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

-------
         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

-------
                                  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

-------
                                 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

-------
                                  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

-------
                            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

-------
                                  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.

-------
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

-------
       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.

-------
(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

-------
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).

-------
           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)

-------
                           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.

-------
   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)

-------
                           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.

-------
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

-------
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

-------
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

-------
          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

-------
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

-------
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

-------
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

-------
          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

-------
          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

-------
          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

-------
          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

-------
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

-------
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

-------
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

-------
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

-------
          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

-------
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

-------
          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

-------
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

-------
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

-------
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

-------
          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

-------
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

-------
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

-------
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

-------
          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

-------
          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

-------
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

-------
          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

-------
          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

-------
          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

-------
          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

-------
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

-------
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

-------
          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

-------
          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

-------
          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

-------
          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

-------
                                    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)

-------