The usefulness to this review is limited only by the goal
of intermittent (40 h/wk) exposure. Several sources reported eye
effects at < 20 ppm, so the TLV was set below that, at 10 ppm.
4-340 ACGIH, American Conference of Governmental Industrial Hygienists
TLV Airborne Contaminants Committee. 1978. TLVs Threshold Limit
Values for Chemical Substances and Physical Agents in the Workroom
Environment with Intended Changes for 1979. ACGIH. Cincinnati,
Ohio.
D--. The time-weighted-average TLV was 15 mg/m3 and the short-term-
exposure limit was 27 mg/m3.
5-175 ACGIH, American Conference of Governmental Industrial Hygienists
TLV Airborne Contaminants Committee. 1980. TLVs Threshold Limit
Values for Chemical Substances and Physical Agents in the Workroom
Environment with Intended Changes for 1980. ACGIH, Cincinnati,
Ohio. p. 20.
A--. The time-weighted-average TLV value for H2S is 14 mg/m3 and
the tentative short-term-exposure limit is 21 mg/m3.
4-310 Adams, D. F., F. A. Young, and R. A. Luhr. 1968. Evaluation of
an Odor Perception Threshold Test Facility. TAPPI 51(3):62A-67A.
B-ll. Four groups of subjects, totaling 998, had calculated thres-
holds of detection for H2S from 3.39 ppb to 6.44 ppb. Differences
between groups were seen. Extensive data manipulation was done.
4-121 Adelson, L., and I. Sunshine. 1966. Fatal Hydrogen Sulfide In-
toxication. Arch. Pathol. 81:375-380.
D-5. Case report of three fatalities due to inhalation of sewer
gas containing unknown but high levels of H2S. It was rapidly
fatal due to paralysis of the central nervous system.
* MRI document acquisition numbers are given in the left margins.
89
-------
4-122 Ahlborg, C. 1951. Hydrogen Sulfide Poisoning in Shale Oil In-
dustry. AMA Arch. Ind. Hyg. Occup. Med. 3:247-266.
B-9. Case reports and large group studies of workers exposed to
20-^600 ppm H2S. Symptoms range from conjunctivitis to neurasthenic
symptoms and unconsciousness. Studies are poorly designed and
confounded by the presence of other gases.
4-341 AIHA, American Industrial Hygiene Association. 1962. Hygienic
Guide Series; Hydrogen Sulfide. American Industrial Hygiene
Association, Akron, Ohio. 2 pp.
D--. Brief review.
4-001 Aitbaev, T. K., V. M. Almaniyazova, N. A. Strelyukhina, A. S.
Abylkasymova, and U. A. Rysbekova. 1976. Combined Effect of
Some Industrial Gases. Zdravookhr. Kaz. No. 1:69-72 (Russ).
B-9. Albino rats were exposed to H2S at the MAC level (the MAC
in 1972 was 10 mg/m3) for 6 h/d for 4 mo. A slight decrease in
body weight gain, fluctuations in peripheral blood values, and an
ultimate decrease in 2 indexes of 02 consumption were seen. An
interaction study of H2S, HF, and S02 was done, indicating summa-
tion-type action.
4-195 Aizenshtad, V. S., E. G. Dolmatova-Guseva, V. P. Perkhurova, A. V.
Shtifel'man, L M. Bogomolova, and S. M. Nerubai. 1971. Work
Hygiene and the State of Workers' Health in the Production of
Carbophos. Gig. Tr. Prof. Zabol. 15(3):49-51 (Russ).
D--. Workers engaged in the production of carbophos (malathion)
were exposed to dimethyldithiophosphoric acid, diethyl maleate,
the product, methanol, and xylene as well as to H2S. The latter
four compounds exceeded their maximum allowable concentrations
(MAC) in 11 to 17% of the air samples. Carbophos exceeded its
MAC, however, in 35% of the cases. Acute conjunctivitis and der-
matitis were possibly due to H2S since the incidence of these
maladies decreased from 18 to 2 persons when the H2S concentra-
tion was reduced by control measures.
4-129 American Industrial Hygiene Association. 1962. AIHA Hygienic
Guide Series. Hydrogen Sulfide. American Industrial Hygiene
Association, Akron, Ohio. 2 pp.
D--. Very authoritative summary, recommending a maximum atmos-
pheric concentration (8 h) of 20 ppm.
4-130 American Petroleum Institute Toxicological Review. 1948. Hydro-
gen Sulfide. Department of Safety, A.P.I., New York, New York. 6
pp.
90
-------
D—. A review of H2S poisoning: occurrence, effects, treatment,
and precautionary measures. The threshold is below 50 ppm.
4-131 American Standards Association. 1941. Allowable Concentration
of Hydrogen Sulfide. ASA Z37.2-1941, A.S.A., New York, New York.
6 pp.
D--. Old, very short review giving 20 ppm as the MAC for 8 h.
4-196 Andreescu, M. 1970. Comparative Investigation of Some Adenocar-
cinomas of the Mammary Glands in Mice of Lines WHT/Ht, A2G and R
III, Developed Under the Influence of Harmful Exogenous Factors.
Nats. Kongr. Onkol., Sb. Dokl. 1st; Vol. 3. pp. 43-48 (Fre).
C--. Three strains of mammary-tumor-bearing mice were exposed to
one of several factors, including an unknown level of H2S. The
character of the tumor chromosomes didn't change.
4-273 Andrew, F. D., R. A. Renne, and W. C. Cannon. 1979. Toxic Effects
of Geothermal Effluents: Reproductive Toxicity Testing for Effects
of H2S in Rats. In: Pac. Northwest Lab. Annu. Report 1979 DOE.
Assist. Seer. Environ. Pt. 1: Biomedical Science. pp. 276-278.
D-9. An abstract of work in progress. Short, repeated exposure
to 220 ppm H2S did not induce dominant lethal effects during
spermatogenesis in male rats or embryotoxicity in the progeny of
female rats. Minor rib anomalies were found in some of the fetuses
(authors' summary).
4-197 Andriasian, G. K. 1969. Certain Side Effects of Hydrogen Sulfide
Baths of Matsesta. Vestn. Dermatol. Venerol. 43(l):72-73 (Russ).
D--. The incidence and case histories of skin problems in people
using baths containing 100-150 mg H2S/L are described.
4-240 Anichkov, S. V., and M. L. Belen'kii (R. Crawford, Trans.). 1963.
Pharmacology of the Carotid Body Chemoreceptor. The Macmillan
Co. New York, New York. pp. 49-60.
D--. A review of the mechanisms of toxicity of sulfides, includ-
ing H2S, through several routes of exposure. Inhalation of H2S
caused erythrocytosis and hyperglycemia, involving reflexes from
the carotid chemoreceptors.
4-132 Anonymous. 1952. Four Workers Overcome by Hydrogen Sulfide when
Digging in Marshy Land. Occup. Health 12:39.
C-6. Case report of exposure to 300-500 ppm H2S causing uncon-
sciousness, nausea, and stomach pains.
4-133 Anonymous. 1966. Gas Hazards in Underground Tanks and Wells.
Mich. Occup. Health 11:1-2.
91
-------
C-7. Case reports of two accidental poisonings, in one of which
> 1,000 ppm H2S was fatal.
4-003 Anonymous. 1978. Hydrogen-Sulphide Poisoning. Lancet 1(0054):
28-29.
D--. A short review of the occurrence and toxicity of H2S. In-
cludes fatal and nonfatal case reports.
4-343 Anonymous. 1981. Deaths Associated with Liquid-Manure Systems--
United States. Morb. Mortal. Wkly. Rep. 30(13):151-152, 157.
D--. A report of 8 deaths and 2 cases of near-fatal illness, in
3 separate accidents. H2S was believed to be the most likely
causative agent along with decreased 02 and increased C02. In-
vestigation after one accident led to an estimate of > 570 ppm
H2S at the time of the incident. No symptoms are described.
4-005 Arimatsu, T., and K. Kesado. 1978. Intoxication due to Hydrogen
Sulfide During the Application of a Mixture of Lime-Sulfur and
Primary Calcium Phosphate. Nippon Noson Igakkai Zasshi (Jap. J.
Rural Med.). 27(3):452-453 (Japan).
C-7. A woman accidentally exposed to ~ 5,000 ppm H2S lost con-
sciousness for 4 h, and suffered nausea and vomiting lasting 4 d
and leukocytosis.
4-134 Aufdermaur, F., and 0. Tb'nz. 1970. Poisoning of Children by
Liquid Manure Gas When Using "Rustic" Latrines. Schweiz. Med.
Wochenschr. 100:894-896 (Ger).
C-8. Case reports of 3 accidental poisonings with unconsciousness,
coma, convulsions, irritation of mucous membranes, lung edema,
and leukocytosis.
4-241 Aves, C. M. 1929. Hydrogen Sulphide Poisoning in Texas. Texas
State J. Med. 24:761-766.
C--. An analysis of the air in some Texas oilfields found 2,000-
140,000 ppm H2S. Several acute, fatal cases are reported. Chronic
effects included: slow healing of minor skin wounds, eye irrita-
tion, weight loss, and insomnia. Increased inflammation of air
passages or respiratory infections was not seen. Specific H2S
concentrations for the case reports are not given.
4-285 Baikov, B. K. 1963. Maximum Permissible Concentration of Carbon
Disulfide and Hydrogen Sulfide when Present Together in the Atmosphere.
Gig. Sanit. No. 28:3-8 (Russ).
A-9. The odor threshold for H2S was found to be 0.014-0.03 mg/m3.
Light sensitivity of the eye wasn't affected by 0.01 mg/m3. Effects
when combined with CS2 were additive and possibly synergistic,
respectively.
92
-------
4-006 Baltaitis, V., Y. M. Markovich, I. F. Yarembash, and A. S.
Grebtsova. 1975. Razrab. Mestorozhd. Polezn. Iskop. (Kiev).
39:158-166 (Russ).
D--. CO and HC1 were released in high concentrations from burning
poly(vinyl chloride). Additional combustion products measured
were N0x, S02, COC12, HCN, and H2S.
4-007 Barilyak, I. R., and I. A. Vasil'eva. 1974. Antimitotic and Cyto-
genetic Activity of Small Concentrations of Carbon Bisulfide and
Hydrogen Sulfide. Tsitol. Genet. 8(2):126-129 (Russ).
D--. The exposure of rats to 10 mg H2S/m3 and CS2 (whether that
is each or the total concentration is unclear) for 70-90 d caused
decreased mitotic activity of liver and kidney embryonic cells
and increased incidence of aneuploidy and structural chromosomal
aberrations in adult bone marrow cells.
4-008 Barilyak, I. R. , I. A. Vasil'eva, and L. P. Kalinovskaya. 1975.
Effect of Small Concentrations of Carbon Bisulfide and Hydrogen
Sulfide on the Intrauterine Bevelopment of Rats. Arkh. Anat.
Gistol. Embriol. 68(5):77-81 (Russ).
B--. Exposing pregnant rats to H2S and CS2 (at 10 mg/m3 [not clear
whether this is the concentration of each component]) under condi-
tions of the viscose industry for prolonged periods was embryolethal
at the pre- and post-implantation stage. Abnormalities, primarily
of the urogenital and bone systems, were seen in a small number
of the embryos. Blood formation and ossification were disturbed
in the embryos, and there were severe changes in parenchymatous
cells of the liver and kidneys of the rat embryos.
4-278 Barthelemy, M. L. 1939. Ten Years' Experience with Industrial
Hygiene in Connection with the Manufacture of Viscose Rayon. J.
Ind. Hyg. Toxicol. 21:141-151.
C-6. Bescriptive study correlating conjunctivitis and visual
symptoms with avg. concentrations of H2S (12-41 mg/m3), CS2
(63-162 mg/m3), and H2S04 (31-55 mg/m3). Controls are absent.
The authors assume that H2S is the culprit because workers in
another department exposed to 400 mg CS2/m3 for a few hours had
no such symptoms. If this assumption is accepted, the threshold
level for H2S for conjunctivitis is < 25 mg/m3. The authors be-
lieve that the presence of CS2 and H2S04 create a hypersensitivity
of the conjunctiva and cornea to H2S.
4-290 Basmadzhieva, K., Z. Rashev, and M. Argirova. 1969. Adaptation
of Rats to Low Atmospheric Concentrations of Hydrogen Sulfide and
Phenol. Khig. Zdroveopazvane. 12(l):33-37.
D--. Rats exposed to a mixture of H2S (0.03 mg/m3) and phenol
(0.06 mg/m3) for 3 mo exhibited a general adaptation syndrome.
93
-------
4-010 Baynes, C. J., and A. G. Scott. 1977. Estimating the Probability
of a Lethal Exposure During an Episodic Release of a Toxic Gas.
In: Proc., Annu. Meet. - Air Pollut. Control Assoc., 70th (Vol. 4),
77-445, 14 pp.
D--. A theoretical, statistical model for predicting exposure is
described. It may be relevant to estimating margins of safety to
allow for fluctuations.
4-136 Beasley, R. W. R. 1963. The Eye and Hydrogen Sulfide. Br. J.
Ind. Med. 20:32-34.
C-5. Description of the same cases as in Carson (1963).
4-011 Beck, J. F., F. Cormier, and J. C. Donini. 1979. The Combined
Toxicity of Ethanol and Hydrogen Sulfide. Toxicol. Lett. (AMST).
3(5):311-314.
C-12. An interaction study. Rats injected with ethanol had shorter
times to unconsciousness when exposed to 800 ppm H2S than rats
without alcohol exposure.
4-012 Becker, B. 1978. Hazards Through Hydrogen Sulfide—G 11.
Zentralbl. Arbeitsmed. Arbeitsschutz. Prophyl. 28(8):224-226
(Ger).
D--. A review with no references for occupational physicians.
4-199 Benini, F., and V. Colamussi. 1969. Various Chronic or Relapsing
Skin Manifestations, Observed in Refinery Workmen Exposed to Long
Term Action of Hydrogen Sulfide. Arcisp. S. Anna Ferrara 22:973-983
(Ital).
B-8. Workers were exposed to unknown levels of S02 and "lower
aliphatic compounds" as well as 5-10 ppm H2S. Various respira-
tory symptoms, eye irritation, and skin sensitization were found.
4-198 Benini, F. , and V. Colamussi. 1970. Possibility of Absorption
of Hydrogen Sulfide in Workers Employed in a Confined Place.
Arcisp. S. Anna Ferrara 23(6):54l-548 (Ital).
B-6. Environmental conditions (including H2S, 0-7 ppm), serum Fe
and transferrin levels, and the elimination of various fractions
of urinary sulfate were measured in 13 workers in a gasoline desul-
furizing plant. Only slight changes were found. Results were
too variable (irregular) to be useful--i.e., there was no dose-
response relationship.
4-200 Benson, F., and T. Karlsson. 1972. Hydrogen Sulfide Intoxication--
Toxicity and Therapy. Lakartidningen 69(6):627-631 (Swe).
94
-------
C--. A good review with two case reports of acute poisoning and
treatment.
4-013 Bersch, W., U. Meinhof, G. Ule, H. Berlet, and A. M. Thiess. 1974.
Proceedings: Pathomorphologic and Pathochemical Findings in Acute
H2S-Poisoning in Man. Verb. Dtsch. Ges. Pathol. 58:502 (Get).
D--. Review.
4-323 Berushvili, Ts. A. 1980. Hygienic Evaluation of Hydrogen Sul-
fide-Containing Hot Springs Used in Hot Water Supply Systems.
Gig. Sanit. No. 6:11-13 (Russ).
D--. Tests with these waters in guinea pigs and white rats were
concerned only with the effects on the skin and effects after in-
gestion.
4-014 Biesold, J., M. Bachofen, and H. Bachofen. 1977. Pulmonary Edema
due to Hydrogen Sulfide. Lung 154(2):146.
D-7. A morphological examination of the lungs of the victim of a
fatal H2S inhalation.
4-201 Bittersohl, G. 1971a. On Relationships in Action Between Carbon
Bisulfide and Hydrogen Sulfide. Med. Lav. 62(12):554-556.
D--. A hypothesis for the mechanisms of action and interaction
of H2S and CS2.
4-202 Bittersohl, G. 1971b. lexical Effect of Hydrogen Sulfide. Z.
Gesamte Hyg. 17(5):305-308 (Ger).
D--. Mechanism review.
4-624 Blaser, E. 1946a. A Contribution to the Study of Hydrogen Sul-
fide Poisoning of Animals by Manure Gases. Schweiz. Arch. Tierheilkd.
88:401-413 (Ger).
D-8. Case report of deaths of two horses due to sewer gas. No
analysis of constituents. Pathological-anatomical study of the
bodies is reported.
4-324 Blaser, E. 1946b. A Contribution to the Study of Hydrogen Sul-
fide Poisoning of Animals by Manure Gases. Schweiz. Arch. Tierheilkd,
88:433-446 (Ger).
C--. Small numbers of rabbits, guinea pigs, mice, and doves were
exposed to high levels of H2S (0.24 or 0.40%) and NH3 (0.10% or
0.24-0.362%) together for several hours. Histological examina-
tions were done showing effects in the lungs, heart, liver, kidney,
and spleen.
95
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4-016 Blaxland, J. D., J. Sheratob, G. H. Francis, and G. E. Jones. 1978.
Mortality in a Battery Laying House Attributed to the Presence of
Noxious Gases from Slurry. Vet. Rec. 103(11):24l-242.
D-7. H2S levels may have reached as high as 90 ppm near the most
exposed chickens, causing increased mortality. On autopsy, several
abnormalities were found, including lung edema. Confounded by
the possibility of other factors present.
4-017 Booras, S. G. 1974. Hydrogen Sulfide Health Effects and Recom-
mended Air Quality Standard. PB 233-843, National Technical In-
formation Service, U.S. Dept. of Commerce, Springfield, Virginia.
34 pp.
A—. The thrust of this review is similar to that of the current
project. Review contains atmospheric H2S data, acute and subacute
poisoning of humans, and a recommended air quality standard of
0.015 mg/m3.
4-138 Breysse, P. A. 1961. Hydrogen Sulfide Fatality in a Poultry
Feather Fertilizer Plant. Am. Ind. Hyg. Assoc. J. 22:220-222.
C-6. The victim was apparently exposed to 2,000-4,000 ppm H2S
for up to 15 min.
4-139 Breysse, P. A. 1970. Three Men Rendered Unconscious While Work-
ing in Sewer Manhole. Occup. Health Bull. 25:1-3.
D-4. The authors believe the effect (unconsciousness after 2 min)
was due to H2S, though there are very few data. Several days after
the incident, no H2S was detected.
4-140 Brown, K. E. 1969. Some Toxicological Problems in a Rubber Industry.
Med. J. Aust. 1:534-538.
C-4. H2S level of about 100 ppm caused unconsciousness, with ap-
parent full recovery in 1 day.
4-019 Buevich, V. A., and G. M. Mel'nikova. 1973. Biophysical Aspects
of Muscle Tone. Dokl. Akad. Nauk. SSSR, Ser. Biol. 212(2):490-491
(Russ).
D--. The muscle tone of workers exposed to both H2S and CS2 was
compared to those of workers not exposed to sulfur compounds at
the same plant and of persons with influenza.
4-141 Bulatova, F. D., L. I. Geller, I. S. Genadinnik, and V. A. Sukhanova.
1968. Influence of Products from the Conversion of High-Sulfur
Petroleum on the Extent arid Clinical Manifestations of Chronic
Bile Duct Disease. Gig. Tr. Prof. Zabol. 12:22-26 (Russ).
96
-------
D--. Oil refinery workers exposed to hydrocarbons and H2S at con-
centrations 4-6 times the maximum allowable concentrations showed
a higher incidence of diseases implicating the bile duct than did
railroad depot workers or lathe operators. Inflammatory signs in
patients with chronic cholecystitis were mild. Functional dis-
orders of the gall bladder and gastrointestinal tract and deranged
liver and gastric secretory functions were prevalent.
4-293 Burnett, W. W., M. Grace, W. F. Hall, and E. G. King. 1975. The
Problem of Hydrogen Sulfide Poisoning. Alberta Med. Bull. 40:68-69.
D--. A brief discussion of H2S exposure in the petrochemical in-
dustry in Alberta, Canada; symptoms and treatment, but no concen-
trations .
4-020 Burnett, W. W. , E. G. King, M. Grace, and W. F. Hall. 1977.
Hydrogen Sulfide Poisoning: Review of 5 Years' Experience. Can.
Med. Assoc. J. 117(11): 1277-1280.
C-8. Review of observed symptoms but no exposure data. The acute
problems in the 221 cases studied were coma, dysequilibrium, and
respiratory insufficiency with pulmonary edema. Survivors had no
apparent long-term adverse effects.
4-142 Carson, M. B. 1963. Hydrogen Sulfide Exposure in the Gas Industry.
Ind. Med. Surg. 32:63-64.
D-5. An account of five men with varying exposures (intermittent,
over 4 wk) to an atmosphere containing H2S and NH3 in unknown con-
centrations. The three affected men complained of blurred vision,
seeing colored rings around lights, and "gritty" eyes. Symptoms
lasted only a day.
4-022 Chelikanov, K. N. 1978. Nature of the Combined Action of Carbon
Bisulfide, Hydrogen Sulfide, and Sulfur Dioxide When All are Present
in the Air. Nauch. Tr. Ryazan. Med. In-t. No. 63:45-47 (Russ).
D--. Rats were exposed to a mixture of 0.005 mg CS2/m3, 0.003 mg
H2S/m3, and 0.05 mg S02/m3 or one of 0.00172 mg CS2/m3, 0.0026 mg
H2S/m3, or 0.0169 mg S02/m3. Changes were seen in the blood
chemistries of these two groups compared to the controls. The
gases were said to have a summation effect showing neither syn-
ergism nor antagonism.
4-023 Chepikova, N. R. 1974. Effect of Hydrogen Sulfide Baths on the
Resistance of Animals to Acute Hypoxia. Vop. Kurortol., Fizioter.
Lech. Fiz. Kul't. No. 1:70-76 (Russ).
D--. One-time bathing of mice in solutions containing 25 or 50
mg H2S/L increased their resistance to experimentally induced
hypoxia. The increase in resistance was explained by mobiliza-
tion of blood from the spleen to increase the respiratory capa-
city of the blood.
97
-------
4-143 Chertok, 0. M. 1968. Acute Poisoning with Hydrogen Sulfide.
Zh. Nevropatol. Psikhiatr. 68:381-384 (Russ).
C-5. The 29 workers studied were divided into three groups of
light, moderate, and severe intoxication, and the symptoms are
described. However, no actual exposure information is given.
The group with light exposure experienced headaches, vertigo, a
feeling of fainting, difficulty in breathing, nausea and vomiting,
photophobia, pain in the eyes, and a short loss of consciousness
sometimes with convulsions.
4-025 Combaz, M. 1976. Gas Intoxications in a Petroleum Refinery (1969
to 1974). Staub - Reinhalt. Luft. 36(1):15-19 (Fre).
D-8. Among 40 instances of gas intoxication within 5 y at a pe-
troleum refinery employing an average 2,000 people, 15 instances
were due to the presence of H2S. Toxicity due specifically to
H2S and H2S concentrations causing the intoxications were not
stated.
4-266 Comberg, G. 1965. Stall Climate as a Performance Factor in Ani-
mal Confinement. Tierzuechter. 17(14):81-82 (Ger).
D--. Review of animal exposure to H2S, NH3, and C02 in closed
barns.
4-026 Cordasco, E. M. , and E. D. Stone. 1973. Pulmonary Edema of
Environmental Origin. Chest 64(2):182-185.
D--. A review of treatment used in cases of pulmonary edema
caused by chemical agents, including H2S. Includes a very brief
summary of the effects of H2S, as low as 50 ppm being toxic.
4-144 Cralley, L. V. 1942. The Effect of Irritant Gases Upon the Rate
of Ciliary Activity. J. Ind. Hyg. Toxicol. 24:193-198.
D-6. Ciliary activity in freshly excised rabbit tracheal tissue
was completely stopped, without recovery in air, by exposure to
600 ppm H2S for 5 min.
4-027 Curtis, S. E., C. R. Anderson, J. Simon, A. H. Jensen, D. L. Day,
and K. W. Kelley. 1975. Effects of Aerial Ammonia, Hydrogen Sul-
fide and Swine-House Dust on Rate of Gain and Respiratory-Tract
Structure in Swine. J. Anim. Sci. 41(3):735-739.
C-10. H2S, alone at 8.5 ppm or at 2 ppm in combination with 50 ppm
NH3, had little effect on the growth rates of three pigs, exposed
for 17-19 d.
4-028 Dalgaard, J. B., F. Dencker, B. Fallentin, P. Hansen, B. Kaempe,
J. Steensberg, and P. Wilhardt. 1972. Fatal Poisoning and Other
Health Hazards Connected with Industrial Fishing. Br. J. Ind.
Med. 29(3):307-316.
98
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D-7. Several case reports of fatal and nonfatal accidents, prob-
ably due to the presence of noxious gases (H2S, NH3, HCHO, C02)
and/or low oxygen levels. The H2S levels found in the holds of
several ships (not done at the time of the accidents) ranged from
3 to > 2,000 ppm.
4-145 Davenport, S. J. 1945. Hydrogen Sulfide Poisoning as a Hazard
in the Production of Oil. Bureau of Mines, U.S. Dept. of the
Interior, Information Circular 7329. 10 pp.
O-. General discussion of H2S, its toxicology, and workplace
precautions. Review includes several cases of poisoning in min-
ing operations.
4-029 Demaret, D., and J. Fialaire. 1974. Hydrogen Sulfide Poisoning
in a Natural Gas Refinery. J. Eur. Toxicol. 7(l):32-36 (Fre).
C-9. Workers in natural gas refineries experienced a wide range
of symptoms: light (euphoria, staggering, colored vision),
moderate (unconsciousness, headache, nausea, respiratory irrita-
tion), and severe (unconsciousness and coma, polypnea, tachycardia,
convulsions). All eventually recovered. No levels of H2S in the
air were given, only in the gas being refined (14.5% - 145,000
ppm).
4-258 Denmead, C. F. 1962. Air Pollution by Hydrogen Sulfide from a
Shallow Polluted Tidal Inlet, Auckland, New Zealand; Paper No. 4,
In: Proceedings of the First Technical Session of the Clean Air
Conference, University New South Wales, Auckland, New Zealand.
17 pp.
D--. Microbial action in polluted waters caused atmospheric H2S
levels of < 1 ppm from ~ 2,000-6,000 ft away. Public complaints
of paint blackening and odor were blamed on the H2S present.
4-235 Deveze [no initial]. 1956. Hydrogen Sulfide, a Pathological Fac-
tor in Coal Mining. Evidence Drawn from 100 Observations. Rev.
Med. Miniere. 9(32-33):14-18 (Fre).
B-8. In over 4 years, 120 workers complained of eye irritation
of widely varying severity. A doubtful spot value of 100 ppm H2S
was measured.
4-031 Dirnhofer, R. 1977. The Morphology of Hydrogen Sulfide Poisoning.
Beitr. Gerichtl. Med. 39:145-159 (Ger).
C-9. Case report of a fatility due to cardiac failure several
days after sewer gas intoxication. There were alterations of the
central nervous system and serious disturbances in the cell metab-
olism of the myocardium and liver. Authors believe the effects
were due to H2S (unknown level). The report implies that any
cardiac patient (or atherosclerotic) who already has myocardial
cell problems belongs to a susceptible group.
99
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4-326 Division of Industrial Hygiene, U.S. Public Health Service. 1941.
Hydrogen Sulfide: Its Toxicity and Potential Dangers. Public
Health Rep. 56:684-692.
C--. Review of the toxicology of H2S and the pathology of poi-
soning. Effects of exposure are similar to other reports.
4-033 Donham, K. J., M. Rubino, T. D. Thedell, and J. Kammermeyer.
1977. Potential Health Hazards to Agricultural Workers in Swine
Confinement Buildings. J. Occup. Med. 19(6):383-387.
D-7. The H2S levels in 13 different swine confinement units varied
with time, from 0 to 10 ppm, along with dust and high levels of
NH3, CO, and C02. The 11 workers and 35 veterinarians interviewed
complained of several adverse symptoms, including coughing and
eye irritation.
4-262 Dougherty, R. W., R. Wong, and B. E. Christensen. 1943. Studies
of Hydrogen-Sulfide Poisoning. Am. J. Vet. Res. 4:254-256.
D-6. The toxicity of H2S gas to dogs and sheep, introduced through
the rectum, was affected by the amount of C02 in the air breathed.
Artificial respiration wasn't sufficient to keep a guinea pig alive
after receiving a toxic H2S dose.
4-146 Duan Fyn-Zhui. 1959. Data for Determining the Maximum Permissible
Concentration of Hydrogen Sulfide in the Atmospheric Air. Gig.
Sanit. 10:12-17 (Russ); English translation in: USSR Literature
on Air Pollution and Related Occupational Diseases. A Survey.
B. S. Levine (trans.). Vol. 5, U.S. Public Health Service,
Washington, D.C. pp. 66-73.
A-10. The minimum concentration at which H2S odor was detected
was 0.012-0.030 mg/m3. Light sensitivity of the eye wasn't af-
fected at 0.008 mg/m3, and was affected at 0.01-0.013 mg/m3.
Motor chronaxy studies (indicating the functional state of the
brain cortex) and autopsies show definite changes in rats exposed
to 10 mg H2S/m3 for 12 h/d, 3 mo. Those exposed to 0.02 mg/m3
showed weaker symptoms. Authors suggest 0.008 mg H2S/m3 as the
allowable daily avg. concentration.
4-035 Dubrovskaya, F. I., M. S. Katsenelenbaum, Y. K. Yushko, S. A.
Ipatova, and R. P. Vlasov. 1976. Hygienic Evaluation of Air
Protection Measures at the Volga Industrial Complex. Gig. Aspekty
Okhr. Okruzhayushchei Sredy 123-127 (Russ).
D—. Exposure of children living in the vicinity of the Volga
industrial complex to HCHO, S02, aldehydes, H2S, and NH3 increased
morbidity. Effects were not ascribed to particular substances
and the levels of the compounds were not stated except that they
exceeded their limits.
100
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4-037 Dvoriantseva, M. V. 1973. Treatment of Chronic Dermatoses Using
Hydrogen Sulfide Baths from Sokolovogorskii Spring. Vopr. Kurortol.
Fizioter. Lech. Fiz. Kult. 38(3):252-254 (Russ).
D~. Mineral baths containing NaCl and 20-32 mg H2S/L improved
conditions of eczema and psoriasis in 88.1 and 84.9% of the pa-
tients. Improvement was seen in 81.5% of the patients with
neurodermatitis.
4-036 Dwornicki, J. 1979. Effect of Experimental Poisoning with Hydrogen
Sulfide on the Cardiac Muscle. Bromatol. Chem. Toksykol. 12(3):256-
265 (Pol).
C--. Exposing rabbits for 1 h/d for 14 d to 100 mg H2S/m3 caused
disorders of rhythm, mineral balance, and enzyme activity in their
hearts.
4-039 Elebekova, R. S., T. K. Aitbaev, and V. M. Almaniyazova. 1976.
Functional State of the Liver under the Chronic Combined Effect
of Hydrogen Fluoride and Hydrogen Sulfide. Tr. Nauchn.-Issled.
Inst. Kraev. Patol. (Alma Ata). 29(Part 1?):27-31 (Russ).
B-ll. Good work. Omits explicit statement of "no observed toxic
signs." Little experimental detail is given, but appears consistent
internally. Rats were exposed to 5 or 10 mg H2S/m3 for 6 h/d, 6
d/wk, for 4 mo. Changes in liver function and peripheral blood
values were seen. Interaction study with HF was also done. In-
cludes an extensive review of other Russian work with H2S (both
oral and inhalation routes).
4-040 Elovaara, E. , A. Tossavainen, and H. Savolainen. 1978. Effects
of Subclinical Hydrogen Sulfide Intoxication on Mouse Brain Protein
Metabolism. Exp. Neurol. 62(l):93-98.
D-9. Adult female mice exposed to 100 ppm H2S for 2 h had reduced
labelled leucine incorporation in cerebral protein and myelin 24
and 48 h after exposure. Incorporation returned to control level
72 h after exposure.
4-147 Evans, C. L. 1967. The Toxicity of Hydrogen Sulphide and Other
Sulphides. Quart. J. Exp. Physiol. 52:231-48.
C-9. The injection of ~ 130 umole/ml H2S into rats and rabbits
generally first increased then decreased respiration and blood
pressure. Sometimes bradycardia appeared. H2S appeared in the
exhaled air. Rate and appearance of these responses varied with
the site and rate of injection, suggesting detoxification in the
blood. The action on nerve centers was reversible. Inhalation
experiments (no data given) are supposed to have shown similar
results.
101
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4-334 Fischer, 0., and E. Starkenstein. 1932. Chronic Occupational
Hydrogen Sulfide Poisoning. Samml. Vergiftungsfalien. 3:27-31
(Ger).
C-9. Extensive data on one case of chronic H2S poisoning of a
lab worker preparing thiourea. Classic symptoms are described,
and apparent increasing sensitivity with time.
4-302 Flury, F. 1928. Modern Tissue Poisons in Pharmacological-
Toxicological View. Arch. Exp. Path. Pharmakol. 138:65-82.
D--. Review.
4-041 Foderman, V. M. , N. S. Grishko, V. I. Rodin, A. M. Trankovski,
and I. A. Nakrasova. 1979. Experimental Substantiation in In-
halation of Aerosols as Prophylaxis for Occupational Diseases of
the Upper Respiratory Tract in Workers of Coal and Metal Mining
Industries. Zh. Ushn. Nos. Gorl. Bolezn. (4):17-21 (Russ).
D--. H2S in water (40 mg/L) was less effective than other pro-
phylactics in delaying the development of experimentally induced
silicosis and anthracosis in rats.
4-204 L. V. Fomicheva, and A. I. Gymrya. 1973. Eyes During Experimental
Chronic Mercury Poisoning. Vestn. Oftal'mol. No. 2:77-80 (Russ).
D--. Changes in the eyes of rats induced by chronic mercury poison-
ing were improved by inhalation of H2S aerosols.
4-336 Frankisek, M. V. 1950. Lesions of the Eye Due to Hydrogen Sulfide.
Ceskoslovenka Oftal. 6:5-8 (Czech).
D--. Eye irritation was seen in workers in a sugar factory:
blepharospasm, light sensitivity, and epithelial edema. Experi-
mental studies with rats showed similar effects.
4-149 Freireich, A. W. 1946. Hydrogen Sulfide Poisoning—Report of
Two Cases, One with Fatal Outcome, from Associated Mechanical As-
phyxia. Am. J. Pathol. 22:147-155.
D-4. Results of the autopsy of the victim of sewer gas intoxi-
cation. No exposure data - time or concentration.
4-242 Fyn-Djui, D. 1961. See Duan Fyn-Zhui (1959).
4-205 Gaultier, M., J. Lecoeur, R. Le Breton, P. Gervais, and J. P.
Frejaville. Case of Extremely Acute Hydrogen Sulfide Poisoning
with Symptoms of Pulmonary Involvement. J. Fr. Med. Chir. Thorac.
21(l):23-26 (Fre).
102
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C-6. Brief description of 2 fatal and 3 light exposure cases.
The fifth victim's symptoms included those described in most ac-
cidental H2S exposure reports, plus abnormal electroencephalograms
and slight jaundice. The same cases are described in Piva et al.
(1974).
4-300 Glebova, L. F. 1960. Establishing Maximum Allowable Concentration
of Hydrogen Sulfide. In: Atmospheric Air. B. S. Levine, Trans-
lator. U.S.S.R. Literature on Air Pollution and Related Occupa-
tional Diseases. 3:98-101.
B-8. Breast-fed babies whose mothers were employed in a viscose
spinning shop were exposed to 0.028-0.055 mg H2S/m3 (no CS2) from
the mothers' clothing. They were anemic, poorly developed, and
susceptible to frequent and severe infectious diseases.
4-044 Gofmekler, V. A., I. I. Brekhman, V. G. Golotin, A. A. Sheparev,
E. B. Krivelevich, L. N. Kamynina, A. I. Dobryakova, and V. A.
Gonenko. 1977. The Embryotropic Action of Nitrogen Dioxide and
a Complex of Atmospheric Pollutants. Gig. Sanit. No. 12:22-27
(Russ).
D--. An increased percentage of intrauterine destruction of embryos,
various types of hemorrhages, and other developmental anomalies
were seen in rabbits exposed to an atmosphere containing N02 or a
mixture of atmospheric pollutants in which CO, phenol, and H2S
concentrations exceeded their maximum allowable concentrations.
4-206 Golyakova, L. P. 1971. Present-Day State of Industrial Hygiene
Problems in Hydrometallurgical Production of Tungsten and Moly-
bdenum Salts and Oxides. PB254580T, National Technical Informa-
tion Service, U.S. Dept. of Commerce, Springfield, Virginia, 10 pp.
D-6. Dust, NH3, H2S, and HC1 were encountered. H2S concentrations
were as high as 21-124 mg/m3. No real exposure or toxicity data.
4-045 Goryacheva, I. G. 1979. Mathematical Experimental Planning in
the Study of the Effect on a Living Organism of Several Harmful
Elements Found in the Air. Khim. Tekhnol. (Kiev) No. 2: 50-54
(Russ).
D--. Typical factorial design. Use of regression analysis to
evaluate the effect of CO, H2S, CS2, and CO, H2S, and S02 on an
organism.
4-259 Grant, W. M. 1962. Toxicology of the Eye. Charles C. Thomas,
Pubisher, Springfield, Illinois, pp. 271-274.
103
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D—. A review of ocular symptoms caused by H2S, which generally
start after several hours' exposure and include irritation, tear-
ing, and burning. May increase to photophobia, colored haloes
around lights, redness and swelling of lids, and fine gray stip-
pling of the corneal epithelium. 100 ppm H2S can cause immediate
effects, but most H2S keratoconjunctivitis caused by much lower
concentrations.
4-283 Gurinov, B. P. 1952. Limits of Allowable Concentrations of Hy-
drogen Sulfide in the Atmospheric Air of Inhabited Localities.
In: Limits of Allowable Concentrations of Atmospheric Pollutants.
Book 1. V. A. Ryazanov, Ed. B. S. Levine, Transl. Office of
Tech. Services, U.S. Department of Commerce, Washington, B.C.
pp. 46-51.
A--. Recommendations for community H2S standards of 0.05 mg/m3
for a one-time limit and 0.015 mg/m3 for a maximum avg. concentra-
tion. A review of Russian studies on atmospheric H2S levels near
various industries (0.01-1.25 mg/m3) and toxic effects, many in-
vestigators maintaining that chronic H2S poisoning will follow
prolonged continuous exposure to extremely low concentrations of
H2S. Inhabitants exposed to tenths and hundredths of mg/m3 com-
plained of general debility, vertigo, nausea, and headaches.
4-296 Haggard, H. W. 1924. Action of Irritant Gases upon the Respir-
atory Tract. J. Ind. Hyg. 5(10):390-398.
D--. A general review. No specific mention of H2S.
4-236 Haggard, H. W. 1925. The Toxicology of Hydrogen Sulfide. J.
Ind. Hyg. Toxicol. 7:113-121.
D—. Review of older data, mostly high dose, in near lethal to
lethal concentrations.
4-243 Haggard, H. W., Y. Henderson, and T. J. Charlton. 1922. The In-
fluence of Hydrogen Sulfide upon Respiration. Am. J. Physiol.
61:289-297.
D-6. Experiments on single dogs. Exposure for 18 min to 1,000
ppm. H2S caused respiratory difficulty with apparent recovery.
Death occurred at 2,000 ppm H2S in 16 min, and in 34 min in a vago-
tomized dog.
4-234 Haider, S. S., M. Hasan, and P. Islam. 1980. Effect of the Air
Pollutant Hydrogen Sulfide on the Levels of Total Lipids, Phos-
pholipids, and Cholesterol in Different Regions of the Guinea Pig
Brain. Indian J. Exp. Biol. 18(4):418-420.
104
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D-ll. Guinea pigs exposed to 20 ppm H2S for 1 h/d for 11 d showed
decreased lipid and phospholipid levels in some areas of the brain.
Authors believe this to be due to increased peroxidation of endo-
genous lipids. A mechanistic study, with questionable applicability
to this report. What is the significance of these changes?
4-150 Hand, B. M. 1939. Carbon Bisulfide and Hydrogen Sulfide Hazards
in the Viscose Rayon Industry. Hahnemannian Mon. 74:117-125.
D--. A review of the effects of CS2.
4-047 Hays, F. L. 1972. Studies of the Effects of Atmospheric Hydrogen
Sulfide in Animals. No. 73-21, 783, University Microfilms, Ann
Arbor, Michigan. 217 pp.
B-13. Mice showed some signs of stress after 24 h exposure to 10
or 20 ppm H2S, with at least partial recovery within several days.
Goats and lactating dairy cows were generally unaffected until
exposed to 50 ppm (exposure times from 24 h to 3 wk) . Includes a
review of effects and mechanism.
4-208 Hayes, F. L., E. Goret, H. D. Johnson, and L. Hahn. 1972. Hydro-
gen Sulfide Exposure in Ruminants. J. Anim. Sci. 35(1):189.
C—. An abstract of work completely presented in Hays (1972)
[4-047].
4-325 Hays, F. L., and H. D. Johnson. 1972. Effect of Atmospheric Hy-
drogen Sulfide (H2S) on Mice. Trans. Mo. Acad. Sci. 6:176.
C—. An abstract of work completely presented in Hays (1972)
[4-047].
4-314 Henderson, Y., and H. Haggard. 1943. Noxious Gases and the Prin-
4-295 ciples of Respiration Influencing their Action. 2nd ed. Reinhold
Publishing Corporation, New York, New York. pp. 140-141, 243-245.
D—. A short review of H2S toxicity and mechanisms.
4-048 Henkin, R. I. 1976. Effects of Vapor Phase Pollutants on Nervous
System and Sensory Function. In: Chemical Implications of Air
Pollution Research. A. J. Finkel and W. C. Duel, Eds. Publish-
ing Sciences Group, Acton, Massachusetts, pp. 193-216.
D—. Brief reviews of the toxicity of several gases, including
H2S.
4-049 Higuchi, Y. 1977. Behavorial Studies on Toxicity of Hydrogen
Sulfide by Means of Conditioned Avoidance Responses in Rats. Folia
Pharmacol. Jap. 73(3):307-320 (Japan).
105
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D--. Discriminated avoidance response and Sidman-type avoidance
response were inhibited by 200 and 300 ppm H2S respectively, at
the minimum. There was recovery in 1 h after exposure to low levels,
but persistance of inhibition for a day after exposure to higher
H2S levels.
4-292 Holasova, P. 1969. Pathology of Children in an Area Polluted
with Carbon Bisulfide and Hydrogen Sulfide in Comparison with a
Control Group. Cesk. Hyg. 14(7-8):260; Chem. Abstr. 72:35459v (1970).
D--. Children living near an industrial plant emitting 32 kg/h
H2S and 55.5 kg/h CS2 had a 10% higher incidence of upper respira-
tory tract diseases than control children living in a rural area.
4-052 Horton, A. D. , and M. R. Guerin. 1974. Quantitative Determina-
tion of Sulfur Compounds in the Gas Phase of Cigarette Smoke. J.
Chromatogr. 90(1):63-70.
C--. H2S levels in cigarettes: 81 pg/cig (nonfliter), 89 H8/ci§
(cellulose acetate filter), 25 pg/cig (charcoal filtered), and
112 pg/cig (filtered little cigar).
4-152 Howes, H. S. 1944. Eye Inflammation as the Only Symptom of In-
cipient Hydrogen Sulphide Poisoning. Analyst 69:92.
D-4. Eye trouble in a tannery was attributed to H2S. No real
data were given.
4-291 Hromadka, M. 1965. Fatal Intoxication with Hydrogen Disulfide
[Hydrogen Sulfide and Carbon Disulfide] in a Spinning Tank.
Pracouni Lekar. 17(2): 68-69; Chem. Abstr. 62:l6872e (1965).
D--. Description of a death occurring in an atmosphere of 6.1 mg
H2S/L and 3.8 mg CS2/L, in the manufacture of viscose cords.
4-244 Hurwitz, L. J. , and G. I. Taylor. 1954. Poisoning by Sewer Gas
with Unusual Sequelae. Lancet 1:1110-1112.
D-5. Case report of severe, but nonfatal, intoxication due to a
30-min exposure to sewer gas, probably containing a high level of
H2S.
4-053 Husain, M. M. 1976. In Vitro Effect of Hydrogen Sulfide on the
Activity of Some Enzymes of Rat Lung Homogenate. Ind. Health
14(3-4):93-96.
D-6. H2S concentrations of 18.2-502 ppm in the homogenate caused
changes in the activity of 6/7 rat lung enzymes, even at the lowest
concentration. Pattern and degree of changes varied with the enzyme.
Includes the same results reported in Husain and Zaidi (1977) plus
two additional enzymes.
106
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4-054 Husain, M. M. , and S. H. Zaidi. 1977. An in Vitro Study on the
Interaction of Hydrogen Sulfide with Enzymes of Rat Lung. In:
Proceedings of the 1st International Symposium of Environmental
Pollution and Human Health, pp. 458-464.
D-ll. Concentrations of 18.2-502 ppm H2S were bubbled through
rat lung homogenates, inhibiting acid phosphatase, alkaline phos-
phatase, and glutamic-pyruvic transaminase, even at 18 ppm. Ar-
ginase activity increased with increased H2S concentration. The
authors suggested that these changes could lead to the deprivation
of amino acids heeded for protein biosynthesis in lung tissue.
4-055 Hysing, E. S., and E. Wergeland. 1975. Gas Exposure and Health
Problems in Herring Oil and Fish Flour Industry. Tidsskr Nor.
Laegeforen. 95(4):226-228 (Nor).
C—. Review of toxic gases to which employees in the herring oil
and fish flour industry are exposed. Also includes a case report.
i The autopsy revealed the typical results of H2S poisoning.
1-0172 ILO. 1970. Permissible Levels of Toxic Substances in the Working
Environment. Occupational Safety arid Health Series 20, Inter-
national Labour Office, Geneva, pp. 194-198.
C—. Maximum Acceptable Concentrations in Czechoslovakia.
Normal Short, Single
MAC (mg/m3) Exposure MAC (mg/m3)
Acrolein 0.5 1.0
NH3 . 40 80
HCHO 2 5 . .
HCN 3 15
MeOH 100 500
H2S 30
4-153 ILO/WHO, International Labour Office/World Health Organization,
Committee on Occupational Health. 1970. Permissible Levels of
Toxic Substances in the Working Environment. In: Proceedings of
the Sixth Session of the Joint ILO/WHO Committee on Occupational
Health, Geneva, Switzerland. June 4-10, 1968. International Labour
Office, Geneva, Switzerland, pp. 190, 195, 202, 218, 235, 242,
and 334.
D—. The Maximum Acceptable Concentration (MAC) for H2S in several
countries ranges from 10 to 30 mg/m3.
4-056 Ivanenko, N. A. 1976. Clinical Aspects and Treatment of Severe
Hydrogen Sulfide Poisoning. Vrach. Delo. No. 8:126-128 (Russ).
C-6. An extensive description of two victims of sewer gas poisoning.
No H2S concentration data. Complications and remote sequelae didn't
occur. Used cyanide-type treatment.
107
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4-318 Jaensch, P. A. 1930. Symptomology and Therapy of Eye Injuries
Caused by Hydrogen Sulfide. Arch. Gewerbepathol. Gewerbehyg.
1:397-407 (Ger).
D--. Review of clinical aspects of H2S exposure with regard to
the eye. Jaensch recommends that work room air contain i500 ppm
to avoid eye injury and preferably much less.
4-306 Jonek, J., and J. Konecki. 1966. Histochemical Examination of
Pulmonary Enzyme Level Changes in Experimental Hydrogen Sulfide
Poisoning. Med. Pracy. 17(4):329-335 (Pol).
C--. The exposure of rabbits to 0.1 mg H2S/L (this is the best
guess of the dose from the unclear photocopy we received of the
article) for 0.5 h/d for 7, 10, or 14 d caused decreased activity
of 4 enzymes in the lung.
4-057 Jones, J. P. 1975. Hazards of Hydrogen Sulfide Gas. Sel. Pap.
Annu. Gas Meas. Inst. 23rd, 16. 4 pp.
D—;. A general discussion of the dangers of H2S to humans. Some
workplace precautionary measures are given.
4-154 Kaipainen, W. J. 1954. Hydrogen Sulfide Intoxication—Rapidly
Transient Changes in the Electrocardiogram Suggestive of Myocar-
dial Infarction. Ann. Med. Intern. Fenniae. 43:97-101.
D-4. Case report of probable H2S intoxication contracted in shov-
elling manure, of unknown strength and duration. Unconsciousness
and convulsions resulted. Changes in the electrocardiogram re-
sembling a myocardial infarction lasted several days. '
4-209 Kami'nski, M., and P. Mikolajczyk. 1967. Changes of the Activity
and Localization of Acid Phosphatase, Alkaline Phosphatase and
Desoxyribonuclease II in Motoric Cells of the Anterior Horn of
the Spinal Cord in Rabbits in Acute Hydrogen Sulfide Poisoning.
Med. Pr. !8(l):42-46 (Pol).
C--. Rabbits exposed to 100 mg/m3 for 0.5 h/d for 7, 10, or 14 d
were decapitated at the end of the exposure periods, and tissue
sections were examined.
4-322 Kamnev, V. M. , and T. M. Lyutikova. 1965. The Action of a Mix-
ture of Hydrocarbons and Hydrogen Sulfide on the Histological
Structure of the Central Nervous System. Tr. Omsk. Med. Inst.
61:141-146 (Russ).
D--. Microscopic changes in the brains of mice exposed to the
title mixture are described. The concentrations of the components
in the mixture to which the mice were exposed and of the total
mixture itself were not given. The mixture was generated by a
thermal cracking unit.
108
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4-060 Kaplun, S. Ya., and E. G. Koptyeva. 1973. Age-Related Character-
istics of Reactions to Hydrogen Sulfide by its Indices in Blood
and Changes of Arterial Pressure and Respiration. Fiziol. Zh.
(Kiev) 19(3):328-332 (Ukr).
D--. Dogs were dosed i.v. by H2S.
4-059 Kaplun, S. Ya. , E. G. Kopteva, E. E. Grechishcheva, and L. K.
Briukhanova. 1975. Development of Experimental Myocarditis under
Conditions Using Various Concentrations of Hydrogen Sulfide Baths.
Vopr. Kurortol. Fizioter. Lech. Fiz. Kult. No. 1:56-60 (Russ).
C--. Fewer rats and rabbits succumbed to experimentally induced
myocarditis if they were subsequently given H2S baths containing
150 or 300 mg H2S/L. The resistance of their erythrocytes to
hemolysis decreased under the influence of the H2S baths.
4-061 Kappus, H. 1979. Toxicology of Hydrogen Sulfide. Staub - Reinhalt.
Luft. 39(5):153-155 (Ger).
D--. A review with 6 references.
4-155 Kemper, F. D. 1966. A Near-Fatal Case of Hydrogen Sulfide Poison-
ing. Can. Med. Assoc. J. 94:1130-1131.
D-4. Duration of exposure and the concentration of the gas are
unknown. A detailed description of the treatment is given, in-
cluding hypothermia.
4-063 Khusainov, Z. K., and A. N. Titov. 1977. Hygienic Evaluation of
the Air in Pig-Sties of the Large-Scale Farming Type. Vestn. S-kh.
Nauki Kaz. 20(5):75-78 (Russ).
D--. Pig-sty air contained 15.0-22.5 mg NH3/m3, 0.055-0.102 vol.
% C02, and 1.26-1.50 mg H2S/m3.
4-065 Kiryakov, K., T. S. Vodichenska, V. Markovska, and E. Tsutsulova.
(2-0018) 1978. Contamination of the Atmospheric Air and Morbidity with
Temporary Loss of Working Capacity Among Agrarian Workers. Khig.
Zdraveopaz. 21(l):42-48 (Bulg).
D-5. An epidemiological study of 2 similar groups of people showed
an increase in general morbidity and in specific groups of diseases
(respiratory and neuritis) in the group exposed to a mixture of
H2S, phenol, and HCN in the atmosphere.
4-156 Kleinfeld, M. 1965. Acute Pulmonary Edema of Chemical Origin.
Arch. Environ. Health 10:942-946.
D-5. Only a brief mention of H2S. A 15-min exposure to unknown
level of H2S caused pulmonary edema, clearing in 24 h.
109
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4-157 Kleinfeld, M., C. Giel, and A. Rosso. 1964. Acute Hydrogen Sulfide
Intoxication—An Unusual Source of Exposure. Ind. Med. Surg.
33:656-660.
C-5. Several case reports from the accidental exposure of 89 people
to unknown, but high, levels of H2S. Dizziness, nausea, pulmonary
edema, apnea, unconsciousness, respiratory arrest, and death were
seen.
4-066 Klentz, R. D., and M. R. Fedde. 1978. Hydrogen Sulfide: Effects
on Avian Respiratory Control and Intrapulmonary C02 Receptors.
Respir. Physiol. 32(3):355-368.
B-12. Acute exposure of chickens to high levels of H2S caused
changes in lung function and intrapulmonary C02 receptors, and
death at 4,000 ppm.
4-284 Kononova, V. A., and V. B. Aksenova. 1961. Contamination of the
Atmosphere by Emissions from a Plant Producing Synthetic Alcohol
and their Effect on the Morbidity and Sanitary-Domestic Life of
the Population. Gig. Sanit. 26:3-7 (Russ).
D--. The plant contaminated its environs with S02, H2S, and hydro-
carbons up to a distance of 3 km and with unsaturated hydrocarbons
for a distance of 500 m. The disease incidence for children living
near the plant in 1957-1959 was greater than that for children of
the control group.
4-067 Koptyeva, E. G. , S. Ya. Kaplun, and L. K. Bryukhanova. 1973.
Absorption Properties of Tissues with Experimental Myocardial
Dystrophy. Fiziol. Zh. (Kiev) 19(6):824-829 (Ukr).
C--. The author abstract of this Ukrainian article states that
the effects of H2S baths, taken before drug-induced myocardial
dystrophy, on the metabolic processes and resistivity of tissues
depended on the H2S concentration in the baths. The baths con-
tained 150 or >300 mg H2S/L.
4-298 Kosmider, S., and E. Rogala. 1967a. Electrolyte Balance Distur-
bances in Serum and Tissues in Subacute Experimental Poisoning
with Hydrogen Sulfide. Int. Arch. Gewerbepathol. Gewerbehyg.
23:12-18 (Ger).
C-10. Rabbits exposed to 100 mg H2S/m3 for 1 h/d for 5 d showed
electrolyte disturbances in the blood serum and tissues (especially
the brain) and heart rhythm disturbances. P, Fe and Cu values
were high in the tissues (liver and brain), but not in the serum.
4-211 Kosmider, S., and E. Rogala. 1967b. Mineral Metabolism Disorders
in Blood Serum and Tissues in Experimental Subacute Hydrogen Sul-
fide Poisoning. Int. Arch. Arbeitsmed. 23(1):12-18 (Ger).
110
-------
C-8. Rabbits were exposed to 100 mg H2S/m3 for 1 h/d for 5 d.
Significant changes were observed relative to the controls in the
concentrations of P and Na in the blood serum; Na, P, Fe, and Cu
in brain homogenate; and Fe in liver homogenate.
4-212 Kosmider, S., and K. Zajusz. 1966. Various Enzyme and Mineral
Metabolism Disorders in the Cerebellum in Experimental Subacute
Hydrogen Sulfide Poisoning. Zentrabl. Allg. Pathol. Anat.
109(4):411-417 (Ger).
C-8. Rabbits were exposed to 100 mg H2S/m3 for 1 h/d for 7 d,
which disturbed the concentrations of Na and Fe and the activity
of alkaline phosphatase in the brain compared to those of the con-
trols .
4-213 Kosmider, S., E. Rogala, and A. Pacholek. 1966. Studies on the
Toxic Action Mechanism of Hydrogen Sulfide. Int. Arch. Gewerbepathol,
Gewerbehyg. 22(l):60-76 (Ger).
C-9. Rabbits were exposed to 100 mg H2S/m3 for 1.5 h or for 0.5
h/d for 5 d, which caused enzyme, mineral, protein, and EKG dis-
turbances. Inhibition of the activity of aerobic enzymes and of
those concerned with active transport in the cerebellum and heart
may depend causally on the functional disturbances of these organs.
The decrease of alkaline phosphatase activity is traceable to the
reaction of H2S with the enzymatically active Mg ions, and the Na
citrate-reversible heart-rhythm disturbances observed in the sub-
acute poisoning are attributed to the increase of biologically
active Ca ions within the heart muscle.
4-158 Kosmider, S., E. Rogala, and A. Pacholek. 1967. Electrocardio-
graphic and Histochemical Studies of the Heart Muscle in Acute
Experimental Hydrogen Sulfide Poisoning. Arch. Immunol. Ther.
Exp. 15:731-740.
C-9. Both acute (1.5 h) and repeated (0.5 h/d, 5 d) exposure of
rabbits to 100 mg H2S/m3 caused abnormal EKG's, though of different
types. Enzyme activity in myocardial cells decreased, and possible
calcium disorder was seen.
4-159 Kosmider, S., E. Rogala, J. Dwornicki, and Z. Szulik. 1971. The
Influence of Vitaral on some Mineral and Enzyme Disturbances in
Subacute Poisoning with Hydrogen Sulfide. Int. Arch. Arbeitsmed.
29:64-84.
C-10. Rabbits exposed to 100 mg H2S/m3 1 h/d for 14 d had pro-
tein, mineral, and enzymatic disturbances in the blood, liver,
kidney, and brain. These were normalized by the repeated inges-
tion, during H2S exposure, of a vitamin and mineral supplement.
Ill
-------
4-068 Kosmider, S., E. Rogala, Z. Szulik, and J. Dwornicki. 1973. Ef-
fect of Trace Metals on Disorders of Acid-Base Equilibrium and
Mineral Metabolism in Subacute Poisoning with Hydrogen Sulfide.
Patol. Pol. 24(1):171-186 (Pol).
C—. Exposing rabbits to 100 mg H2S/m3 for 1 h/d for 14 d caused
mineral and acid-base balance disorders in the blood, which distur-
bances were improved by Vitaral (vitamin-mineral preparation) treat-
ment in the course of the poisoning.
4-069 Kosmodamianskaya, D. M., and S. F. Sorokina. 1976. Characteristics
of Allergic Pathologies of the Child Population in an Industrial
Center. Gig. Sanit. No. 11:101-102 (Russ).
D--. Children in an industrial center who were exposed to num-
erous chemicals (including CO, H2S, S02, and NH3) in concentra-
tions often exceeding maximum permissible levels showed a 1.5-3
times greater incidence of respiratory afflictions and 10 times
greater incidence of allergic dermatitis than for children living
in an area where the chemicals were below acceptable limits.
4-070 Kostlan, J. 1976. Contribution to the Analysis of the Possibil-
ity of Escape of Workers during Accidental Emission of Gases.
Sb. Pr. Vyzk. Chem. Vyuziti Uhli, Dehtu Ropy. 14:253-264 (Czech).
D--. The maximum atmospheric concentration of H2S through which
a man might run with restricted breathing, with the assumption
that the worker can reach a safe area within 1 min, is 1,000 ppm.
4-160 Kranenberg, W. R. H. , and H. Kessener. 1925. Hydrogen Sulfide
and Carbon Bisulfide Poisoning. Zentralbl. Gewerbehyg. Unfallverhuet,
2:348-350 (Ger).
B-9. Workers in a sugar beet processing plant, exposed to ~l4-37
mg H2S/m3, had repeated eye irritations. Includes a review of
the viscose rayon industry, with workers exposed to H2S (~9-86
mg/m3), CS2, and H2S04. The acid may have played a role in the
eye problems that occurred.
4-214 Krasovitskaya, M. L., T. A. Shirinkina, S. G. Zinov'eva, and T.
N. Novoselova. 1970. A Sanitary Evaluation of a Chemical Combine
as the Source of Contamination of the Atmospheric Air. Tr. Permsk.
Med. Inst. 82:40-45 (Russ).
D--. Children living in an area polluted by H2S, S02, N oxides,
phenol, H2SC>4, and dust showed a lag in physical development,
elevation in incidence of anemia and chronic rhinitis, and more
frequent central nervous system disturbances than controls.
4-286 Krekel, K. 1964. Electrocardiographic (ECG) Changes in Two
Workers after Hydrogen Sulfide Poisoning. Zentralbl. Arbeitsmed.
Arbeitsschutz. 14(7):159-163 (Ger).
112
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C-6. Two men were briefly exposed to an unknown (probably low)
level of H2S. Extensive physical exam found no real problems ex-
cept for some EKG abnormalities and moderate dyspnea. One com-
plained of continuing dizziness and fatigue, but had a complica-
ting head injury so symptoms cannot be attributed only to H2S.
4-071 Kriz, J., L. Pelech, Z. Madlo, and D. Wokounova. 1976. Bone Age
in Children from Areas with Polluted Atmospheres. Cesk. Hyg.
2l(6-7):326-330 (Czech).
D--. Bone maturation and serum alkaline phosphatase were reduced
in two groups of 9-y-old children exposed to various chemicals.
One group was exposed to H2S, CS2, S02, C12, and H2S04 in the am-
bient air; the other, to S02, dust, and emissions from a synthetic
rubber manufacturing plant.
4-161 Kuwai, S. 1960. Experimental Studies on Gas Inhalation of Respec-
tive and Combined H2S. Shikoku Igaku Zasshi. 16:144-164 (Japan).
B-10. Includes an English abstract. Nice study, including inter-
action. Exposing rabbits to 20-25 ppm H2S for 4 h/d for 150 d
caused no change in general state or body weight, and a temporary
increase in free cholesterol. Combined inhalation with 20-25 ppm
CS2 caused more symptoms than either gas alone.
4-073 Langner, R. R., S. K. Norwood, G. E. Socha, and H. R. Hoyle. 1979.
Two Methods for Establishing Industrial Hygiene Priorities. Am.
Ind. Hyg. Assoc. J. 40(12):1039-1045.
D--. A theoretical discussion, with H2S as one of several com-
pounds briefly used for demonstration.
4-237 Larsen, V. 1944. Eye Disease Caused by Hydrogen Sulfide in Tunnel
Workers. Acta Ophthalmol. 21:271-286 (Fre).
A-9. Eye irritation was seen in workers exposed to ~40-185 mg
H2S/m3.
4-245 Larson, C. P., C. C. Reberger, and M. J. Wicks. 1964. The Purple
Brain Death. Med. Sci. Law 4:200-202.
D-4. Case report of a fatality in a plant making fertilizer from
chicken feathers. The death is attributed to H2S poisoning, and
the brain color to sulphaemoglobin. A more detailed description
is given in Breysse, 1961.
4-162 Laug, E. P., and J. H. Draize. 1942. The Percutaneous Absorp-
tion of Ammonium Hydrogen Sulfide and Hydrogen Sulfide. J. Phar-
macol. Exp. Therap. 76:179-188.
D-8. No inhalation exposure. H2S exposure of rabbits was through
the skin, at unknown concentrations, and death was the endpoint
measured.
113
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4-311 Layton, D. , Ed. 1980. An Assessment of Geothermal Development
in the Imperial Valley of California, Volume 1-Environment, Health
and Socioeconomics. DOE/EV-0092, National Technical Information
Service, U.S. Department of Commerce, Springfield, Virginia, pp.
10-3 to 10-9.
D--. Includes a 7-page review of public health considerations
(particularly odor theshold) of H2S, as the major health problem
related to thermal energy utilization.
4-215 Lebedeva, E. K., and M. I. Skorospeshkina. 1970. The Morbidity
Among Children of the Town of Perm Living Near Chemical Factories.
Tr. Permsk. Med. Inst. 82:73-76 (Russ).
D--. A group of 1,000 infants (<1 y) living in an area with sev-
eral sources of atmospheric pollutants (dust, carbon black, S02,
H2S, HF, S03, NO , and hydrocarbons) was compared to a control
group of 1,000. xThere was more respiratory illness (pneumonia,
bronchitis) and exudative diathesis in the exposed group.
4-216 Leduc, G. 1967. Report of a Study of the Pathological Conse-
quences of Chronic Exposure to Sulfur Dioxide, Hydrogen Sulfide,
and Chlorine Dioxide. Arch. Mai. Prof. 28(1):307-311 (Fre).
C-5. A review of several industries in France, stating that most
H2S levels encountered had no effect, but didn't give any concen-
tration information. During "bad periods," workers complained of
headaches, epistases, itching, and digestive troubles (vomiting,
constipation, diarrhea).
4-163 Legge, T. M. 1934. Industrial Maladies. Oxford University Press,
London, pp. 146-151.
D--. Reminiscences of many years of experience. Eye inflammation
was the major symptom.
4-238 Lehmann, K. B. 1892. Experimental Studies on the Habituation to
Industrial Gases. VI. Hydrogen Sulfide. Arch. Hyg. 14:135-189
(Ger).
B-9. The original studies. Also reviews much work done earlier.
Cats, rabbits, and dogs were exposed to very high levels (1,420-
48,280 mg/m3) for up to several hours. The lower levels caused
minor mucous membrane irritation, and the higher levels caused
convulsions. Most recovered. Human exposure ranged from 284 to
8,165 mg/m3, with no apparent symptoms at the lowest level.
5-149 Leonardos, G., D. Kendall, and N. Barnard. 1969. Odor Threshold
Determinations of 53 Odorant Chemicals. J. Air Pollut. Control
Assoc. 19(2):91-95. Data also appear in A.D. Little, Inc., Research
on Chemical Odors, Manufacturing Chemists Assoc., Washington, D.C.
1968.
114
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A-ll. Definitive paper. The odor recognition threshold for H2S
was 0.00047 ppm, and 0.0047 ppm when H2S was derived from Na2S.
4-299 Lewey, F. H. 1938. The Health Hazards in the Viscose Rayon In-
dustry. In: Pennsylvania Dept. of Labor and Industry. Survey
of Carbon Bisulfide and Hydrogen Sulphide Hazards in the Viscose
Rayon Industry. Bull. 46, Occupational Disease Prevention Division,
Pennsylvania Dept. of Labor and Industry, Harrisburg, Pennsylvania.
pp. 17-22.
D--. A review of the occurrence and toxicity of CS2. A brief
mention of H2S, that workers exposed to 16-25 ppm H2S had con-
junctivitis and those exposed to 12-16 ppm had no complaints.
4-074 Lewicki, L. , and W. Turkiewicz. 1979. Problems of the Maximum
Permissible Concentrations of Toxic Substances in Air. Cuprum.
6(l):32-36 (Pol).
D--. A discussion of the problems of determining the maximum per-
missible concentrations of CH4, C02, N02, S02, Hg, and H2S in the
air of mines.
4-316 Loginova, R. A. 1957. Basic Principles for the Determination of
Limits of Allowable Concentrations of H2S in Atmospheric Air.
In: Limits of Allowable Concentrations of Atmospheric Pollutants
III, V. A. Riazanov, Ed. National Technical Information Service,
U.S. Department of Commerce, Springfield, Virginia, pp. 52-68.
A-10. An extensive review of Russian work on the toxicity of H2S
to humans, as well as reports of 2 new studies. The odor threshold
is given as ~0.04 mg/m3. H2S air pollution in the presence of
hydrocarbons is considered to pose a greater danger than H2S alone.
Authors recommend 0.03 mg/m3 as the limit of allowable concentra-
tions for pure H2S, and 0.015 mg/m3 for H2S as a constituent of
natural gas.
4-344 Ludvich, D. 1981. The Hydrogen Sulfide Technical Manual. Safety
Technology and Oilfield Protectors, Inc. Lafayette, Louisiana.
123 pp.
D--. A safety and handling training manual.
4-164 Lund, 0. E., and H. Wieland. 1966. Pathologic-Anatomic Findings
in Experimental Hydrogen Sulfide Poisoning (H2S)--A Study on Rhesus
Monkeys. Int. Arch. Gewerbepathol. Gewerbehyg. 22:46-54 (Ger).
B-8. Acute exposure (^35 min) of monkeys to 500 ppm H2S caused
frequent rubbing of the eyes (mucous membrane irritation), gasping,
and unconsciousness in ~15 min. One died immediately, one 5 d
later, and one survived. Autopsies were done on all 3, emphasiz-
ing the brain.
115
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4-217 Lutsenko, L. A. 1970. Industrial Hygiene in the Concentration
of Sulfide Copper Ores at Mills in the Urals. Gig. Tr. Prof. Zabol.
14(10):11-15 (Russ).
D--. Any health effects observed in this study would be confounded
by all the possible chemical and physical exposures at an ore bene-
ficiation plant. H2S, HCN, and CS2i for example, are decomposition
products of the flotation reagents.
4-218 Manz, A. 1968a. On the Behavior of Tissue Oxidase and the Effect
of Oxygen Administration in Hydrogen Sulfide Poisoning in the Animal
Experiment. Zentralbl. Arbeitsmed. 18(11):325-333 (Ger).
D--. Mechanism study. Rabbits and/or guinea pigs were exposed
to 1,500 or 1,900 ppm H2S for S210 s and also to 5 and 20% H2S.
4-219 Manz, A. 1968b. On a Case of Survival after Acute Poisoning by
a Mixture of Hydrogen Sulfide and Hydrocyanic Acid. Zentralbl.
Arbeitsraed. 18(6):167-171 (Ger).
D--. Cannot separate H2S and HCN effects.
4-076 Matsuo, F., J. W. Cummins, and R. E. Anderson. 1979. Neurologi-
cal Sequelae of Massive Hydrogen Sulfide Inhalation. Arch. Neurol.
36(7):451-452.
C-5. The results of a computerized tomography scan of the head
of a victim of H2S poisoning (level unknown, but high).
4-220 Mattina, C. F., Jr. 1972. A Potentiometric Method for the Deter-
(2-0167) mination of Hydrogen Cyanide and Hydrogen Sulfide in Cigarette
Smoke. Tob. Sci. 16:113-114.
C--. Unfiltered cigarettes contained 4.3 (Jg H2S/puff and 35.0 |jg
HCN/puff.
4-269 Mazanowski, A., and A. Mazanowska. 1964. Ventilation in Henstalls
and Egg-Laying Performance. II. Mitt. Drobiarstwo, Warsaw.
12(11):10-11 (Pol). i
D--. 15-75 mg H2S/m3 were reported in livestock quarters.
4-167 McCabe, L. C., and G. D. Clayton. 1952. Air Pollution by Hydro-
gen Sulfide in Poza Rica, Mexico. Arch. Ind. Hyg. Occup. Med.
6:199-213.
C-8. Extensive description of an accident hospitalizing 320 people
because of exposure to unknown levels of H2S. There was extensive
irritation of the respiratory, gastrointestinal, and nervous sys-
tems. There were no respiratory or digestive sequelae.
116
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4-168 McCormack, M. F. 1975. Sewer Fume Poisoning. J. Am. Coll. Emer-
gency Physicians 4:141-142.
D-4. Case report of 2 acute H2S poisonings, resulting in 1 death
and 1 successfully treated victim. That man was unconscious, cy-
anotic, hyperventilating, and suffering from pulmonary edema and
various central nervous system effects.
4-246 McDonald, R. 1938. Ophthalmological Aspects of CS2 Intoxication.
In: Pennsylvania Dept. of Labor and Industry. Survey of Carbon
Disulfide and Hydrogen Sulphide Hazards in the Viscose Rayon In-
dustry. Bull. 46, Occupational Disease Prevention Division,
Pennsylvania Dept. of Labor and Industry, Harrisburg, Pennsylvania.
pp. 38-40.
D--. Includes a short discussion of eye irritation due to H2S.
No concentrations given. Mentions large differences in individual
susceptibility.
s4-l69 McDougall, J. W. G., and T. 0. Garland. 1954. Hydrogen Sulphide
Gas Poisoning at Rotorua. N. Z. Med. J. 53:471-475.
D-6. Data on gases in a thermal springs area: 63% by vol. H2S
in one manhole. Descriptions of 3 fatalities, with H2S implicated.
4-077 McQuitty, J. B., and J. R. Feddes. 1978. Warning: Manure Gases
are Dangerous. Agric. For. Bull. 1(1):10-14.
D--. Short review of the occurrence and possible problems of
several gases in barns, including NH3 and H2S.
4-247 Medvedev, V. M. 1959. The Effect of Certain Industrial Poisons
on the Mechanism of the Nerve Impulse Transmission in Superior
Cervical Sympathetic Ganglion. Report I. Acute Experiments with
Hydrogen Sulfide, Ethylene and Propylene in Healthy Animals. Byull.
Eksp. Biol. 47(4):79-82 (Russ).
D--. The upper cervical sympathetic ganglia of cats were perfused
by an injected solution of H2S in saline. The effect on the con-
traction of the nictitating membrane upon application of an elec-
trical current was measured. H2S lowered the humoral, not the
electrical, transfer of the nerve impulse.
4-221 Mel'nichenko, R. K. 1968. Combined Effect of Carbon Monoxide
and Hydrogen Sulfide. Vrach. Delo. 7:87-90 (Russ).
B-7. Rats were exposed to 300 mg H2S/m3 and 300 mg CO/m3 or 300 mg
CO/m3 alone for 4 h/d for 6 mo. The study indicated that the ac-
tion of the combined gases elicited a more expressed toxic effect
than CO alone, in terms of the lowering of the 02 absorption by
the animals, inhibition of the phagocytic reactions, strengthening
of the permeability of the vessels, and a tendency to the absence
of a weight increment in the animals.
117
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4-170 Milby, T. H. 1962. Hydrogen Sulfide Intoxication—Review of the
Literature and Report of Unusual Accident Resulting in Two Cases
of Nonfatal Poisoning. J. Occup. Med. 4:431-437.
C-6. A review of toxicity and treatment of H2S inhalation. H2S
level estimated to have been around 2,000 ppm. Victims suffered
loss of consciousness, convulsions, and no pulmonary edema. Rapid
recovery.
4-222 Misiakiewicz, Z., G. Szulinska, and A. Chyba. 1972. Effect of a
Carbon Bisulfide-Hydrogen Sulfide Mixture in Air on White Rats
during Several Months of Continuous Exposure. Rocz. Panstw. Zakl.
Hig. 23(4):465-475 (Pol).
D-6. Rats exposed for 6 mo to 0.1 mg/m3 each CS2 and H2S (com-
bined) showed a 30% increase in blood cholinesterase activity, a
14% increase in coproporphyrin excretion in the urine, a 64% in-
crease in aspartate aminotransferase serum activity, and bronchitis.
The only change observed in rats exposed to 0.1 mg CS/m3 for 6 mo
was a 16% increase in blood cholinesterase.
4-239 Mitchell, C. W. , and W. P. Yant. 1925. Correlation of the Data
Obtained from Refinery Accidents with a Laboratory Study of Hydrogen
Sulfide and its Treatment. Bull. No. 231. Bureau of Mines, U.S.
Dept. of Commerce, pp. 59-80.
A-10. Review of human accidental/occupational exposure. A small
amount of human experimental data. Definite irritation was seen
at 100 ppm. Recovery was rapid in acute cases, and slower (days)
in subacute cases. Acute exposure of canaries, rats, dogs, guinea
pigs, and goats to a range of H2S concentrations (35-1,600 ppm).
Authors believe that man behaves similarly to cats and dogs in
H2S exposure.
4-223 Morie, G. P. 1971. Determination of Hydrogen Sulfide in Ciga-
rette Smoke with a Sulfide Ion Electrode. Tob. Sci. 15:107.
C--. Unfiltered cigarettes contained 30-49 |Jg H2S/cig. The
amount was reduced by certain types of filters (18.7 pg/cig with
acetate-carbon filter).
4-319 Moser, P. 1940. Effect of Prolonged Inhalation of Hydrogen Sul-
fide in Dogs. Arch. Exp. Pathol. Pharmakol. 196:446-454 (Ger).
B-ll. Dogs exposed to 14 mg H2S/m3 for 7 h/d for 14 d showed only
increased drinking. Exposure to ~150 mg/m3 for 2 mo (7 h/d) caused
some eye and respiratory problems, which cleared up after exposure
stopped each day, and some slight blood changes.
4-081 Muller, P. H., L. Lenoir, D. Furon, M. Willot, A. Debarge, and J.
P. deMendonca. 1973. Double Poisoning by Hydrogen Sulfide. Med.
Lag. Domm. Corpor. (Paris). 6(3):284-286 (Fre).
118
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C-8. Case report of 2 deaths attributed to H2S in sewer gas, with
intense tracheal congestion, alveolar and interstitial edema of
the lungs, and congestion of the viscera.
4-082 Nabiullin, R. G., F. S. Khusainova, A. G. Zaerov, V. I. Nikulicheva,
and N. M. Zagidullina. 1976. Role of Hydrogen Sulfide in the
Development of Impairment of the Bronchopulmonary Apparatus in
Petroleum Industry Workers. V Sb., Gig. Tr. Zabol. Neft. Neftekhim.
Prom-st1. 74-77 (Russ).
D--. Petroleum workers, who are exposed to hydrocarbons as well
as H2S, showed more chronic bronchitis if they had worked ^10 y
compared to workers who had been exposed <10 y. The levels of
H2S and hydrocarbons as well as the numbers of workers examined
were not given.
4-083 Nakajima, K., S. Tsuchiya, T. Nakajima, and K. Harada. 1975.
The Effect of Nasal Obstruction on the Susceptibility of Mice to
Noxious Gases (author's transl). Exp. Anim. (Tokyo). 24(2):45-52
(Japan).
D--. The threshold values for loss of righting reflex and respi-
ratory arrest were higher for mice forced to breathe through the
mouth (1,200 and 1,600 ppm) than for nasal breathing mice (1,000
ppm).
4-086 Natusch, D. F. S., and B. J. Slatt. 1978. Hydrogen Sulfide as
an Air Pollutant. Air Pollut. Control 3:459-518.
B--. Review of natural and industrial sources of atmospheric H2S,
sampling and analytical methodologies, and corrosion of metals
and paint. Reported odor threshold was 0.025-0.1 ppm normally,
but lower when oil vapor is present, 0.006-0.02 ppm.
4-172 Nesswetha, W. 1969. Eye Lesions Caused by Sulphur Compounds.
Arbeitsmed. Sozialmed. Arbeitshyg. 4:288-290 (Ger).
D--. Review.
6-124 Newsome, J. R., V. Norman, and V. L. Zaratzian. 1965. Vapor
Phase Analysis of Cigarette Smoke. Tob. Sci. 9:102-110; or
Tobacco 161(4):24-32.
D--. Levels in tobacco smoke (pg/40 mL puff):
Unfiltered Filtered
Methanol 13 10
HCHO 4.1 3.6
Acrolein 8.2 7.9
HCN 32 29
H2S 3.4 3.1
NH3 12 13
119
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4-086 Nikolov, S. K., N. A. Kambulin, and M. V. Kolupaeva. 1976. Prob-
lems of Labor Hygiene in Modern Stock Breeding. Gig. Sanit. No.
12:80-84 (Russ).
D--. Review. Various authors have found up to 39 mg H2S/m3 and
3-135 mg NH3/m3 in large cattle, swine, and poultry-breeding estab-
lishments.
4-084 NRC, National Research Council, Subcommittee on Hydrogen Sulfide.
1979. Medical and Biological Effects of Environmental Pollutants.
Hydrogen Sulfide. University Park Press. Baltimore, Maryland.
172 pp.
A--. Authoritative and extensive review of the effects of H2S.
4-088 Odera, G. M. 1975. Fatality Produced by Accidental Inhalation
of Drain Cleaner Fumes. Clin. Toxicol. 8(5):547-551.
D-4. Grossly incomplete data for the purpose of this study.
Just a description of the accident, and a discussion of the safety
of drain cleaners.
4-270 O'Donoghue, J. G. 1961. Hydrogen Sulphide Poisoning in Swine.
Can. J. Comp. Med. Vet. Sci. 25:217-219.
C-8. The acute exposure of a few pigs and rabbits to increasing
H2S concentrations (50-1,200 ppm) caused death at longer exposures
to the highest concentrations, and symptoms with apparent recovery
after brief high exposures.
4-249 Oliver, T. 1911. The Sulphur Miners of Sicily: Their Work,
Diseases, and Accident Insurance. Br. Med. J. 2:12-14.
D-4. Just a mention of the presence of H2S in the mines and of a
fatal accident claiming 11 lives.
4-233 Ostrow, D. N., J. Manfreda, K. S. Tse, T. Dorman, and R. M.
Cherniack. 1978. Alpha^Antitrypsin Phenotypes and Lung Func-
tion in a Moderately Polluted Northern Ontario Community. Can.
Med. Assoc. J. 118(6): 669-672.
D-8. Just mentions the presence of H2S, at levels >20 ppm. Any
abnormalities in the tested lung functions seem more likely to be
due to dust exposure, which was also heavy. No comparisons with
nonpolluted areas. The aim was to find differences in lung func-
tion due to phenotypes, not air quality.
4-271 Petkov, G. 1964. A Study of the Microclimate in Large Poultry
Houses. Veterinarnomed. Nauki. Sofia 1(4):81-85 (Bulg).
D--. The levels of NH3, H2S, and C02 in poultry houses were above
acceptable levels, and caused decreased hemoglobin and erythrocytes
in the chickens.
120
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4-175 Petrun, N. M. 1965. Indications of Poisoning by Hydrogen Sulfide
Entering the Body Through the Skin. Farmakol. Toksikol. 28:488-490
(Russ).
C-9. Rabbits whose skin (except that of the head) was exposed to
air containing 1,000 or 2,000 mg/ra3 showed inhibition of blood
carboanhydrase and cholinesterase activities, reduced erythrocyte
respiration rate, changes in the gaseous composition of the blood,
and reduced hemoglobin.
4-176 Pettigrew, G. L. 1976. Preliminary Report on Hydrogen Sulfide
Exposure in the Oil and Gas Industry. Public Health Service, Dallas
Regional Office, U.S. Dept. of Health, Education, and Welfare.
4 pp.
D--. A brief review of the occurrence of H2S poisoning, and sug-
gestions for reducing the hazard. No concentration or effects
information given.
4-090 Piva, C., 0. Diamant-Berger, J. P. Frejaville, and E. Fournier.
1974. Intoxication by Hydrogen Sulfide. Eur. J. Toxicol. Environ.
Hyg. 7(1):30-31 (Fre).
C-5. No exposure data. Does show nice gradation of effects.
The same cases are described in Gaultier et al. (1967) [4-205].
4-250 Poda, G. A. 1966. Hydrogen Sulfide Can Be Handled Safely. Arch.
Environ. Health 12:795-800.
B-4. A discussion of the occurrence (123 cases in 7 y) and the
symptoms of H2S in a heavy water plant which had an alarm system
set for 10 ppm H2S (it never went off). Contrary to other reports,
little eye irritation was seen. Weakness, dizziness, nervousness,
and nausea were the main effects. Work practices, treatment, and
precautionary measures are also given.
4-305 Pohl, J. 1887. The [Toxicological] Action of Hydrogen Sulfide
and Alkali Sulfides. Arch. Exp. Pathol. Pharmakol. 22:1-25 (Ger).
D--. Most animal experiments studied the toxicity of Na2S. In
two experiments, convulsions were induced by H2S in rabbits by
nasal insufflation or by introduction directly into the trachea.
4-091 Pollard, G. D., and D. W. Hirsch. 1978. In-Flight Toxicology of
Fixed and Rotary Wing Aircraft Crew Stations. Paper No. 18, AGARD
[Advisory Group for Aeronautical Research and Development] Conf.
Proc. Vol. 225. 7 pp.
D--. After the firing of the guns, 2 air samples contained 63 or
126 ppm H2S and 21 or 18 ppm HCN, as well as other gases.
121
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4-313 Preuschen, G. 1974. Air Pollution and Human Work Capacity. In:
Proceedings of the International Livestock Environment Symposium.
University of Nebraska, Lincoln, Nebraska. April 17, 18, and 19,
1974. American Society of Agricultural Engineers. St. Joseph,
Michigan, pp. 195-198.
D--. Workers exposed to animal house atmospheres experienced
coughing, dizziness, shortness of breath (no numbers given) and
decreased respiratory functions (no statistical evaluations done).
No listing of contaminants or concentrations given.
4-177 Prouza, Z. 1970. Group Poisoning with Hydrogen Sulphide in an
Unusual Situation on a Viscose Plant. Prakt. Lek. 50:27-29 (Czech);
English translation available John Crerar Library, Chicago, Illinois.
Order No. 5828.4F (22836).
B-5. Brief exposure to ~15-35 mg H2S/m3 caused minor symptoms
in 4/9 workers. All 9 fully recovered. One man exposed to 4,000
mg/m3 died very quickly.
4-276 Renne, R. A., and K. E. McDonald. 1979. Toxic Effects of Geo-
thermal Effluents: Acute and Subacute Inhalation Toxicology of
Hydrogen Sulfide and Ammonia in Rodents. In: Pac. Northwest Lab.
Annu. Rep. 1979 DOE. Assist. Seer. Environ. Pt. 1: Biomedical
Science, p. 275.
C--. Part of an annual report, just a summary provided. An ini-
tial 7-d exposure to 100 ppm H2S (alone or in combination with
250 ppm NH3) caused no significant changes in rats or guinea pigs.
Subsequent 7-d exposure to 220 ppm H2S caused a mild increase in
the incidence of acute respiratory tract inflammatory lesions in
guinea pigs. Subsequent 7-d exposure instead to 250 ppm NH3 caused
the same changes as well as mild interstitial pneumonitis and mild
chronic nephritis.
4-337 Renne, R.A., and K.E. McDonald. 1980. Toxic Effects of Geothermal
Effluents: Subacute Inhalation Toxicology of Hydrogen Sulfide
and Ammonia in Rodents. In: Pac. Northwest Lab. Annu. Rep. 1980
DOE. Assist. Seer. Environ. Pt. 1: Biomedical Science, p. 240.
C--. Part of an annual report, so this is only a summary. Expo-
sure for 22 d to 220 ppm H2S, 250 ppm NH3, or a combination of
these gases had no effect on the major organs in rats and only
slight respiratory and renal effects in guinea pigs.
4-274 Robinson, A. V. 1979. Toxic Effects of Geothermal Effluents:
Effect of in Vitro Exposure to Hydrogen Sulfide on Cultured Rabbit
Alveolar Macrophages. In: Pac. Northwest Lab. Annu. Rep. 1979
DOE. Assist. Seer. Environ. Pt. 1: Biomedical Science, pp. 279-
281.
122
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C-6. A summary of work in progress. Cultured rabbit alveolar
macrophages were exposed to 50 or 200 ppm H2S under various ex-
posure regimes and times. Relative phagocytic ability and via-
bility decreased with increasing concentration and time.
4-338 Robinson, A.V. 1980. Toxic Effects of Geothermal Effluents:
Effect of in Vitro Exposure to Hydrogen Sulfide on Rabbit Alveolar
Macrophages Cultured on Gas Permeable Membranes. In: Pac. North-
west Lab. Annu. Rep. 1980 DOE. Assist. Seer. Environ. Pt. 1:
Biomedical Science, pp. 235-239.
C--. Exposure of rabbit alveolar macrophages to 60 ppm H2S for
24 h caused a decrease to ~5% of the controls when cultured on
gas-permeable membranes (more similar to ^n vivo exposure), and
had no effect when cultured on gas-impermeable flasks. Cytotox-
icity was more pronounced under continuous than intermittent ex-
posure. Full expression of phagocytic ability depended on the
length of time after the end of exposure as well as the duration
and level of exposure.
4-275 Robinson, A. V., K. E. McDonald, and R. A. Renne. 1979. Toxic
Effects of Geothermal Effluents: Effect of in Vitro Exposure of
Hydrogen Sulfide on Free Cells Obtained from Lungs of Rats and
Guinea Pigs. In: Pac. Northwest Lab. Annu. Rep. 1979 DOE.
Assist. Seer. Environ. Pt. 1: Biomedical Science, pp. 282-283.
C-6. An abstract of work in progress. The numbers and types of
lavaged lung cells from rats and guinea pigs exposed to 200 ppm
H2S for 24 h were indicative of an inflammatory response in the
respiratory tract.
4-294 Robinson, L. F. , M. N. Camp, and E. C. Chamberlain. 1942. A
Source of Industrial Hazard from Hydrogen Sulfide Gas. Southern
Med. J. 35(6)=621-623.
D—. A short review of the effects of H2S. And a case report of
acute and subacute H2S poisonings (no concentrations given) caus-
ing unconsciousness or eye inflammation.
4-272 Rosenberger, G., Ed. 1970. Sulfur. In: Diseases of Cattle.
Paul Paley Verlag, Berlin and Hamburg, Federal Republic of Germany.
pp. 1172-1174 (Ger).
D--. Atmospheric concentrations of H2S >0.03 vol. % (300 ppm)
are unhealthy for cattle. Concentrations of 0.1 vol. % H2S are
fatal within a short time. Symptoms and histopathology are des-
cribed. The recommended maximum concentration to be allowed is
0.01 vol. %.
4-092 Rotenberg, Y. S. 1974. Correlation Between the Toxicity of
Chemical Agents and Their Inhibitory Action on Isolated Mito-
chondria. Byull. Eksp. Biol. Med. 78(7):65-68 (Russ).
123
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D--. A correlation was found between the LD50 and CL5o values
for 29 compounds and their concentrations causing 50% inhibition
of mitochondrial respiration. H2S was included.
4-251 Rubin, H., and A. Arieff. 1945. Carbon Disulfide and Hydrogen
Sulfide: Clinical Study of Chronic Low-Grade Exposures. J. Ind.
Hyg. Toxicol. 27:123-129.
D-10. A study of 100 workers, confounded by exposure to both H2S
(1-5.5 ppm) and CS2 (1.9-20.5 ppm); the average length of employ-
ment was not given. Subjective symptoms, such as fatigue, and
objective neurological signs were diverse and vague, leading authors
to believe that the adverse effects, if any, were minimal. No
comparison to workers without this exposure.
4-288 Ryazanov, V. A. 1960. New Data on Maximum Allowable Concentra-
tions of Pollutants in the Air in the U.S.S.R. In: Proceedings
of the Diamond Jubilee International Clean Air Conference, London,
1959. Arnold Marsh, Ed. pp. 175-176.
D-—. A brief review of the types of information used to set stand-
ards in the U.S.S.R., including a description of the "electro-
cortical conditioned reflex" frequently used. The MAC's for 30
compounds are given. The one-time MAC for H2S was 0.03 mg/m3,
and the 24-h avg. was 0.01 mg/m3.
4-093 Safiullina, S. I. 1978. Effect of Hydrogen Fluoride, Phosphine,
and Hydrogen Sulfide on Rats. Tr. Nil Kraev. Patol. No. 32:28-33
(Russ).
D--. Because workers involved in the flotation of phosphorite
ores are subjected to the action of PH3 with H2S or HF, albino
rats were exposed to 0.39 mg PH3/m3 and 1.21 mg HF/m3 or 12.1 mg
H2S/m3 for 4 mo. Since such combinations are unlikely from auto-
mobile exhausts, this paper was not examined further.
4-185 St. Hill, C. A. 1966. Occupation as a Cause of Sudden Death.
Trans. Soc. Occup. Med. 16:6-9.
D-4. Case reports of fatalities. Two were probably caused by
loss of consciousness due to H2S, followed by inhalation of sludge.
4-224 Saitanov, A. 0. 1969. Heart Disease in Severe Acute Hydrogen
Sulfide Poisoning. Kardiologiya 9(8):92-95 (Russ).
C-6. Another case report, complicated by x-ray evidence of tuber-
culosis. A description of the symptoms and treatment of the fe-
male victim is given. Heart damage seen belonging to the class
of toxic myocardiodystrophy. Slow recovery. No exposure informa-
tion given.
124
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4-180 Sandage, C. 1961. Tolerance Criteria for Continuous Inhalation
Exposure to Toxic Material--!. Effects on Animals of 90-Day Ex-
posure to Phenol, CC14, and a Mixture of Indole, Skatole, H2S,
and Methyl Mercaptan. (ASTIA AD 268 783). Armed Services Tech-
nical Information Agency, Arlington, Virginia. 33 pp.
D-10. The mixture containing 20 ppm H2S caused varying occurrence
and degrees of lung, liver, and kidney damage in the 3 different
species (monkeys, rats, and mice). Weight loss and low grade,
fluctuating anemia occurred in all species.
4-225 Sarin, M. I., N. V. Sarina, N. D. Topolianskii, L. G. Karavchenko,
and V. J. Bugaev. 1972. Acute Hydrogen Sulfide Poisoning. Klin.
Med. (Mosk.) 50(1):99-101 (Russ).
C-7. Case histories of 6 accidental poisonings, with extensive
medical information. In 2 cases, exposure to ~1,300 mg H2S/L
caused death in minutes to an hour. The authors hypothesize that
the symptoms were caused in significant measure by the "disorder
of the function of the reticulohypothalamic system of the brain
stem."
4-094 Sartorius, R., and W. Jaeschke. 1977. The [German] Air Pollu-
tion Control Standards for Hydrogen Sufide are Correct. Umwelt.
No. 1:30-31 (Ger).
D--. Some atmospheric H2S levels in Germany, ranging from 0.05
to 1.09 (Jg/m3 (near an industrial region).
4-320 Savio, T. , and H. D. Johnson. 1972. The Effect of Acute Expo-
sure to H2S on the Sympatho-Adrenal System of the Goat. Trans.
Mo. Acad. Sci. 6:177-178.
C--. Abstract only. Exposure of female goats to 10, 50, and
100 ppm H2S for 11 d caused increased urinary secretion of the
catecholamine metabolite 3-methoxy-4-hydroxymandelic acid (a mea-
sure of sympatho-adrenal function). The change may be due to the
H2S or to anxiety.
4-253 Sayers, R. R., C. W. Mitchell, and W. P. Yant. 1923. Hydrogen
Sulfide as an Industrial Poison. U.S. Bureau of Mines, Depart-
ment of the Interior. Reports of Investigations, Serial No. 2491,
U.S. Department of the Interior, Washington, D.C. 6 pp.
C-7. Review of the general properties and toxicology of H2S.
Limited description of animal experiments—all eventually lethal.
Concluded that acute poisoning in humans occurs at 0.07-0.08%
(700-800 ppm) H2S and subacute poisoning at levels as low as
0.005% (50 ppm).
4-095 Schaffernicht, H., D. Suessenbach, and P. Wedekind. 1975. Hydro-
gen Sulfide and Noise Exposure in Industrial Animal Production.
Z. Gesamte Hyg. Grenzgeb. 19(3):177-180 (Ger).
125
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D--. Incidence and industrial hygiene data.
4-255 Scheler, W. , and R. Kabisch. 1963. The Antagonistic Action on
Acute H2S Poisoning in the Mouse via Methemoglobin Formation.
Acta Biol. Med. Ger. 11:194-199 (Ger).
Oil. The LC50 in control mice was 430 ppm H2S compared to 1,380
ppm H2S when the mice were pretreated with 108 mg NaN02/kg due to
the protective action of methemoglobin formation induced by NaN02.
4-226 Schmitz, W. 1971. Appearance and Manifestation of a Disease with
Psychomotor Symptoms Due to an Acute Manure Pit Gas Intoxication
in a Boy Who Previously Had Sustained Brain Damage. Z. Gesamte
Hyg. Grenzgeb. 17(8):628-632 (Ger).
D--. Confounded by the earlier trauma and the presence of other
gases.
4-342 Schulze, B. , R. Ullmann, and H. Kirsch. 1979. Problems of Air
Pollution with Hydrogen Sulfide Emitted from Rivers. Z. Gesamte
Hyg. Ihre Grenzgeb. 25(3):219-221 (Ger).
D--. Three instances of communal air pollution by H2S from waste-
waters are described: (1) no H2S concentrations were measured,
but the citizens suspected that H2S was causing health problems
(not specified). The air pollution discolored Pb-based house paints;
(2) three people died; no H2S measurements were made; and (3) H2S
measurements were made but are not reported here. A connection
between H2S and health problems could not be established.
4-227 Schwander, D. 1972. Toxic Pulmonary Edema After Inhalation
of Hydrogen Sulfide. Successful Treatment by Continuous Positive
Pressure Ventilation. Cah. Anesthesiol. 20(7): 785-792 (Fre).
C-6. Case report of exposure to fumes from liquid manure causing
unconsciousness, irritation of the mucous membranes, neurological
symptom, and pulmonary edema.
4-097 Seuren, P. 1979. A Case of Hydrogen Sulfide Poisoning and
Stench Nuisance in a Broiler Stockbreeding Farm Caused by Storage
Finished Mushroom Manure. Tijdschr. Diergeneeskd. 104(9):383-384
(Dut).
D--. Symptoms of workers are described and attributed to H2S
poisoning. Histological study of one patient described. No ex-
posure levels given.
4-228 Shaparenko, B. A., V. M. Foderman, and N. S. Drevniak. 1972.
Use of Antidote Hydrogen Sulfide Prophylactic Inhalations in Per-
sons Exposed to Metallic Mercury Vapor. Zh. Ushn. Nos. Gorl.
Bolezna. 32(4):1-3 (Russ).
126
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D--. Four courses a year of antidote inhalations of solutions
containing 30-60 mg H2S/L were a useful prophylaxis for mercury
poisoning.
4-098 Shaparenko, B. A., R. I. She'inin, 0. A. Lastkov, V. M. Foderman,
and N. S. Drevniak. 1973. Morphological Changes of the Nasal
Mucous Membrane in Experimental Animals in Micromercurialism and
the Effect of Hydrogen Sulfide-Carbonate Inhalations. Zh. Ushn.
Nos. Bolezn. 33(4): 37-39 (Russ).
D--. Inhalation of steam from a solution containing C02 and 30
mg H2S/L was a useful method for prophylaxis or treatment when
rats had been exposed to 40 mg Hg/m3 for 20 min/d for up to 5 mo.
4-332 Shtrum, I. Ya. 1938. The Combined Action of Carbon Monoxide and
Hydrogen Sulfide. Fiziol. Zh. SSSR. 24:624- 629 (Russ).
D--. At lethal concentrations, a mixture of H2S and CO required
a total dosage of 130% that of either poison alone to cause death
in mice. When the "time of reflex" in rabbits was used as the
criterion, it required 160% of either poison's dose alone to elicit
the same effect with a mixture of H2S and CO. The lowest H2S
concentration tested was 300 mg/m3.
4-182 Simson, R. E., and G. R. Simpson. 1971. Fatal Hydrogen Sulphide
Poisoning Associated with Industrial Waste Exposure. Med. J. Aust.
1:331-334.
C-6. Post-mortem findings of the victim, exposed to H2S levels
possibly as high as 12,000 ppm.
4-099 Smith, R. P., and R. E. Gosselin. 1979. Hydrogen Sulfide Poisoning.
J. Occup. Med. 21(2):93-97.
D--. A review of the use of antidotes and some discussion of the
mechanisms of toxicity and the similarities to cyanide poisoning.
4-229 Sof'ina, L. I. 1969a. Effect of a Complex of Saturated and Unsat-
urated Hydrocarbons and Hydrogen Sulfide on the Activity of Certain
Enzymes of the Brain, Liver, and Blood Serum. Gig. Tr. Prof. Zabol.
13(7):41-43 (Russ).
D--. Albino rats were exposed to cracking gases 6 h/d for 4 mo.
The cracking gas in the exposure chamber contained 100 mg H2S/m3.
The effects of H2S on the enzymes would be confounded by those of
the saturated and unsaturated hydrocarbons in the cracking gas.
4-230 Sof'ina, L. I. 1969b. Effect of Sulfur Petroleum Reprocessing
Gaseous Products on the Activity of Some Rat Brain Enzymes. Tr.
Ufim. Nauch.-Issled. Inst. Gig. Prof. Zabol. 5:64-68 (Russ).
127
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D--. Exposing rats to 1,200 mg H2S/m3 for 2 h/d for 5 d lowered
the activities of glutaminase (by 34.5%), alkaline phosphatase
(by 29%), and malate dehydrogenase. Sorbitol dehydrogenase activ-
ity was increased. (Cracking gas caused the most expressed changes
in brain enzyme activities.)
4-183 Sorokin, G. E., and N. M. Olshanskaya. 1941. Electrocardiographic
Studies on Changes in Cardiac Activity Induced by Hydrogen Sulfide.
Fiziol. Zh. 30:530-532 (Russ).
D--. Solutions containing 265 mg H2S/L were injected intravenously
into rabbits.
4-184 Spolyar, L. W. 1951. Three Men Overcome by Hydrogen Sulfide in
Starch Plant. Ind. Health Monthly 11:116-117.
C-6. H2S levels of 300-400 ppm caused unconsciousness, and 1
death.
4-101 Spurgeon, J. C. 1978. The Correlation of Animal Response Data
With the Yields of Selected Thermal Decomposition Products for
Typical Aircraft Interior Materials. NTIS No. AD-A062938, National
Technical Information Service, U.S. Department of Commerce,
Springfield, Virginia. 40 pp.
C-12. The times to incapacitation and death of at least 9 rats
exposed to mixed combustion products, the gas containing 0-14.2
mg H2S/g sample.
4-102 Stine, R. J., B. Slosberg, and B. E. Beacham. 1976. Hydrogen Sul-
fide Intoxication: A Case Report and Discussion of Treatment.
Ann. Intern. Med. 85(6):756-758.
D-4. A case report of cyanide-type treatment for H2S poisoning.
4-103 Stolpe, J., R. Sedlag, and B. Bresk. 1976. Single and Complex
Effect of Ammonia and Hydrogen Sulfide in the Air on Small Labor-
atory Animals (Rats) Under Various Environmental Conditions. 2.
Effect of Hydrogen Sulfide Alone and Hydrogen Sulfide with Ammonia
and Dust. Arch. Exp. Veterinaermed. 30(4):541-545 (Ger).
B-10. Rats exposed to 10 ppm H2S, 10 ppm H2S and 50 ppm NH3, 5
ppm H2S and 30 ppm NH3, or 5 ppm H2S and 30 ppm NH2 and dust
caused varying decreases in weight gain and food utilization.
All test groups were at 10°C. Cold controls and optimal tempera-
ture controls were done.
4-104 Strack, W. 1977. Danger from Hydrogen Sulfide Used in Modern
Technologies for Leather Production. Koza Obuca. 26(11):283-285
(Croat).
128
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D--. The occurrence of an accidental death from H2S used in the
drum bating and pickling process (short liquor) is described.
4-186 Sukhanova, V. A. 1962. The Influence of the Products of Proces-
sing High-Sulfur Crude Oil on the Functional State of the Gastro-
intestinal Tract (Experimental Study). Gig. Tr. Prof. Zabol. 6:7-11
(Russ).
D--. Rats and dogs were exposed to atmospheres containing cracking
gases with 75-77 vol. % saturated hydrocarbons, 13-15 vol. % unsat-
urated hydrocarbons, 4-7 vol. % hydrogen, and 3-6 vol. % H2S.
Four dogs exposed 4 h/d for 5 mo in a chamber containing 50-70 mg
H2S/m3 and the other components did not show any change in blood
amylase. Rats exposed similarly for 4 mo showed a drop in uropep-
sin level in the urine and reduced intensity of incorporation into
the pancreas proteins of radiolabeled methionine.
4-289 Taiganides, E., and R. K. White. 1969. The Menace of Noxious
Gases in Animal Units. Trans. Am. Soc. Agric. Eng. 12(3):
359-362.
D--. A review of the occurrence of H2S, NH3) C02, and CH4 in animal
units, and their toxicities to different species. Includes a dis-
cussion of potentially lethal situations and preventive measures.
4-327 Teleky, L. 1931. Industrial Hygienic Studies on Hydrogen Sulfide
Poisoning. Dtsch. Med. Wochenschr. 57:1026-1027 (Ger).
C--. Case histories of H2S poisoning are described. Among them
is the chronic poisoning of a family by H2S (no concentrations
given) emanating from a wall constructed of porous bricks in their
apartment. On the other side of the wall was an accumulator (stor-
age battery) room. The sulfuric acid vapors apparently reacted
with the construction materials to form H2S.
4-105 Thiele, V. 1979. Experimental Studies on Determining an Odor
Threshold Value for Hydrogen Sulfide. Staub-Reinhalt. Luft.
39(5):159-160 (Ger).
C-9. The odor threshold value was 0.0016 mg/m3, the 50-percentile
value of a dose-response curve from 2 groups. The responses for
"annoyance" values were more widely distributed, the 50% value
ranging from -0.002 to -0.030 mg/m3.
4-231 Thiess, A. M. 1968. Case Contribution of Hydrogen Sulfide Poi-
soning with Fatal Outcome. Zentralbl. Arbeitsmed. 18(12):366-368
(Ger).
C-7. Short exposure to unknown levels of H2S caused only slight
symptoms of H2S intoxication: headache, vomiting, and light ir-
ritation of mucous membranes and conjunctiva of the eye. Death
was due to a skull fracture, not H2S poisoning.
129
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4-187 Thoman, M. 1969. Sewer Gas—Hydrogen Sulfide Intoxication. Clin.
Toxicol. 2:383-386.
D-5. The accidental exposure of 5 people to H2S fumes, symptoms
ranging from mild discomfort to near fatal. Concentrations and
exposure times unknown.
4-106 Timofeev, V. P. 1974. Biological Effect of Natural Human Metabol-
ites in a Dwelling Environment. Tr. Leningr. Sanit.-Gig. Med.
Inst. 105:168-171 (Russ).
D--. White male rats (18 per group) were exposed to a five-component
mixture of human metabolites for 100 d. In the eight tests, the
average concentrations of the components were 0.92 to 74.4 mg CO/m3,
0.20 to 148.3 mg NH3/m3, 0 to 8.75 mg H2S/m3, 0.3 to 240.1 mg ace-
tone per cubic meter, and 0.009 to 5.6 mg phenol per cubic meter.
H2S was judged from partial coefficients of multiple linear regres-
sion as contributing 16% to the animals' deaths.
4-107 Tomaszewska, Z. 1978. Multiple Fatal Hydrogen Sulfide Poisonings.
Arch. Med. Sadowej Kryminol. 28(l):55-57 (Pol).
C-8. Four men exposed to ^944 mg H2S/m3 were fatally poisoned
while cleaning a settler for sewage from a carriage washer.
4-108 Tonzetich, J., and S. K. Ng. 1976. Reduction of Malodor by Oral
Cleansing Procedures. Oral Surg., Oral Med. Oral Pathol. 42(2):
172-181.
B-9. A group of 8 people found the threshold of objectionability
(not odor detection) for H2S to be 0.15 mg/ra3. This was a small
part of a larger study.
4-188 United States of America Standards Institute. 1967. Acceptable
Concentrations of Hydrogen Sulfide, USAS Z37.2-1966, USASI, New
York, New York. 8 pp.
C--. Summary of properties and toxic effects of H2S, similar to
other reports. Has recommended acceptable concentrations: ten-
min-peak exposure 50 ppm; 8-h 5 d/wk, 20 ppm; and level to avoid
any discomfort, 10 ppm. More recent issues of this H2S standard
are available.
4-189 United States of America Standards Institute. 1972. Acceptable
Concentrations of Hydrogen Sulfide. USAS Z37.2-1972, USASI, New
York, New York. 8 pp.
A—. A review of H2S occurrence, properties (physical, chemical,
toxic), and detection methods. At low concentrations the predom-
inant effects are on the eyes (£10 ppm) and respiratory tract
(^50 ppm). No permanent after-effects in cases of recovery un-
less there was prolonged 02 depletion. No evidence of accumula-
tive or systemic effects following repeated exposures.
130
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5-424 Urban, C. M., and R. J. Garbe. 1980. Exhaust Emissions from Mal-
functioning Three-Way Catalyst-equipped Automobiles. S.A.E. Tech.
Pap. Ser. 800511. 11 pp.
C--. Maximum emission rates (mg/m3) in 4 malfunctioning, 3-way
catalyst-equipped automobiles:
NH3 254
CN 67
H2S . 8
HCHO 3
4-174 U.S. Geological Survey Outer Continental Shelf. 1976. Outer Con-
tinental Shelf Standard—Safety Requirements for Drilling Opera-
tions in a Hydrogen Sulfide Environment. Report No. GSC-OCS-1.
Geological Survey Conservation Division, U.S. Department of the
Interior,-Reston, Virginia. 15 pp.
D--. An outline of safety procedures and equipment to be used.
Protective breathing apparatus to be worn when H2S levels reach
20 ppm, and nonessential personnel evacuated at 50 ppm.
4-173 U.S.P.H.S. United States Public Health Service. 1964. The Air
Pollution Situation in Terre Haute, Indiana with Special Reference
to the Hydrogen Sulfide Incident of May-June, 1964. PB 227 486.
National Technical Information Service, U.S. Department of Commerce,
Springfield, Va. 28 pp.
A-6. Limited by the lack of tests for non-sulfide contaminants.
Mild (non-hospitalization) complaints of odors and symptoms at
20-30 ppb H2S. Recommends an ambient air quality level of 50 ppb/
In.
4-337 U.S.S.R. State Committee of the Council of Ministers for Construc-
tion. 1972. Sanitary Norms for Industrial Enterprise Design.
Publishing House of Literature on Construction, Moscow. 92 pp.
(Russ).
C--. In the USSR, the MAC for H2S in workplaces was 10 mg/m3,
and in populated places was 0.008 mg/m3 (one-time and avg.).
5-413 Van Gemert, L. J. , and A. H. Nettenbreijer. 1977. Compilation
of Odour Threshold Values in Air and Water. National Institute
for Water Supply. Leidschendam, the Netherlands, and Central In-
stitute for Nutrition and Food Research, TNO, Zeist, the Netherlands,
131
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A--. Compilation of odor threshold values reported by different
researchers, for many compounds, including:
Ammonia 0.03-37 mg/m3
HCN < 1.1-6
H2S 0.001-2
HCHO 0.033-2.2
Methanol 4.3-11,700
Acrolein 0.05-4.1
4-110 Vasil'eva, I. A. 1973. Effect of Small Concentrations of Carbon
Bisulfide and Hydrogen Sulfide on the Menstrual Function of Women
and the Estrous Cycle of Experimental Animals. Gig. Sanit.
38(7):24-27 (Russ).
D--. Interaction study. Workers were exposed to ^5 mg H2S/m3 in
71.1% of the samples and no sample exceeded the MAC. They were
also exposed to CS2 in concentrations up to 12.6 mg/m3. They
showed a higher incidence of ovarian function disturbances. The
estrous cycle of rats similarly exposed was prolonged.
4-1111 Vasil'eva, I. A. 1975. State of Reproductive Functions in Chemi-
cal Industry Workers. Gig. Tr. 11:179-182 (Russ).
C-4. During pregnancy, an unknown number of women workers in a
viscose spinning plant exposed to unknown concentrations of H2S
and CS2 experienced incidences of 15.0 and 16.8% toxicosis of
early and late pregnancy compared to 7.8 and 8.6% in rewinding-
sorting plant workers and 10.7 and 2.9% in housewives. The spin-
ning plant workers experienced significantly (p<0.001) more blood
loss during birth, and their offspring showed twice as many de-
velopmental flaws and malformations than those of the housewives.
The spinning plant workers had chromosomal aberrations.
4-261 VDI, Verein Deutscher Ingenieure [Society of German Engineers]
Committee on Air Purification. 1970. Permissible Immisson Concen-
trations of Hydrogen Sulfide. PB-221 243-T, National Technical
Information Service, U.S. Department of Commerce, Springfield,
Virginia. 12 pp.
D—. Review of the occurrence and properties of H2S, and its ef-
fects on man, animals, and plants. The exposure limits given are:
~0.15 mg/m3 (as half-hour mean value) for the Permissible Immission
Concentration (PIC) for continuous exposure; ~0.3 mg/m3 (3 x a
day half-hour mean value) for the PIC for intermittent exposure;
and ~30 mg/m3 for the Permissible Work-Station Concentration.
4-308 Vigil, P. J. 1979. A State-of-the-Art Review of the Behavioral
Toxicology of Hydrogen Sulfide. UCRL-15093. Reference Dynamics,
Santa Rosa, California. 55 pp.
132
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B--. Review of studies of acute, subacute, chronic, and low level
H2S exposure of humans. It concludes that behavior toxicology as
a minimum toxic effect is likely, but not proven, and no threshold
is definable due to lack of good low-dose data.
4-113 Vilisov, B. A., L. M. Kremko, Z. N. Pavlyutina, and V. M. Ermakova.
1975. Working Conditions and Illness Rate of Workers in the Biolog-
ical Flax-Retting Division. Gig. Tr. Prof. Zabol. No. 6:43-45
(Russ).
D--. The above named workers were exposed not only to H2S but
also to NH3, C02, aliphatic amines, monocarboxylic acids, bacteria,
and molds.
4-260 von Rad [no initial], and Scheidemantel. 1933. Late Consequences
of a Hydrogen Sulfide Intoxication (Perturbation of the Heart Ac-
tivity and Lesions of the Central Ganglia). Munchen. Med. Wochenschr.
80:1494-1495 (Ger).
D-4. Description of an accidental exposure, where 0.5 h after
the accident there was 0.83 mg (volume not given) H2S. For several
months, the victim complained of insomnia, and later had an epi-
leptic attack. Victim still suffered from high blood pressure
and abnormal irritability of the vasomotoric center 1.5 y after
the accident.
4-114 Wachnik, Z. 1974. Gases Harmful to Birds. Med. Weter. 39(10):
605-608 (Pol).
D--. A Polish review of bird intoxication by NH3, H2S, and CO.
4-190 Wakatsuki, T. 1959. Experimental Study on the Poisoning by Car-
bon Disulfide and Hydrogen Sulfide. Shikoku Igaku Zasshi. 15:671-
700 (Japan).
C-8. Rated only from English abstract. Rabbits exposed to 100
ppm H2S 30 min/d for 4 mo showed only slight changes in peripheral
blood picture, returning to normal shortly after exposure stopped.
"General condition," body weight, and serum calcium and protein
were unaffected. No direct respiratory information.
4-191 Walton, D.C., and M. G. Witherspoon. 1926. Skin Absorption of
Certain Gases. J. Pharmacol. Exp. Therap. 26:315-324.
C-6. No inhalation exposure. Pure H2S caused swelling and black-
ening when contacting small areas of guinea pigs skin, and death
in 45 min when half of the guinea pig was exposed.
4-256 Weedon, F. R., A. Hartzell, and C. Stetterstrom. 1940. Toxicity
of Ammonia, Chlorine, Hydrogen Cyanide, Hydrogen Sulphide, and
Sulphur Dioxide Gases. V. Animals. Contrib. Boyce Thompson Inst.
11:365-385.
133
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B-8. 8 rats and 4 mice were exposed to 16, 63, 250 or 1,000 ppm
H2S for a maximum of 23 h. There were no symptoms at 16 ppm for
16 h, and increasing morbidity and mortality for the other tests
with increasing concentrations and exposure times.
4-328 Weise, W. 1933. Gastrointestinal Diseases from Chronic Inhala-
tion of Carbon Bisulfide and Hydrogen Sulfide. Arch. Gewerbepathol.
Gewerbehyg. 4:219-279 (Ger) .
B-9. Repeated exposure of very small numbers of rats and rabbits
to 10, 100, or 1,000 ppm H2S caused noticeable disturbance or
changes in the gastrointestinal tract only at the higher levels.
4-232 Westbye, 0. 1971. Composition and Toxicology of Manure Gas.
Nor. Vet. Tidsskr. 83(10) :522-525 (Nor).
D — . Review. Dose-response generalizations are tabulated for
ammonia and hydrogen sulfide. The hygienic limit is given as 10
ppm for H2S.
4-116 Westermann, H. D. , A. Thalmann, and H. Kummer. 1975. The Toxicity
of Hydrogen Sulfide in Animal Feeding: A Survey of the Literature.
Landwirtsch. Forsch. 28(1): 70-80 (Ger).
D--. A review with 42 references. Not pertinent to this study.
4-117 Williams, F. D. , J. F. Emele, and M. C. Alford. 1977. The Appli-
cation of the Dynamic Triangle Olfactometer to the Evaluation of
Oral Odor. Chem. Senses Flavour. 2(4) :497-502.
A-13. The odor threshold for H2S was 0.27 mg/m3 (0.19 ppm). Part
of a larger study.
4-257 Winek, C. L. , W. D. Collom, and C. H. Wecht. 1968. Death from
Hydrogen-Sulphide Fumes. Lancet 1:1096.
D-5. Case report of a fatality after short exposure to 1,900-6,100
ppm H2S. Autopsy revealed extensive respiratory pathology, and
congested spleen and liver.
4-118 Winneke, G. , J. Kotalik, H. 0. Keldenich, and J. Kastka. 1979.
Perception of Hydrogen Sulfide in Laboratory- and Field-Conditions.
Staub-Reinhalt. Luft 39(5) : 156-159 (Ger).
C--. Using a group of 31 people, a detection limit for ^S of
2.65 (Jg/m3 was determined.
4-192 Yant, W. P. 1930. Hydrogen Sulphide in Industry-Occurrence,
Effects, and Treatment. Am. J. Public Health 20:598-608.
134
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B--. Review of toxicology of H2S, both acute and subacute, and
the occurrence and prevention of poisoning in the petroleum in-
dustry. Indicates a physiological threshold <50 ppm and an odor
threshold of 0.13 ppm.
4-193 Yant, W. P., and H. C. Fowler. 1926. Hydrogen Sulphide Poisoning
in the Texas Panhandle, Big Lake, Texas, and McCamey, Texas Oil-
fields. Bull. No. 2776. Bureau of Mines, U.S. Dept. of Commerce.
20 pp.
D—. H2S concentrations in several different locations ranged
from ~100 ppm to 100,000 ppm. Workers exposed to the lower con-
centrations had no symptoms while those at the higher levels had
symptoms ranging from eye irritation and nausea to unconsciousness
and death (at 1,000 ppm). Many dead rabbits and birds were found
around one field. A long discussion on safety practices and equip-
ment and treatment is included.
4-119 Zaitseva, D. M. 1976. Immunobiological Reactivity of the Bodies
of Workers Producing the Sulfonate Additive PMS. Sb. Nauchn. Tr.
Bashk. Cos. Med. Inst. 23(1):111-112 (Russ).
D--. Exposure of the title workers to S02, S03, NH3, H2S, hydro-
carbons, acetic acid, and excessive noise and microclimatic condi-
tions caused high morbidity due to acute respiratory diseases.
4-194 Zander, R. 1950. Carbonization Gas Intoxications. Dtsch.
Gesundheitswes. 5:1422-1444 (Ger.).
C-6. Carbonization gas contains an avg. 2.6 vol % H2S. This is
confounded with the presence of other gases, particularly carbon
monoxide (avg. 10.3 vol %). No patient exposure data are given.
Several case reports given, no fatalities. Some EKG changes were
noted in the patients.
4-126 Zhigunov, N. F. 1975. Techniques for Studying Industrial Environ-
mental Factors on the Heterogeneity of 0- and Vi Antibodies. Gig.
Sanit. No. 11:767 (Russ).
D--. Effects due to H2S are confounded by the higher concentra-
tions of CS2.
4-329 Ziaber, Z. 1978. Effect of Sulfide-Hydrogen Sulfide Bath on
Sulfohydryl Groups (SH) in the Serum of Patients with Rheumatoid
Arthritis. Pol. Tyg. Lek. 33(29):1147-1150 (Pol).
D--. Taking S-H2S for ^90 min significantly increased the SH
groups in the serum in patients with rheumatoid arthritis. No
information was given on the concentration of H2S the patients
might have inhaled or been exposed to by skin absorption.
135
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TECHNICAL REPORT DATA
(Please read Instructions on the reverse before completing/
i. REPORT NO.
EPA 460/3-81-028
2.
3. RECIPIENT'S ACCESSIOf*NO.
4. TITLE AND SUBTITLE
Hydrogen Sulfide Health Effects
5. REPORT DATE
September 1981
6. PERFORMING ORGANIZATION CODE
7. AUTHOR(S)
Bonnie L. Carsom
Cecily M. Beall.
8. PERFORMING ORGANIZATION REPORT NO.
Harry V. Ellis III,
Larrv H. Baker» and
Joy L. McCann
9. PERFORMING ORGANIZATION NAME AND ADDRESS
Midwest Research Institute
425 Volker Boulevard
Kansas City, Missouri 64110
1O. PROGRAM ELEMENT NO.
11. CONTRACT/GRANT NO.
68-03-2928
12. SPONSORING AGENCY NAME AND ADORER.1;
Environmental Protection Agency
Office of Mobile Source Air Pollution Control
Emission Control Technology Div., 2565 Plymouth Road
Ann Arbor. Michigan 48102
13. TYPE OF REPORT AND PERIOD COVERED
Final Report
14. SPONSORING AGENCY CODE
15. SUPPLEMENTARY NOTES
16. ABSTRACT
Health effects literature primarily related to inhalation exposures to hydrogen
sulfide was collected, evaluated, tabulated, and summarized. Approximately 350 docu-
ments were collected from computerized and manual literature searches covering the
period 1887-1981. Pharmacologists and an M.D. epidemiologist rated the documents
according to their applicability to the study and their methodology. The 40 docu-
ments considered useful for deriving a range of concern for human exposure to hydrogen
sulfide from automotive emissions were tabulated. The 60 pages of tables detail the
results of acute, repeated dose, and chronic testing of canaries, mice, rats, guinea
pigs, chickens, rabbits, cats, monkeys, dogs, pigs, goats, cows, and humans as well
as human occupational studies. Most of the documents evaluated are described in an
annotated bibliography.
17.
KEY WORDS AND DOCUMENT ANALYSIS .
DESCRIPTORS
b.lDENTIFIERS/OPEN ENDED TERMS
c. COSATI Field/Croup
Toxicity
Hydrogen Sulfide
Mammals
Bibliographies
Toxic Tolerances
Occupational Diseas
Respiratory System
Inhalation Health Effect
06T
>S
13. DISTRIBUTION STATEMENT
Release Unlimited
19. SECURITY CLASS (This Report)
TTnrlaagn
20. SECURITY CLASS (Thispage)
Unclassified
21. NO. OF PAGES
139
22. PRICE
EPA Form 2220-1 (9-73)
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