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) ------- |