The following information was generated from the 

Toxicology Bibliographic Information (TOXLINE), 

a database of the National Library of Medicine's TOXNET system 

(http://toxnet.nlm.nih.gov) on August 30, 2007. 

Query: The phrase hydrogen sulfide (All Fields). 

Singular and plural forms were searched. 

The chemical name hydrogen sulfide was identified. 

The following terms were added from ChemIDplus: 

hydrogen sulfide 

zwavelwaterstof 

sulfureted hydrogen 

sulfur hydride 

stink damp 

siarkowodor 

schwefelwasserstoff 

idrogeno solforato 

acide sulfhydrique 

hydrogen sulphide 

CAS Registry Number: 7783-06-4 

1 

TITLE: 

 Hydrogen sulfide: Human health aspects 

AUTHORS: 

 Anonymous 

SOURCE: 

 Concise International Chemical Assessment Document (CICAD) Vol:53 (2003) 

 31 p 

ABSTRACT: 

 This CICAD on hydrogen sulfide was prepared by the US Agency for Toxic 

 Substances and Disease Registry. Data identified as of 1998 were 

 considered in the source document (ATSDR, 1999). A comprehensive 

 literature search of several on-line databases was conducted in March 2002 

 to identify any references published subsequent to these incorporated in 

 the source document. Information on the nature of the peer review and the 

 availability of the source document is presented in Appendix 1. 

 Information on the peer review of this CICAD is presented in Appendix 2. 

 This CICAD was approved as an international assessment at a meeting of the 

 Final Review Board, held in Monks Wood, United Kingdom, on 16-19 September 

 2002. Participants at the Final Review Board meeting are listed in 

 Appendix 3. The International Chemical Safety Card (ICSC 0165) for 

 hydrogen sulfide, produced by the International Programme on Chemical 

 Safety (IPCS, 2000), has also been reproduced in this document. Hydrogen 

 sulfide (CAS No. 7783-06-4) is a colourless, flammable gas with a 

 characteristic odour of rotten eggs. It is produced naturally and as a 

 result of human activity. Natural sources include non-specific and 

 anaerobic bacterial reduction of sulfates and sulfur-containing organic 

 compounds. Hydrogen sulfide is found naturally in crude petroleum, natural 

 gas, volcanic gases, and hot springs. It is also found in groundwater. It 

 is released from stagnant or polluted waters and manure or coal pits. 

 Hydrogen sulfide may be produced by a variety of commercial methods. The 

 principal source of hydrogen sulfide is recovery as a by-product in the 

 purification of natural and refinery gases. It is also a by-product of 

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 kraft pulp and paper manufacturing and carbon disulfide production. It is 

 used as an intermediate in the manufacture of sulfuric acid and inorganic 

 sulfides and as an agricultural disinfectant. Hydrogen sulfide is also 

 produced as a decomposition product of xanthates (used in the mining 

 industry) when they come into contact with water. Accidental release or 

 improper disposal of materials resulting from these processes may result 

 in hydrogen sulfide emissions. Releases to the environment are primarily 

 in emissions to the ambient air, where the chemical is likely to remain 

 for less than 1 day, but may persist for as long as 42 days in winter. 

 Hydrogen sulfide may evaporate easily from water, depending on temperature 

 and pH. It is unlikely to bioconcentrate and biomagnify in the food-chain. 

 The concentration of hydrogen sulfide in air in unpolluted areas is very 

 low, between 0.03 and 0.1 ug/m3. Humans may be exposed to hydrogen sulfide 

 from endogenous production and from exogenous sources. Most endogenous 

 production results from the metabolism of sulfhydryl-containing amino 

 acids (e.g., cysteine) by bacteria present in both the intestinal tract 

 and the mouth. Hydrogen sulfide is also produced in the brain and several 

 smooth muscles (e.g., thoracic aorta, ileum, and portal vein) by enzymes 

 found in these tissues. In the rat, the endogenous level of hydrogen 

 sulfide is 50-160 umol/litre in the brain and 1 umol/litre in the ileum. 

 Human exposure to exogenous hydrogen sulfide is principally via 

 inhalation, and the gas is rapidly absorbed through the lungs. Hydrogen 

 sulfide is metabolized through three pathways: oxidation, methylation, and 

 reactions with metalloproteins or disulfide-containing proteins. Oxidation 

 in the liver is the major detoxification pathway. The major oxidation 

 product is thiosulfate, which is then converted to sulfate and excreted in 

 the urine. The methylation pathway also serves as a detoxification route. 

 The toxicity of hydrogen sulfide is a result of its reaction with 

 metalloenzymes. In the mitochondria, cytochrome oxidase, the final enzyme 

 in the respiratory chain, is inhibited by hydrogen sulfide; this disrupts 

 the electron transport chain and impairs oxidative metabolism. Nervous and 

 cardiac tissues, which have the highest oxygen demand, are especially 

 sensitive to the disruption of oxidative metabolism. In the central 

 nervous system, this effect may result in death from respiratory arrest. 

 In experimental animals, single inhalation exposures to hydrogen sulfide 

 result in death and respiratory, immunological/lymphoreticular, 

 cardiovascular, and neurological effects. Reported health effects in 

 animals following short-term exposures include ocular, cardiovascular, 

 neurological, metabolic, hepatic, and developmental effects. 

 Medium-duration inhalation studies of hydrogen sulfide in animals have 

 reported respiratory, neurological, and olfactory effects. There are no 

 long-term inhalation studies in animals. The most sensitive target organ 

 for medium-term exposure in animals is the nasal olfactory mucosa. Nasal 

 olfactory lesions were reported in Sprague-Dawley CD rats exposed to 

 hydrogen sulfide at 42 or 110 mg/m3; the no-observed-adverse-effect level 

 (NOAEL) was 14 mg/m3. This NOAEL is used as a basis for the development of 

 a medium-term tolerable concentration. Most human data are derived from 

 acute poisoning case reports, occupational exposures, and limited 

 community studies. The odour threshold varies depending on the individual; 

 the geometric mean odour threshold is 11 ug/m3. At concentrations greater 

 than 140 mg/m3, olfactory paralysis occurs, making hydrogen sulfide very 

 dangerous, because a few breaths at 700 mg/m3 can be fatal. Short-term 

 inhalation exposure to high concentrations of hydrogen sulfide causes 

 health effects in many systems; reported health effects in humans 

 following exposure to hydrogen sulfide include death and respiratory, 

 ocular, neurological, cardiovascular, metabolic, and reproductive effects. 

 Respiratory, neurological, and, ocular effects are the most sensitive 

 end-points in humans following inhalation exposure. The 

 lowest-observed-adverse-effect level (LOAEL) is 2.8 mg/m3 in asthmatic 

 individuals for respiratory and neurological effects. This LOAEL is used 

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 as a basis for the development of a short-term tolerable concentration. 

 Ingestion is of no relevance for humans. There are no human ingestion 

 data. The genotoxicity of hydrogen sulfide has been inadequately 

 investigated; there is only a single negative Salmonella mutagenicity 

 test. It is not possible to evaluate the carcinogenic potential of 

 hydrogen sulfide, as long-term animal studies are missing and studies on 

 human populations are inadequate. Tolerable concentrations for hydrogen 

 sulfide in air of 100 ug/m3 and 20 ug/m3, respectively, have been derived 

 based on respiratory effects for short-term (for exposure durations of 

 1-14 days) and medium-term (for exposure durations of up to 90 days) 

 inhalation exposures. Environmental exposures to malodorous emissions are 

 usually to a mixture of sulfur-containing gases. The exact concentration 

 of hydrogen sulfide in these types of mixtures cannot be determined. In 

 estimating exposure, there is also uncertainty about the dose and duration 

 of exposure. Based on limited information, rodents appear to be less 

 sensitive to hydrogen sulfide than humans. Since the respiratory tract is 

 the major target organ of hydrogen sulfide toxicity, humans with asthma, 

 the elderly, and young children with compromised respiratory function 

 represent sensitive subpopulations. Due to the serious toxic effects 

 associated with exposures to high concentrations of hydrogen sulfide for 

 very short durations, all exposure should be avoided. 

2 

TITLE: 

 Hydrogen sulfide 

AUTHORS: 

 WHO Working Group 

SOURCE: 

 Environmental Health Criteria Vol:19 (1981) pp 1-48 

ABSTRACT: 

 Properties Hydrogen sulfide is a colourless gas with a characteristic 

 odour that is soluble in various liquids including water, alcohol, ether, 

 and solutions of amines, alkali carbonates, and bicarbonates. it can 

 undergo a number of oxidation reactions to yield principal products 

 consisting of sulfur dioxide, surfuric acid, or elemental sulfur. Reaction 

 rates and oxidation products depend on the nature of the oxidizing agent. 

 Effects on experimental animals In experimental animals, the effects of 

 high doses of hydrogen sulfide and high doses of cyanide are very similar. 

 Cyanide inhibits the enzyme cytochrome c oxidase [EC 1.9.3.1] a, thereby 

 interfering with tissue use of oxygen to the point where metabolic demands 

 cannot be met. Hydrogen sulfide also exhibited an inhibitory action on a 

 purified preparation of cytochrome c oxidase. Results of studies on a 

 number of animal species including canary, rat, guineapig, cat, dog, and 

 goat showed that inhalation of hydrogen sulfide at a concentration of 

 150--225 mg/m3 (100--150 ppm) resulted in signs of local irritation of 

 eyes and throat after many hours of exposure; at 300--450 mg/m3 (200--300 

 ppm), eye and mucous membrane irritation appeared after 1 h inhalation and 

 slight general effects after prolonged inhalation; at 750--1050 mg/m3 

 (500--700 ppm), local irritation and slight systemic signs appeared within 

 1 h and death after several hours; at 1350 mg/m3 (900 ppm), serious 

 systemic effects appeared in less than 30 min and death within 1 h; at 

 2250 mg/m3 (1500 ppm), collapse and death occurred within 15--30 min; and, 

 at 2700 mg/m3 (1800 ppm), there was immediate collapse with respiratory 

 paralysis, and death. There is little information on the effects on 

 experimental animals of long-term, low-level exposure to hydrogen sulfide 

 gas. Water containing a hydrogen sulfide concentration as low as 0.86 mg/l 

 was toxic to trout, after exposure for 24 h. Effects on man General 

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 toxicological considerations Hydrogen sulfide is both an irritant and an 

 asphyxiant gas. Its direct irritant action on the moist tissues of the eye 

 produces keratoconjunctivitis, known as "gas eye". When inhaled, hydro,gen 

 sulfide exerts an irritant action throughout the entire respiratory tract, 

 although the deeper structures suffer the greatest damage. A consequence 

 may be pulmonary oedema. At concentrations of 1500--3000 mg/m3 (1000--2000 

 ppm), hydrogen sulfide gas is rapidly absorbed through the lung into the 

 blood, which initially induces hyperpnoea (rapid breathing). This is 

 followed by respiratory inactivity (apnoea). At higher concentrations, 

 hydrogen sulfide exerts an immediate paralysing effect on the respiratory 

 centres. Death due to asphyxia is the certain outcome, unless spontaneous 

 respiration is re-established or artificial respiration is promptly 

 provided. This sequence of events represents the most important toxic 

 effect of hydrogen sulfide. Acute hydrogen sulfide intoxication can be 

 defined as the effects from a single exposure Its massive concentrations 

 of hydrogen sulfide that rapidly produce signs of respiratory distress. 

 Concentrations exceeding about 1500 mg/m3 (1000 ppm) produce such acute 

 effects. Subacute hydrogen sulfide intoxication is the term applied to the 

 effects of continuous exposure for up to several hours to concentrations 

 ranging from 150 to 1500 mg/m3 (100--1000 ppm). In this range of exposure, 

 eye irritation is the most commonly observed effect. However, some reports 

 have indicated that the threshold for eye irritation occurs after several 

 hours of exposure to hydrogen sulfide at levels of 16--32 mg/m3 

 (10.5--21.0 ppm). Pulmonary oedema may be a more important and potentially 

 fatal complication of subacute hydrogen sulfide intoxication. Chronic 

 intoxication is a largely subjective state characterized by fatigue and 

 believed by some to be a consequence of intermittent exposure to hydrogen 

 sulfide concentrations of 75--150 mg/m3 (50--100 ppm). Not all research 

 workers accept the existence of such a condition. The characteristic 

 "rotten egg" odour of hydrogen sulfide is well known. The threshold of 

 perception of this odour varies considerably depending on individual 

 sensitivity, but, under laboratory conditions, it ranges from 0.0008 to 

 0.20 mg/m3 (0.0005--0.13 ppm). Above about 225 mg/m3 (150 ppm), the gas 

 exerts a paralysing effect on the olfactory apparatus, thus neutralizing 

 the value of its odour as a warning signal. At these concentrations, ~the 

 odour of the gas has been reported to be sickeningly sweet. Occupational 

 exposure Exposure to hydrogen sulfide in high concentrations occurs in 

 numerous occupations. Workers in the oil, gas, and petrochemical 

 industries are occasionally exposed to hydrogen sulfide in concentrations 

 sufficient to cause acute intoxication. In one survey of the petrochemical 

 industry, among 221 cases of hydrogen sulfide poisoning, the overall 

 mortality was 6% and a high proportion of victims exhibited neurological 

 signs and symptoms. Forty percent of all cases required some form of 

 respiratory assistance; 15 % developed pulmonary oedema. Persistent 

 sequelae following acute intoxication have been reported among workers in 

 a number of occupations including sewer workers, chemical plant employees, 

 farmers, shale-oil workers, and laboratory attendants. Most victims who 

 develop sequelae experience a state of unconsciousness during the acute 

 phase of their illness. However, sequelae following acute intoxication 

 without unconsciousness have also been reported. Exposure of the general 

 population Several episodes of general population exposure to hydrogen 

 sulfide have been reported. The effects of such exposure have ranged from 

 minor nuisance to serious illness and death. In a small community adjacent 

 to an oilfield installation, large quantities of hydrogen sulfide were 

 release~d into the air when an oilfield flare malfunctioned. Three hundred 

 and twenty persons were hospitalized, 22 of whom died. Nine exhibited 

 manifestations of pulmonary oedema. Four victims developed neurological 

 sequelae. The air levels of hydrogen sulfide were not measured. A 

 community of 40 000 people, located in the vicinity of a large geothermal 

 field, was exposed in some areas to hydrogen sulfide levels in air 

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 (measured on a continuous basis over a 5-month period) exceeding 0.08 

 mg/m3 (0.05 ppm), for, on average, 35 % of the time. Although fatal cases 

 of hydrogen sulfide intoxication associated with improper ventilation in 

 geothermal steam-heated dwellings in this area were occasionally reported 

 until 1962, the major problem has been the nuisance caused by the odour of 

 the gas. In a moderately sized community, hydrogen sulfide was released 

 from a small industrial waste lagoon resulting in a 1-h average 

 concentration of hydrogen sulfide in air of 0.45 mg/m3 (0.3 ppm). 

 Complaints were mostly related To the odour of hydrogen sulfide gas. 

 However, the severity of complaints of nausea, vomiting, headache, loss of 

 appetite, and disturbed sleep exceeded the mere nuisance level. No 

 community studies of the long-term, low-level effects of hydrogen sulfide 

 exposure have been reported. Evaluation of health risks Hydrogen sulfide 

 in ambient air in concentrations of the order of the odour threshold has 

 not been shown to have any significant biological activity in man or 

 animals. In controlled laboratory studies, the odour threshold for 

 hydrogen sulfide has been reported to range from 0.0008 to 0.20 mg/m3 

 (0.0005--0.13 ppm). Little information is available on the odour detection 

 limits for hydrogen sulfide either under experimental field conditions or 

 in the ambient air. However, the Task Group considered that a level of 

 0.008 mg/m3 (0.005 ppm) averaged over 30 min should not produce odour 

 nuisance in most situations. In the occupational setting, the earliest 

 toxic response appears to be eye irritation, which has been reported to 

 occur at 16--32 mg/m3 (10.5--21.0 ppm) after several hours' exposure. The 

 occupational exposure guidelines for hydrogen sulfide recommended by the 

 Task Group included the adoption of a level of 10 mg/m3 (7 ppm) as a 

 workshift time-weighted average value together with a short Term exposure 

 limit of 15 mg/m3 (10 ppm), the latter to be determined as a 10-min or 

 less, average value. 

3 

TITLE: 

 A Critical Review Of The Literature On Hydrogen Sulfide Toxicity 

AUTHORS: 

 Beauchamp RO Jr 

 Bus JS 

 Popp JA 

 Boreiko CJ 

 Andjelkovich DA 

SOURCE: 

 CRC Critical Reviews in Toxicology, Vol. 13, No. 1, pages 25-97, 1274 

 references, 19841984 

ABSTRACT: 

 Hydrogen-sulfide (7783064) toxicity is reviewed. The disposition of 

 hydrogen-sulfide is discussed. The lung is the primary route of exposure. 

 Occupational exposure by way of skin absorption appears to be minimal. No 

 studies of hydrogen-sulfide disposition in humans have been reported. In 

 animals, hydrogen-sulfide is sequentially oxidized, and can be excreted as 

 free or conjugated sulfate. Alternative metabolic pathways involve 

 methylation of hydrogen-sulfide to form methanethiol (74931) and 

 dimethyl-sulfide (75183) or reaction of hydrosulfide with metallo or 

 disulfide containing enzymes. Pathophysiologic effects of 

 hydrogen-sulfide are discussed. The carcinogenic, teratogenic, and 

 reproductive effects of hydrogen-sulfide have not been determined. 

 Studies of genotoxicity have yielded conflicting results. In humans, 

 hydrogen-sulfide gas is highly toxic and can be rapidly fatal. It is both 

 an irritant and asphyxiant. Locally, it irritates the mucous membranes of 

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 the eyes and respiratory tract. Systemically, it affects the central 

 nervous system and may cause paralysis of the respiratory center which 

 usually results in death. There is very little experimental or human 

 health data on long term exposures to low concentrations of 

 hydrogen-sulfide. Environmental emission and effects of hydrogen-sulfide 

 are considered. Environmental hydrogen-sulfide originates from natural 

 and industrial sources. 

4 

TITLE: 

 Metabolism of S-(2-chloro-1,1,2-trifluoroethyl)-L-cysteine to hydrogen 

 sulfide and the role of hydrogen sulfide in 

 S-(2-chloro-1,1,2-trifluoroethyl)-L-cysteine-induced mitochondrial 

 toxicity. 

AUTHORS: 

 Banki K 

 Elfarra AA 

 Lash LH 

 Anders MW 

SOURCE: 

 Biochem Biophys Res Commun. 1986, Jul 31; 138(2):707-13. [Biochemical and 

 biophysical research communications] 

ABSTRACT: 

 The nephrotoxic cysteine S-conjugate 

 S-(2-chloro-1,1,2-trifluoroethyl)-L-cysteine (CTFC) is metabolized by 

 kidney homogenates and subcellular fractions to pyruvate and a reactive 

 thiol, which is cytotoxic and partially decomposes to yield hydrogen 

 sulfide and thiosulfate. Although hydrogen sulfide is a potent 

 mitochondrial poison, the mitochondrial toxicity of CTFC is not 

 attributable to hydrogen sulfide formation, as shown by different sites of 

 inhibition of mitochondrial respiration by CTFC and hydrogen sulfide. The 

 efficient mitochondrial oxidation of hydrogen sulfide apparently serves to 

 protect mitochondria against the toxic effects of hydrogen sulfide 

 generated from CTFC. 

5 

TITLE: 

 Co-worker fatalities from hydrogen sulfide. 

AUTHORS: 

 Hendrickson RG 

 Chang A 

 Hamilton RJ 

SOURCE: 

 Am J Ind Med. 2004, Apr; 45(4):346-50. [American journal of industrial 

 medicine] 

ABSTRACT: 

 BACKGROUND: Hydrogen sulfide is a colorless, odorless gas that may cause 

 rapid loss of consciousness and respiratory depression without warning. It 

 has produced toxicity in workers in numerous industries and occupations. 

 METHODS: A review of the United States Bureau of Labor Statistics (USBLS) 

 Census of Fatal Occupational Injuries (CFOI) for occupational deaths 

 related to hydrogen sulfide from 1993 to 1999 was performed. RESULTS: 

 Fifty-two workers died of hydrogen sulfide toxicity in this 7-year period. 

 Deaths were most commonly reported in workers who were white (85%), male 

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 (98%), and in their first year of employment with the company (48%). 

 Common industries included waste management, petroleum, and natural gas. 

 In 21% of cases, a co-worker died simultaneously or in the attempt to save 

 the workers. CONCLUSIONS: Hydrogen sulfide toxicity is uncommon, but 

 potentially deadly. Toxicity is predominantly in new workers and co-worker 

 fatalities occur in a significant minority of cases. Proper training and 

 education on the warning signs of hydrogen sulfide toxicity may help 

 reduce worker fatalities. 

6 

TITLE: 

 Hydrogen sulfide (H2S) and sour gas effects on the eye. A historical 

 perspective. 

AUTHORS: 

 Lambert TW 

 Goodwin VM 

 Stefani D 

 Strosher L 

SOURCE: 

 Sci Total Environ. 2006, Aug 15; 367(1):1-22. [The Science of the total 

 environment] 

ABSTRACT: 

 The toxicology of hydrogen sulfide (H(2)S) and sour gas on the eye has a 

 long history beginning at least with Ramazzini's observations [Ramazzini 

 B. Diseases of Workers--De Morbis Artificum Diatriba--1713. Wright WC 

 (trans). New York, C. Hafner Publishing Co Inc.; 1964. 98-99 pp.]. In 

 contrast, a recent review by Alberta Health and Wellness (AHW Report) 

 concluded that there is little evidence of eye irritation following 

 short-term exposures to H(2)S at concentrations up to 100ppm and that the 

 H(2)S literature on the eye is a series of unsubstantiated claims 

 reproduced in review articles dating back to the 1930s [Alberta Health and 

 Wellness (AHW report). Health effects associated with short-term exposure 

 to low levels of hydrogen sulfide: a technical review, Alberta Health and 

 Wellness, October 2002, 81pp.]. In this paper, we evaluated this claim 

 through a historical review of the toxicology of the eye. Ramazzini noted 

 the effects of sewer gas on the eye [Ramazzini B. Diseases of Workers--De 

 Morbis Artificum Diatriba--1713. Wright WC (trans). New York, C. Hafner 

 Publishing Co Inc. 1964. 98-99 pp.]. Lehmann experimentally showed eye 

 effects in men at 70-90ppm H(2)S and also in animals [Lehmann K. 

 Experimentalle Studien uber den Einfluss technisch und hygienisch 

 wichtiger Gase und Dampfe auf den Organismus. Arch Hyg 1892;14:135-189]. 

 In 1923, Sayers, Mitchell and Yant reported eye effects in animals and men 

 at 50ppm H(2)S. Barthelemy showed eye effects in animals and men at 20ppm 

 H(2)S [Barthelemy HL. Ten years' experience with industrial hygiene in 

 connection with the manufacture of viscose rayon. J Ind Hyg Toxicol 

 1939;21:141-51]. Masure experimentally showed that H(2)S is the causative 

 agent of eye impacts in animals and men [Masure R. La Keratoconjunctivite 

 des filatures de viscose; etude clinique and experiementale. Rev Belge 

 Pathol 1950;20:297-341]. Michal upon microscopic examination of the rat's 

 cornea, found nuclear pyknosis, edema and separation of cells in the eye 

 following exposures for 3h at 36ppm H(2)S [Michal FV. Eye lesions caused 

 by hydrogen sulfide. Cesk Ophthalmol 1950;6;5-8]. In 1975, in Alberta, 

 irreversible eye damage and photophobia were experimentally produced in 

 calves exposed to 20ppm H(2)S for 1week [Nordstrom GA. A study of calf 

 response of ammonia and hydrogen sulfide gases. Thesis, University of 

 Alberta, Department of Agricultural Engineering, Edmonton Alberta; 1975, 

 218 pp.]. Alberta Environmental Centre documented clinical irritation of 

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 the eye at 40ppm H(2)S in 6 hours in rats [Alberta Environmental Centre. 

 Morphological observations in rats exposed for six hours to an atmosphere 

 of 0, 56, or 420mg/m(3) hydrogen sulfide. AECV86-A1. Alberta Environmental 

 Centre, Vegreville, Alberta; 1986b. 28 pp.]. In two sour gas blow-outs in 

 Alberta, in the early 1980s, eye injury was documented in humans and 

 animals at 0.5 ppm H(2)S. Community studies in the United States, Europe 

 and New Zealand suggest that acute exposure to 25ppb H(2)S is the lowest 

 concentration to irritate the eyes; with chronic exposure, serious eye 

 effects are suggested. In contrast to the conclusion, all of the studies, 

 except one, cited in the AHW Report indicate toxic effects on the eye 

 below 100ppm H(2)S [Alberta Health and Wellness (AHW report). Health 

 effects associated with short-term exposure to low levels of hydrogen 

 sulfide (H(2)S): a technical review, Alberta Health and Wellness, October 

 2002, 81pp.]. In addition, the AHW Report (2002) mis-presented two studies 

 as 'clinical studies', claiming they reported no evidence of eye effects 

 in humans from 2 and 30 ppm H(2)S for 30-40 minutes [Alberta Health and 

 Wellness (AHW report). Health effects associated with short-term exposure 

 to low levels of hydrogen sulfide (H(2)S): a technical review, Alberta 

 Health and Wellness, October 2002, 81pp.]. 

7 

TITLE: 

 Effects of hydrogen sulfide exposure on surface properties of lung 

 surfactant. 

AUTHORS: 

 Green FH 

 Schürch S 

 De Sanctis GT 

 Wallace JA 

 Cheng S 

 Prior M 

SOURCE: 

 J Appl Physiol. 1991, May; 70(5):1943-9. [Journal of applied physiology 

 (Bethesda, Md. : 1985)] 

ABSTRACT: 

 Hydrogen sulfide is an irritant and chemical asphyxiant gas that exerts 

 its primary toxic effects on the respiratory and neurological systems. 

 Exposure to hydrogen sulfide above a threshold value of 200-300 ppm is 

 characterized by the sudden onset of hemorrhagic pulmonary edema. The 

 purpose of this study was to determine whether this response is associated 

 with changes in the surface properties of pulmonary surfactant. 

 Bronchoalveolar lavage fluid was retrieved from the lungs of Fischer 344 

 rats exposed to two concentrations of hydrogen sulfide or fresh air for 4 

 h. Surface tension-lowering properties were assayed using a captive bubble 

 surface tensiometer. Lung injury was assessed by histopathology and 

 measurements of total protein and lactate dehydrogenase activity in the 

 lavagate. Marked abnormalities in surfactant activity were demonstrated in 

 the lavagates from rats exposed to the highest concentration (300 ppm) of 

 hydrogen sulfide. These involved the properties of adsorption to the 

 air-water interface and surface tension lowering under quasi-static 

 interfacial compression. Exposure to 200 ppm hydrogen sulfide had no 

 effect on minimum surface tension despite a significant increase in 

 protein and lactate dehydrogenase in the lavagate. This would suggest a 

 threshold-type response for the inhibition of surfactant activity by 

 hydrogen sulfide. In vitro studies using normal rat surfactant showed that 

 the abnormalities in surfactant activity were due to inhibitors in the 

 edema fluid and not to a direct effect of sulfide on surfactant. The 

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 pathophysiological consequences of increased alveolar surface tension 

 after hydrogen sulfide exposure may need to be considered in the clinical 

 setting. 

8 

TITLE: 

 Cytotoxic mechanisms of hydrosulfide anion and cyanide anion in primary 

 rat hepatocyte cultures. 

AUTHORS: 

 Thompson RW 

 Valentine HL 

 Valentine WM 

SOURCE: 

 Toxicology. 2003, Jun 30; 188(2-3):149-59. [Toxicology] 

ABSTRACT: 

 Hydrogen sulfide and hydrogen cyanide are known to compromise 

 mitochondrial respiration through inhibition of cytochrome c oxidase and 

 this is generally considered to be their primary mechanism of toxicity. 

 Experimental studies and the efficiency of current treatment protocols 

 suggest that H(2)S may exert adverse physiological effects through 

 additional mechanisms. To evaluate the role of alternative mechanisms in 

 H(2)S toxicity, the relative contributions of electron transport 

 inhibition, uncoupling of mitochondrial respiration, and opening of the 

 mitochondrial permeability transition pore (MPTP) to hydrosulfide and 

 cyanide anion cytotoxicity in primary hepatocyte cultures were examined. 

 Supplementation of hepatocytes with the glycolytic substrate, fructose, 

 rescued hepatocytes from cyanide anion induced toxicity, whereas fructose 

 supplementation increased hydrosulfide anion toxicity suggesting that 

 hydrosulfide anion may compromise glycolysis in hepatocytes. Although 

 inhibitors of the MPTP opening were protective for hydrosulfide anion, 

 they had no effect on cyanide anion toxicity, consistent with an 

 involvement of the permeability transition pore in hydrosulfide anion 

 toxicity but not cyanide anion toxicity. Exposure of isolated rat liver 

 mitochondria to hydrosulfide did not result in large amplitude swelling 

 suggesting that if H(2)S induces the permeability transition it does so 

 indirectly through a mechanism requiring other cellular components. 

 Hydrosulfide anion did not appear to be an uncoupler of mitochondrial 

 respiration in hepatocytes based upon the inability of oligomycin and 

 fructose to protect hepatocytes from hydrosulfide anion toxicity. These 

 findings support mechanisms additional to inhibition of cytochrome c 

 oxidase in hydrogen sulfide toxicity. Further investigations are required 

 to assess the role of the permeability transition in H(2)S toxicity, 

 determine whether similar affects occur in other cell types or in vivo and 

 evaluate whether this may provide a basis for the design of more effective 

 therapeutic measures for hydrogen sulfide intoxication. 

9 

TITLE: 

 Reducing sulfur compounds of the colon impair colonocyte nutrition: 

 implications for ulcerative colitis. 

AUTHORS: 

 Roediger WE 

 Duncan A 

 Kapaniris O 

 Millard S 

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SOURCE: 

 Gastroenterology. 1993, Mar; 104(3):802-9. [Gastroenterology] 

ABSTRACT: 

 BACKGROUND: Mercaptides (sodium hydrogen sulfide and sodium methanethiol) 

 and mercapto-fatty acid (sodium mercaptoacetate) are reducing agents that 

 help to maintain anaerobic conditions in the colonic lumen. The metabolic 

 effect of these agents on n-butyrate and glucose oxidation in human 

 colonocytes is unknown. METHODS: Isolated human colonocytes were prepared 

 from 31 colectomy specimens, and generation of oxidative metabolites from 

 [1-14C]n-butyrate and [6-14C]glucose was measured in the presence and 

 absence of reducing agents. Injury to cells was judged by diminished 

 production of metabolites. RESULTS: The injurious action of mercaptides at 

 all sites of the colon was of the order of sodium hydrogen sulfide > 

 methanethiol > mercaptoacetate. Significant inhibition of n-butyrate ( < 

 0.005) but not glucose oxidation was observed with sodium hydrogen sulfide 

 in the ascending colon, splenic flexure, and rectosigmoid region. Hydrogen 

 sulfide more significantly inhibited fatty acid oxidation in the 

 rectosigmoid than in the ascending colon (P < 0.02). CONCLUSIONS: 

 Metabolic effects of sodium hydrogen sulfide on butyrate oxidation along 

 the length of the colon closely mirror metabolic abnormalities observed in 

 active ulcerative colitis, and the increased production of sulfide in 

 ulcerative colitis suggests that the action of mercaptides may be involved 

 in the genesis of ulcerative colitis. 

10 

TITLE: 

 Risk of Pore Water Hydrogen Sulfide Toxicity in Dredged Material 

 Bioassays. 

AUTHORS: 

 Sims JG 

 Moore DW 

SOURCE: 

 Govt Reports Announcements & Index (GRA&I), Issue 21, 2005 

ABSTRACT: Final rept. 

 Generally, hydrogen sulfide is not treated as a contaminant of concern in 

 the regulatory evaluation of dredged material since it undergoes rapid 

 oxidation and dilution during dredging and disposal. However, because 

 dredged material is evaluated using effects-based testing (i.e., whole 

 sediment and elutriate toxicity tests), there is the potential for H2S to 

 exert toxicity and confound the regulatory decision-making process. To 

 evaluate the potential for hydrogen sulfide toxicity in dredged material 

 bioassays, a literature review and survey to U.S. Army Corps of Engineers 

 Divisions and Districts were conducted. Data included (a) reported 

 environmental pore water exposure concentrations of hydrogen sulfide and 

 (b) effects concentrations shown to cause toxicity in laboratory studies 

 with aquatic species. While the majority (&gt;60 percent) of reported 

 environmental pore water concentrations were &gt;100 micronMeter 

 H2S/1, almost all (90 percent) of reported effects were found at 

 concentrations 400 micronMeter HzS/1. This simple comparison of reported 

 exposure and effects concentrations suggests that there is a strong 

 Potential for hydrogen sulfide toxicity in dredged material bioassays. 

 However, a number of biases in this limited data set are discussed that 

 must be considered before any definitive conclusions can be drawn. 

11 

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TITLE: 

 A New Look at Physiologic Respiratory Response to H2S Poisoning 

AUTHORS: 

 Ammann HM 

SOURCE: 

 Journal of Hazardous Materials, Vol. 13, No. 3, pages 369-374, 17 

 references, 19861986 

ABSTRACT: 

 The physiological respiratory response to hydrogen-sulfide (7783064) 

 poisoning was discussed. Toxicological properties of hydrogen-sulfide 

 were summarized. Hydrogen-sulfide exposures of 50 to 100 parts per 

 million (ppm) cause serious eye injury. Exposures of 300 to 500ppm cause 

 pulmonary edema and are life threatening. Exposures of 1000 to 2000ppm 

 cause respiratory paralysis after a breath or two due to inhibition of the 

 respiratory center of the brain. At concentrations of 500 to 1000ppm, 

 respiratory paralysis is preceded by a period of rapid breathing or 

 hyperpnea. Death results unless the victim is removed from exposure and 

 artificially ventilated. Only at relatively low concentrations is the 

 obnoxious, rotten egg like odor of the gas a warning of its presence. At 

 concentrations above 150ppm, the olfactory sense is lost and pain from the 

 irritant effect on the eyes stops as the gas anesthetizes nerve endings in 

 these mucous membranes. Hydrogen-sulfide is metabolized along three 

 general pathways: methylation, oxidation, and reaction with metallic ion 

 or disulfide containing proteins. Reaction with metal ion containing 

 proteins is the primary route of hydrogen-sulfide toxicity. 

 Hydrogen-sulfide inhibits cytochrome-oxidase. This activates carotid and 

 aortic chemoreceptors, and increases signals to the respiratory center. 

 The respiratory center responds with increased signals to the ventilatory 

 muscle, and hyperpnea results. This is the same effect seen when oxygen 

 supply is decreased or oxygen tension in the arterial blood is reduced. 

 The author emphasizes that it is important that workers and potential 

 rescuers of hydrogen-sulfide poisoning victims be aware that hyperpnea is 

 part of the clinical picture of response to hydrogen-sulfide toxicity. 

12 

TITLE: 

 Minimal Risk Levels For Hydrogen Sulfide - Update. 

AUTHORS: 

 Chou SJ 

 Fay M 

 Keith S 

 Ingerman L 

SOURCE: 

 Toxicol Sci 2005 Mar;84(1-S):302-3 

ABSTRACT: 

 The Agency for Toxic Substances and Disease Registry (ATSDR) derives 

 minimal risk levels (MRLs) for hazardous substances based on available 

 toxicological and epidemiologic information, as detailed in the Agency 

 toxicological profiles. An MRL is an estimate of the daily human exposure 

 to a hazardous substance that is likely to be without appreciable risk of 

 adverse, non-cancer health effects. The toxicological profile for hydrogen 

 sulfide was recently updated; revisions of the acute inhalation MRL and 

 the intermediate inhalation MRL were proposed. The acute inhalation MRL of 

 0.2 ppm was based on a lowest-observed-adverse-effect level (LOAEL) of 2 

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 ppm for respiratory effects. Two out of 10 persons with asthma exposed to 

 hydrogen sulfide for 30 minutes had changes in excess of 30% in airway 

 resistance or specific airway conductance, suggestive of bronchial 

 constriction. These individuals showed no significant changes in lung 

 function (Jappinen et al. Br J Ind Med. 1990, 47:824-8). To derive the 

 MRL, an uncertainty factor (UF) of 9 was applied, 3 for use of a minimal 

 LOAEL, and 3 for human variability. The intermediate inhalation MRL of 

 0.02 ppm was based on a no-observed-adverse-effect level (NOAEL) of 10 ppm 

 for respiratory effects in rats exposed to hydrogen sulfide for 6 

 hours/day, 7 days/week for 10 weeks. Olfactory neuron loss and basal cell 

 hyperplasia in the olfactory epithelium of the nose were seen in rats 

 exposed to 30 ppm and 80 ppm (Brenneman et al. Toxicol Pathol 2000, 

 28:326-33). To derive the MRL, a human equivalent concentration NOAEL was 

 calculated and an UF of 30 was applied, 3 for animal to human 

 extrapolation, and 10 for human variabiltiy. As hydrogen sulfide is a gas, 

 inhalation is the major route of exposure. No federal air quality standard 

 presently exists for hydrogen sulfide. Health-based guidance values, such 

 as MRLs, are useful for states and local municipalities when addressing 

 community concerns regarding hydrogen sulfide emissions, for example, 

 those from concentrated agricultural feeding operations. 

13 

TITLE: 

 Twenty-foot fall averts fatality from massive hydrogen sulfide exposure. 

AUTHORS: 

 Gabbay DS 

 De Roos F 

 Perrone J 

SOURCE: 

 J Emerg Med. 2001, Feb; 20(2):141-4. [The Journal of emergency medicine] 

ABSTRACT: 

 Hydrogen sulfide is a colorless irritant and asphyxiant gas with a noxious 

 odor of "rotten eggs." Acute hydrogen sulfide exposure may 

 cause, depending on the level and duration of toxicity, symptoms ranging 

 from mild mucous membrane irritation to permanent neurologic impairment 

 and cardiopulmonary arrest. We present a case of an oil refinery worker 

 exposed to a typically fatal concentration of hydrogen sulfide gas (>1000 

 ppm) while working on top of a 20-foot ladder. The "knockdown" 

 effect of exposure to high concentrations of hydrogen sulfide caused him 

 to lose consciousness and fall from the top of the ladder. He was 

 transported to the Emergency Department as a major trauma victim. 

 Ironically, this 20-foot fall saved his life and possibly those of the 

 rescuers by immediately removing him from the source of the hydrogen 

 sulfide. Treatment of hazardous materials incidents and the 

 pathophysiology and treatment options for hydrogen sulfide poisoning are 

 discussed. 

14 

TITLE: 

 Effects of hydrogen sulfide to Vibrio fischeri, Scenedesmus vacuolatus, 

 and Daphnia magna. 

AUTHORS: 

 Küster E 

 Dorusch F 

 Altenburger R 

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SOURCE: 

 Environ Toxicol Chem. 2005, Oct; 24(10):2621-9. [Environmental toxicology 

 and chemistry / SETAC] 

ABSTRACT: 

 The effects of hydrogen sulfide (H2S) were tested in three 

 ecotoxicological tests in order to evaluate its confounding potential in 

 assessment of pore water and groundwater toxicity. The luminescent 

 bacteria Vibrio fischeri, the water flea Daphnia magna, and the microalgae 

 Scenedesmus vacuolatus often are part of a biotest battery. A new 

 technique for the synthesis of hydrogen sulfide solutions of defined 

 concentrations using an electrochemical generator instead of sodium 

 sulfide solutions was used. Because hydrogen sulfide is volatile, the loss 

 rate of H2S was studied over time to enable estimation of the mean test 

 concentrations over the whole test duration. Loss rates were calculated to 

 be 13 +/- 6% after 30 min, and 39 +/- 11% and 43 +/- 16% after a 24- and 

 48-h exposure time, respectively. Sensitivities of the test organisms in 

 terms of median effective concentration (EC50), corrected for the above 

 loss rates, varied from 0.28 to 0.0036 and 0.055 mM for the luminescent 

 bacteria, the crustacea, and the algae, respectively. A 

 species-sensitivity distribution using EC and mean lethal concentration 

 literature data for marine and freshwater crustaceans and phytoplankton 

 showed a medium sensitivity of the water flea D. magna, though the 

 bacteria V. fischeri and the algae S. vacuolatus were among the 

 least-sensitive group of organisms. This demonstrates that only the algae 

 and the bacteria are easy to use in the assessment of toxicity of matrices 

 with H2S concentrations above 0.06 mM. 

15 

TITLE: 

 A critical review of the literature on hydrogen sulfide toxicity. 

AUTHORS: 

 Beauchamp RO Jr 

 Bus JS 

 Popp JA 

 Boreiko CJ 

 Andjelkovich DA 

SOURCE: 

 Crit Rev Toxicol. 1984; 13(1):25-97. [Critical reviews in toxicology] 

ABSTRACT: 

 The information available on the biological activity of hydrogen sulfide 

 has been examined for present status of critical results pertaining to the 

 toxicity of hydrogen sulfide. This review of the literature is intended as 

 an evaluative report rather than an annotated bibliography of all the 

 source material examined on hydrogen sulfide. The information was selected 

 as it might relate to potential toxic effects of hydrogen sulfide to man 

 and summarized, noting information gaps that may require further 

 investigation. Several recommendations are listed for possible 

 consideration for either toxicological research or additional short- and 

 long-term tests. Two bibliographies have been provided to assist in 

 locating references considered in this report: (1) literature examined but 

 not cited and (2) reference citations. The majority of the references in 

 the first bibliography were considered peripheral information and less 

 appropriate for inclusion in this report. 

16 

TITLE: 

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 [Fatal outcome of an hydrogen sulfide poisoning] 

AUTHORS: 

 Querellou E 

 Jaffrelot M 

 Savary D 

 Savry C 

 Perfus JP 

SOURCE: 

 Ann Fr Anesth Reanim. 2005, Oct; 24(10):1302-4. [Annales francaises 

 d'anesthesie et de reanimation] 

ABSTRACT: 

 We report a case of fatal outcome poisoning by massive exposure to 

 hydrogen sulfide of a sewer worker. This rare event was associated with a 

 moderate intoxication of two members of the rescue team. The death was due 

 to asystole and massive lung oedema. Autopsy analysis showed diffuse 

 necrotic lesions in lungs. Hydrogen sulfide is a direct and systemic 

 poison, produced by organic matter decomposition. The direct toxicity 

 mechanism is still unclear. The systemic toxicity is due to an acute 

 toxicity by oxygen depletion at cellular level. It is highly diffusable 

 and potentially very dangerous. At low concentration, rotten egg smell 

 must trigger hydrogen sulfide suspicion since at higher concentration it 

 is undetectable, making intoxication possible. In case of acute 

 intoxication, there is an almost instantaneous cardiovascular failure and 

 a rapid death. Hydrogen sulfide exposure requires prevention measures and 

 more specifically the use of respiratory equipment for members of the 

 rescue team. 

17 

TITLE: 

 Measurement and distribution of interstitial and overlying water ammonia 

 and hydrogen sulfide in sediment toxicity tests. 

AUTHORS: 

 PHILLIPS BM 

 ANDERSON BS 

 HUNT JW 

SOURCE: 

 MARINE ENVIRONMENTAL RESEARCH; 44 (2). 1997. 117-126. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Hydrogen sulfide and ammonia are naturally 

 occurring and anthropogenically enriched components of marine sediments 

 which may occur in concentrations toxic to marine organisms. In this 

 study, ammonia and hydrogen sulfide were measured in interstitial and 

 overlying water at the initiation and termination of solid phase toxicity 

 tests using amphipods (Rhepoxynius abronius). Interstitial hydrogen 

 sulfide concentrations were generally higher than overlying 

 concentrations, presumably because hydrogen sulfide that diffused from 

 sediments was quickly volatilized in the overlying water. Unionized 

 ammonia concentrations were higher in interstitial water at test 

 initiation, but were often higher in overlying water after 10 day 

 exposures. The pH was higher in overlying water samples than in 

 interstitial samples, and contributed to increased proportions of 

 unionized ammonia in the overlying water. Concentrations of hydrogen 

 sulfide and ammonia above the effects threshold for Rhepoxy 

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18 

TITLE: 

 Capsaicin pretreatment modifies hydrogen sulphide-induced pulmonary injury 

 in rats. 

AUTHORS: 

 Prior M 

 Green F 

 Lopez A 

 Balu A 

 De Sanctis GT 

 Fick G 

SOURCE: 

 Toxicol Pathol. 1990; 18(2):279-88. [Toxicologic pathology] 

ABSTRACT: 

 One of the major target organs of hydrogen sulphide gas is the lung. 

 Exfoliation of upper respiratory epithelia and pulmonary edema are 

 prominent effects. Various neuropeptides contained in afferent C-fibres 

 are intimately associated with the epithelia of the conducting airways and 

 are liberated upon exposure to noxious gases. We sought to determine their 

 role in the pathogenesis of hydrogen-sulphide-induced pulmonary injury by 

 pretreating rats with the neurotoxin, capsaicin, which is known to ablate 

 a subpopulation of vagal afferent C-fibres. Groups of capsaicin and saline 

 (control) pretreated Fischer 344 rats were exposed to an edemogenic 

 concentration of hydrogen sulphide (525-559 mg/m3) for 4 hr. Mortality was 

 significantly greater (p less than 0.01) in the capsaicin treated rats 

 (12/12) compared to the control animals (2/12). Pulmonary injury was also 

 more severe in the capsaicin pretreated animals as assessed by lung water 

 content, histological grade of pulmonary edema and protein in the 

 broncho-alveolar fluid. Animals depleted of substance P exhibited a 

 significantly greater (p less than 0.01) degree of bronchial epithelial 

 cell exfoliation and ulceration following exposure to hydrogen sulphide. 

 These experiments indicate that capsaicin sensitive sensory nerves may 

 play a major role in pulmonary defense against the effects of inhaled 

 toxic gases such as hydrogen sulphide. 

19 

TITLE: 

 Odor and volatile organic compound removal from wastewater treatment plant 

 headworks ventilation air using a biofilter. 

AUTHORS: 

 Converse BM 

 Schroeder ED 

 Iranpour R 

 Cox HH 

 Deshusses MA 

SOURCE: 

 Water Environ Res. 2003 Sep-Oct; 75(5):444-54. [Water environment research 

 : a research publication of the Water Environment Federation] 

ABSTRACT: 

 Laboratory-scale experiments and field studies were performed to evaluate 

 the feasibility of biofilters for sequential removal of hydrogen sulfide 

 and volatile organic compounds (VOCs) from wastewater treatment plant 

 waste air. The biofilter was designed for spatially separated removal of 

 pollutants to mitigate the effects of acid production resulting from 

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 hydrogen sulfide oxidation. The inlet section of the upflow units was 

 designated for hydrogen sulfide removal and the second section was 

 designated for VOC removal. Complete removal of hydrogen sulfide (H2S) and 

 methyl tert-butyl ether (MTBE) was accomplished at loading rates of 8.3 g 

 H2S/(m3 x h) (15-second empty bed retention time [EBRT]) and 33 g MTBE/(m3 

 x h) (60-second EBRT), respectively. In field studies performed at the 

 Hyperion Treatment Plant in Los Angeles, California, excellent removal of 

 hydrogen sulfide, moderate removal of nonchlorinated VOCs such as toluene 

 and benzene, and poor removal of chlorinated VOCs were observed in 

 treating the headworks waste air. During spiking experiments on the 

 headworks waste air, the percentage removals were similar to the unspiked 

 removals when nonchlorinated VOCs were spiked; however, feeding high 

 concentrations of chlorinated VOCs reduced the removal percentages for all 

 VOCs. Thus, biofilters offer a distinct advantage over chemical scrubbers 

 currently used at publicly owned treatment works in that they not only 

 remove odor and hydrogen sulfide efficiently at low cost, but also reduce 

 overall toxicity by partially removing VOCs and avoiding the use of 

 hazardous chemicals. 

20 

TITLE: 

 Hyperbaric oxygen therapy for severe hydrogen sulfide poisoning. 

AUTHORS: 

 Smilkstein MJ 

 Bronstein AC 

 Pickett HM 

 Rumack BH 

SOURCE: 

 J Emerg Med. 1985; 3(1):27-30. [The Journal of emergency medicine] 

ABSTRACT: 

 The optimum therapy for hydrogen sulfide poisoning is unclear. Adjuncts 

 used in the treatment of cyanide poisoning have been advocated because of 

 the shared mechanism of toxicity between hydrogen sulfide and cyanide. 

 Following success in cyanide poisoning, hyperbaric oxygen therapy (HBO) 

 has been suggested for use in treating hydrogen sulfide poisoning. A case 

 of severe hydrogen sulfide poisoning was successfully treated with HBO 

 after standard therapy was apparently ineffective. HBO as a therapeutic 

 adjunct in hydrogen sulfide poisoning and the rationale for its use are 

 discussed. 

21 

TITLE: 

 Hydrogen Sulfide 

AUTHORS: 

 Anonymous 

SOURCE: 

 Hazard Evaluation System and Information Service, State of California, 

 Berkeley, California, 2 pages, 19831983 

ABSTRACT: 

 Guidelines for the diagnosis and treatment of hydrogen-sulfide (7783064) 

 poisoning are presented. Sources of industrial and natural 

 hydrogen-sulfide are given. Mechanisms of toxicity are discussed. 

 Hydrogen-sulfide is an eye and respiratory irritant; exposure route is 

 inhalation; perception of odor of hydrogen-sulfide is not a reliable 

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 warning indicator of its presence. Olfactory fatigue can be rapid, and 

 tolerance to the odor may come from chronic exposure. Clinical 

 manifestations of hydrogen-sulfide poisoning are summarized. Inhalation 

 of concentrations above 500 parts per million (ppm) can cause loss of 

 consciousness and respiratory paralysis; coma can result from the 

 inhalation of a single breath containing 1,000ppm. Treatment procedures 

 are described. Antidotal therapy consists of breaking an ampule of 

 amyl-nitrite (110463) under the nose, followed by the administration of 

 sodium-nitrite (7632000) intravenously. The toxic sulfide ions are 

 removed from the blood by binding with the methemoglobin initiated by the 

 nitrite treatment. The authors note that hydrogen-sulfide poisoning is 

 one of the few industrial poisons for which a specific antidotal therapy 

 is available; however, they caution against over treating with nitrites 

 because of the danger of developing methemoglobinemia. 

22 

TITLE: 

 [Structural-biochemical reorganization of rat liver caused by hydrogen 

 sulfide-containing gas mixture] 

AUTHORS: 

 Poliakova VS 

 Shakhlamov VA 

 Stadnikov AA 

 Solnyshkova TG 

SOURCE: 

 Morfologiia. 2003; 124(4):84-7. [Morfologiia (Saint Petersburg, Russia)] 

ABSTRACT: 

 Morphological equivalents of hepatocyte response to environmental factors 

 of various intensity, associated with biochemical processes and directed 

 at cell survival were studied in white outbred male rat using 

 morphological (light and electron microscopy, histoautoradiography) and 

 biochemical methods. As judged by the responses of intracellular 

 structures, an exposure to hydrogen sulfide-containing gas, a pathogenic 

 environmental factor, results in unequal changes in hepatocytes in 

 different lobule zones. Small doses cause an activation of metabolic 

 processes in hepatocytes that have plastic directivity. High doses of 

 hydrogen sulfide-containing gas mixture result in the appearance of some 

 signs of hepatocyte adaptation to extreme situation. Positive dynamics of 

 structural modifications of the liver after the administration of 

 nootropil and vitamin complex with antioxidant properties as correcting 

 substances, indicates the reversibility of hepatocyte changes following 

 long-term (up to two weeks) exposure to low doses and short-term exposure 

 to high doses of hydrogen sulfide-containing gas mixture. 

23 

TITLE: 

 [The morphofunctional characteristics of the pulmonary air-blood barrier 

 in rats breathing gas mixtures with a high content of hydrogen sulfide] 

AUTHORS: 

 Seredenko MM 

 Rozova EV 

 Velikanov EB 

 Trizno NN 

SOURCE: 

 Morfologiia. 1992, May; 102(5):120-9. [Morfologiia (Saint Petersburg, 

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 Russia)] 

ABSTRACT: 

 The influence of gas mixtures with high concentration of pure hydrogen 

 sulphide and natural gas of the Astrakhan deposit (NGAD) upon the 

 morphofunctional state of the aerohematic barrier (AHB) and the surfactant 

 system of the lungs was studied in 80 albino Wistar rats of 180-250 g body 

 weight. The influence of both hydrogen sulphide and NGAD results in the 

 appearance of morphofunctional alterations in the AHB and surfactant 

 system of the lungs. However, if the action of hydrogen sulphide in 

 concentrations of 300-330 and 600-700 mg/m3 is followed not only by 

 pathological manifestations but also by mobilization of certain 

 compensatory-adaptational mechanisms such as reinforcement of pinocytosis, 

 the action of NGAD with the similar concentration of hydrogen sulphide 

 seems to be too toxic, surpassing the possibilities of compensation, and 

 there occurs the development of purely pathological phenomenon--pulmonary 

 edema. 

24 

TITLE: 

 Hydrogen Sulfide Generation in Shipboard Oily-Water Waste: A Safety Hazard 

 in Ships. 

AUTHORS: 

 Hodgeman DK 

SOURCE: 

 Govt Reports Announcements &amp; Index (GRA&I), Issue 22, 1995 

ABSTRACT: 

 TD3: This report is intended to inform crews of the hazards arising from 

 generation of hydrogen sulfide gas in stored oily-water wastes in ships. 

 It has been written with an audience of sailors in mind. Some background 

 information on the cause of the problem is provided, and questions on the 

 nature and toxicity of hydrogen sulfide answered. The process by which 

 hydrogen sulfide is generated in oily-water waste is discussed and the 

 sailor advised of what he can do to minimize the formation of this toxic 

 gas. Finally, the main hazard from oily-water waste generated hydrogen 

 sulfide is identified, and advice given on what to do in the event of a 

 hazardous incident. jg. 

25 

TITLE: 

 Hydrogen Sulfide 

AUTHORS: 

 Macaluso P 

SOURCE: 

 Kirk-Othmer Encyclopedia of Chemical Technology, Second Revised Edition, 

 Interscience Publishers, New York, Volume 19, pages 375-389, 19691969 

ABSTRACT: 

 The physical, chemical and thermodynamic properties of hydrogen-sulfide 

 (7783064) are described. Its occurrence in petroleum, natural gas and 

 coal deposits, as a result of bacterial metabolism and as a by-product in 

 industrial operations is discussed. The small scale production, and two 

 obsolete large scale processes for hydrogen-sulfide are described. These 

 have been replaced by the conversion of sulfur compounds in petroleum to 

 hydrogen-sulfide, and the recovery of by-product hydrogen-sulfide. The 

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 economic aspects of this recovery are discussed. The materials of 

 construction, and health and safety factors are discussed in relation to 

 its toxicity, flammability and explosiveness. The uses of 

 hydrogen-sulfide as a raw material are described. 

26 

TITLE: 

 Hydrogen sulfide poisoning treated with hyperbaric oxygen. 

AUTHORS: 

 Whitcraft DD 3rd 

 Bailey TD 

 Hart GB 

SOURCE: 

 J Emerg Med. 1985; 3(1):23-5. [The Journal of emergency medicine] 

ABSTRACT: 

 Hydrogen sulfide inhalation injury can be life threatening. The toxic gas 

 is produced, sometimes unexpectedly, from a wide variety of sources. 

 Because its mechanism of toxicity is similar to that of cyanide, hydrogen 

 sulfide poisoning is commonly treated with the nitrite component of the 

 cyanide antidote kit. In this case report, hyperbaric oxygen was 

 successfully used to treat hydrogen sulfide intoxication. Further 

 evaluation of hyperbaric oxygen therapy as adjunctive treatment of 

 hydrogen sulfide poisoning is recommended. 

27 

TITLE: 

 Noxious gas exposure in the outback: two cases of hydrogen sulfide 

 toxicity. 

AUTHORS: 

 Gunn B 

 Wong R 

SOURCE: 

 Emerg Med (Fremantle). 2001, Jun; 13(2):240-6. [Emergency medicine 

 (Fremantle, W.A.)] 

ABSTRACT: 

 Two cases of toxicity from industrial exposure to hydrogen sulfide are 

 presented. Both patients had neurological effects with loss of 

 consciousness and amnesia along with respiratory symptoms and signs. Both 

 were treated with hyperbaric oxygen therapy in addition to standard 

 resuscitative techniques with rapid improvement. Sodium nitrite and 

 hyperbaric oxygen therapy are suggested specific treatments. The 

 literature and the two case reports support the use of hyperbaric oxygen 

 therapy in the treatment of acute hydrogen sulfide toxicity. Hyperbaric 

 oxygen therapy has also been reported to have a role in the prevention of 

 both short- and long-term neurological toxicity. 

28 

TITLE: 

 [Ultrastructural changes in the cortex of cerebral hemispheres in acute 

 and subacute intoxication with natural gas containing hydrogen sulfide] 

AUTHORS: 

 Solnyshkova TG 

 Shakhlamov VA 

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SOURCE: 

 Arkh Patol. 2003 Mar-Apr; 65(2):17-20. [Arkhiv patologii] 

ABSTRACT: 

 Grave destructive changes of myelin nerve fibers in the cortex of the 

 cerebral hemispheres were found in rats intoxicated with hydrogen sulfide 

 gas of the Astrakhan gas deposit. Repeated exposures to natural hydrogen 

 sulfide containing gas in subacute chronic intoxication (100 mg/m3 by H2S) 

 damage predominantly myelin areas corresponding to myelin incisions which 

 are most sensitive to this gas. 

29 

TITLE: 

 Occupational exposure to hydrogen sulfide in the sour gas industry - Some 

 unresolved issues 

AUTHORS: 

 Guidotti TL 

SOURCE: 

 International Archives of Occupational and Environmental Health 1994, 

 Vol.66, No.3, p.153-160. Illus. 54 ref. 

ABSTRACT: 

 This literature survey deals with the effects of exposure to hydrogen 

 sulfide in the natural gas industry. It is stressed that the acute 

 toxicity of hydrogen sulfide is well known. However, exposure-response 

 data are confined to lethal doses. There is some evidence that long-term 

 exposure to hydrogen sulfide causes eye irritation. Further studies are 

 needed for confirmation. 

30 

TITLE: 

 Work-related symptoms and inflammation among sewage plant operatives. 

AUTHORS: 

 Thorn J 

 Beijer L 

SOURCE: 

 Int J Occup Environ Health. 2004 Jan-Mar; 10(1):84-9. [International 

 journal of occupational and environmental health : official journal of the 

 International Commission on Occupational Health] 

ABSTRACT: 

 Sewage operatives at five sewage treatment plants (n = 59) and controls 

 not exposed to sewage (n = 55) were examined to determine work-related 

 symptoms and inflammatory responses. Symptoms were elicited using a 

 questionnaire, and spirometry was performed. Inflammatory markers were 

 determined in blood and nasal lavage. Workplace endotoxin and hydrogen 

 sulfide were measured and adeno- and enterovirus antibodies were evaluated 

 in blood. Gastrointestinal and airway symptoms, joint pains, unusual 

 tiredness, and toxic pneumonitis were more common among operatives, and 

 the proportion of blood neutrophils was higher among operatives as 

 compared with controls. A relationship was found between several reported 

 symptoms and the inflammatory markers. Hydrogen sulfide levels were very 

 low. Endotoxin levels were generally low, but high at some work sites. 

31 

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TITLE: 

 Ultrastructural and morphometric characteristics of nerve cells and 

 myelinated fibers in the cerebral cortex after chronic exposure to natural 

 gas containing hydrogen sulfide in low concentrations. 

AUTHORS: 

 Solnyshkova TG 

 Shakhlamov VA 

SOURCE: 

 Bull Exp Biol Med. 2002, Oct; 134(4):411-3. [Bulletin of experimental 

 biology and medicine] 

ABSTRACT: 

 We studied ultrastructural and morphometric characteristics of nerve cells 

 and myelinated fibers in the cerebral cortex after chronic exposure to 

 natural gas containing hydrogen sulfide in low concentrations. 

 Radioisotope assay revealed activation of protein synthesis in nerve cells 

 after chronic exposure to natural hydrogen sulfide-containing gas in low 

 concentrations (10 mg/m(3)by H2S) for 2 weeks. After 1 month the 

 ultrastructure of myelinated fibers was characterized by sectorial 

 loosening and demyelination. 

32 

TITLE: 

 Exposure to hydrogen sulfide, mercaptans and sulfur dioxide in pulp 

 industry. 

AUTHORS: 

 Kangas J 

 Jäppinen P 

 Savolainen H 

SOURCE: 

 Am Ind Hyg Assoc J. 1984, Dec; 45(12):787-90. [American Industrial Hygiene 

 Association journal] 

ABSTRACT: 

 An hygienic survey for hydrogen sulfide, methyl mercaptan and its 

 derivatives and sulfur dioxide in kraft mills and in sulfite mills 

 revealed concentrations varying from 0 to 20 ppm hydrogen sulfide, 0 to 15 

 ppm methyl mercaptan and comparable amounts of dimethyl sulfide with 

 dimethyl disulfide up to 1.5 ppm. The greatest emissions were detected at 

 chip chutes and evaporation vacuum pumps. Batch operations yielded clearly 

 higher sulfur dioxide concentrations (up to 20 ppm) as compared to a 

 continuous ammonia-base digester. Furthermore, there was a strong 

 correlation with the season in the sulfite mills where higher 

 concentrations were found in the winter when natural ventilation was 

 poorer. As to the health effects, the exposed workers complained of 

 headaches and a decrease in concentration capacity more often than matched 

 controls. The number of sick leaves was greater in the exposed workers 

 than among the controls. 

33 

TITLE: 

 Hydrogen Sulfide 

AUTHORS: 

 Anonymous 

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SOURCE: 

 Medical and biologic effects of environmental pollutants. National 

 research council (1979) 183 p 

ABSTRACT: 

 Hydrogen sulfide intoxication has been classified under three rubrics: 

 acute, subacute, and chronic. Acute intoxication is a dramatic, systemic 

 reaction resulting from a single massive exposure to up to 1,400 ug/liter 

 (1,000 ppm) of hydrogen sulfide in air. This condition is characterized by 

 rapid (often instantaneous) loss of consciousness followed by convulsions 

 and respiratory failure caused by the paralyzing effects of the gas on the 

 centers of respiration. Death due to histotoxic anoxia is the frequent 

 outcome of acute intoxication unless resuscitation is begun immediately. 

 Subacute hydrogen sulfide poisoning is a localized response to the 

 irritant properties of the gas following continuous exposure to 

 concentrations between 140 and 1,400 ug/liter (100 and 1,000 ppm). Eye 

 irritation, manifested as conjunctivitis, keratitis, or both, is the most 

 common form of subacute poisoning. respiratory tract irritation is also an 

 effect of subacute poisoning. If exposure is prolonged, irritation of the 

 deeper regions of the lung may cause pulmonary edema. It is important to 

 emphasize that, at these concentrations, hydrogen sulfide produces rapid 

 paralysis of the olfactory apparatus, thereby neutralizing the sense of 

 smell as a warning system.(Shortened) 

34 

TITLE: 

 Respiratory tract toxicity of inhaled hydrogen sulfide in Fischer-344 

 rats, Sprague-Dawley rats, and B6C3F1 mice following subchronic (90-day) 

 exposure. 

AUTHORS: 

 Dorman DC 

 Struve MF 

 Gross EA 

 Brenneman KA 

SOURCE: 

 Toxicol Appl Pharmacol. 2004, Jul 1; 198(1):29-39. [Toxicology and applied 

 pharmacology] 

ABSTRACT: 

 The goal of this study was to characterize the toxicity of hydrogen 

 sulfide (H2S), including nasal and pulmonary effects, in adult male and 

 female Fischer-344 and Sprague-Dawley rats and B6C3F1 mice. Animals 

 underwent whole-body exposure to 0, 10, 30, or 80 ppm H2S for 6 h/day for 

 at least 90 days. Exposure to 80 ppm H2S was associated with reduced feed 

 consumption during either the first exposure week (rats) or throughout the 

 90-day exposure (mice). Male Fischer-344 rats, female Sprague-Dawley rats, 

 and female B6C3F1 mice exposed to 80 ppm H2S had depressed terminal body 

 weights when compared with air-exposed controls. Subchronic H2S inhalation 

 did not result in toxicologically relevant alterations in hematological 

 indices, serum chemistries, or gross pathology. Histologic evaluation of 

 the nose showed an exposure-related increased incidence of olfactory 

 neuronal loss (ONL) and rhinitis. ONL occurred following exposure to > or 

 =30 ppm H2S in both sexes of all experimental groups, with one exception, 

 male Sprague-Dawley rats demonstrated ONL following exposure to 80 ppm H2S 

 only. A 100% incidence of rhinitis was found in the male and female B6C3F1 

 mice exposed to 80 ppm H2S. In the lung, exposure to H2S was associated 

 with bronchiolar epithelial hypertrophy and hyperplasia in male and female 

 Sprague-Dawley rats following exposure to > or =30 ppm H2S and in male 

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 Fischer-344 rats exposed to 80 ppm H2S. Our results confirm that the 

 rodent nose, and less so the lung, are highly sensitive to H2S-induced 

 toxicity, with 10 ppm representing the NOAEL for ONL following subchronic 

 inhalation. 

35 

TITLE: 

 Toxicological Profile for Hydrogen Sulfide (2006 Update). 

SOURCE: 

 Govt Reports Announcements & Index (GRA&I), Issue 04, 2007 

ABSTRACT: 

 Supersedes PB99-166696. Sponsored by Agency for Toxic Substances and 

 Disease Registry, Atlanta, GA. Div. of Toxicology. 

 This public health statement tells you about hydrogen sulfide and the 

 effects of exposure to it. The Environmental Protection Agency (EPA) 

 identifies the most serious hazardous waste sites in the nation. These 

 sites are then placed on the National Priorities List (NPL) and are 

 targeted for long-term federal clean-up activities. Hydrogen sulfide has 

 been found in at least 35 of the 1,689 current or former NPL sites. 

 Although the total number of NPL sites evaluated for this substance is not 

 known, the possibility exists that the number of sites at which hydrogen 

 sulfide is found may increase in the future as more sites are evaluated. 

 This information is important because these sites may be sources of 

 exposure and exposure to this substance may harm you. When a substance is 

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

 container, such as a drum or bottle, it enters the environment. Such a 

 release does not always lead to exposure. You can be exposed to a 

 substance only when you come in contact with it. You may be exposed by 

 breathing, eating, or drinking the substance, or by skin contact. If you 

 are exposed to hydrogen sulfide, many factors will determine whether you 

 will be harmed. These factors include the dose (how much), the duration 

 (how long), and how you come in contact with it. You must also consider 

 any other chemicals you are exposed to and your age, sex, diet, family 

 traits, lifestyle, and state of health. 

36 

TITLE: 

 Influence of the short-term inhalation of hydrogen sulfide in rats. 

AUTHORS: 

 KOHNO M 

 TANAKA E 

 NAKAMURA T 

 SHIMOJO N 

 MISAWA S 

SOURCE: 

 EISEI KAGAKU; 37 (2). 1991. 103-106. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. The effects of the short-term inhalation of 

 hydrogen sulfide were studied on rats that were exposed to hydrogen 

 sulfide gas (75 ppm) for 20 to 60 min. The levels of hydrogen sulfide were 

 higher in most of the tissues than that of the blood shortly after the 

 exposure to the gas. The highest level of hydrogen sulfide was obtained in 

 the heart, followed by kidney, brain, spleen, liver and lung. Biochemical 

 parameters in the serum increased the level of GOT but those of alkaline 

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 phosphatase, blood urea nitrogen, sodium ion, potassium ion and 

 creatinine remained unchanged. Physiological examination revealed a 

 reduction in the heart beat and delayed P-Q intervals on 

 electrocardiograms during the exposure for 60 min. Histopathological 

 examination demonstrated a slight congestion in the lungs but no abnormal 

 lesions in other tissues. The results indicate that the short-term 

 inhalation of hydrogen sulfide at a concentration of 75 ppm could evoke 

 overall acute toxicity, mainly in 

37 

TITLE: 

 [Reaction of the immune system of the body to combined effects of chemical 

 agents] 

AUTHORS: 

 Setko NP 

 Zheludeva GN 

 Mazaeva SG 

SOURCE: 

 Gig Sanit. 1989, Mar(3):24-6. [Gigiena i sanitariia] 

ABSTRACT: 

 A single and chronic inhalation exposure to a complex of chemical 

 substances being part of hydrogen sulphide-containing natural gas 

 (hydrogen sulphide, hydrocarbon, mercaptan, sulphur dioxide) results in a 

 decline in humoral indicators of non-specific body resistance. At the same 

 time the level of inhibition of lysozyme and complement activity along 

 with the bactericidal activity of blood serum have direct dependence on 

 the duration of chemical exposure and can be used as additional tests for 

 early detection of body changes. 

38 

TITLE: 

 Effects of inhalation exposure to carbon disulfide and its combination 

 with hydrogen sulfide on embryonal and fetal development in rats. 

AUTHORS: 

 Saillenfait AM 

 Bonnet P 

 de Ceaurriz J 

SOURCE: 

 Toxicol Lett. 1989, Jul; 48(1):57-66. [Toxicology letters] 

ABSTRACT: 

 Pregnant rats were exposed to 0, 100, 200, 400 or 800 ppm of carbon 

 disulfide (CS2), 100 ppm of hydrogen sulfide (H2S) alone or in combination 

 with 400 and 800 ppm CS2, 6 h/d during days 6-20 of gestation. Maternal 

 reproduction and fetal parameters were evaluated on gestational day 21. 

 Treatment with 100 or 200 ppm CS2 or with 100 ppm H2S caused no maternal 

 toxicity or adverse effects on the developing embryo or fetus. Exposure to 

 400 or 800 ppm CS2 resulted in a low incidence of club foot and in a 

 significant reduction of maternal weight gain. Significant increases in 

 unossified sternebrae occurred at 800 ppm CS2 and reduction of fetal body 

 weight at 400 and 800 ppm CS2. The latter effect was enhanced by 

 combination with 100 ppm H2S. These results support the conclusion that, 

 at levels of exposure associated with maternal toxicity, CS2 leads to an 

 increase in incidence of club foot and to fetal toxicity which is enhanced 

 by simultaneous exposure to H2S. 

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39 

TITLE: 

 Occupational exposure to hydrogen sulfide in the sour gas industry: some 

 unresolved issues. 

AUTHORS: 

 Guidotti TL 

SOURCE: 

 Int Arch Occup Environ Health. 1994; 66(3):153-60. [International archives 

 of occupational and environmental health] 

ABSTRACT: 

 Occupational exposure to hydrogen sulfide (H2S) and the medical management 

 of H2S-associated toxicity remains a problem in the sour gas industry and 

 some other industrial settings. The acute effects of exposure to H2S are 

 well recognized, but accurate exposure-response data are limited to 

 acutely lethal effects, even in animal studies. Odor followed by olfactory 

 paralysis and keratoconjunctivitis are the characteristics effects of H2S 

 at lower concentrations. H2S-induced acute central toxicity leading to 

 reversible unconsciousness is a "knockdown"; it is controversial 

 whether repeated or prolonged knockdowns are associated with chronic 

 neurologic sequelae but the evidence is suggestive. Knockdowns can be 

 acutely fatal as a consequence of respiratory paralysis and cellular 

 anoxia. Pulmonary edema is also a well-recognized acute effect of H2S 

 toxicity. Human studies of sublethal exposure with satisfactory exposure 

 assessment are almost nonexistent. There are indications, poorly 

 documented at present, of other chronic health problems associated with 

 H2S exposure, including neurotoxicity, cardiac arrhythmia, and chronic eye 

 irritation but apparently not cancer. Rigorous and comprehensive studies 

 in the sour gas industry are difficult, in part because of confounding 

 exposures and uncertain end points. 

40 

TITLE: 

 Objective measures of ocular irritation as a consequence of hydrogen 

 sulphide exposure. 

AUTHORS: 

 Lefebvre M 

 Yee D 

 Fritz D 

 Prior MG 

SOURCE: 

 Vet Hum Toxicol. 1991, Dec; 33(6):564-6. [Veterinary and human toxicology] 

ABSTRACT: 

 Hydrogen sulphide (H2S) exposure has been reported to adversely affect the 

 eyes. Objective information regarding the extent of injury relative to 

 varied exposure concentrations of H2S has not been published. The 

 exfoliative eye cytology procedure has been demonstrated to provide 

 quantitative information regarding the degree of ocular irritation and to 

 allow for comparisons to be made between the irritants. This paper 

 evaluates this procedure's efficiency in determining the degree of ocular 

 irritation resulting from hydrogen sulphide exposure in rats. 

41 

TITLE: 

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 Concentration-time interactions in hydrogen sulphide toxicity in rats. 

AUTHORS: 

 Prior MG 

 Sharma AK 

 Yong S 

 Lopez A 

SOURCE: 

 Can J Vet Res. 1988, Jul; 52(3):375-9. [Canadian journal of veterinary 

 research = Revue canadienne de recherche veterinaire] 

ABSTRACT: 

 Concentration-time interactions were investigated in young male and female 

 Sprague-Dawley, Long Evans and Fischer-344 rats exposed to hydrogen 

 sulphide for two, four or six hours. Higher concentrations caused more 

 deaths, with no significant difference for duration of exposure. A 

 significant sex effect was noted with 30% mortality in males and 20% in 

 females, with no significant difference among strains. Changes in weight 

 were significant: increasing with concentration, higher in males than in 

 females, different among strains (Fischer-344 less than Sprague Dawley 

 less than Long Evans), and affected by duration of exposure. Lethal 

 concentration values (LC50 and LC10) were estimated, for the pooled data 

 set (n = 456); the probit equation was Y = -5.74749 + 3.8259X where X is 

 log10 dose of hydrogen sulphide in parts per million. The LC50/LC10 values 

 were 644/298 parts per million (902/417 mg m-3) respectively. Individual 

 probit analyses were also performed for strain, hours of exposure and sex. 

 The LC50 and LC10 values for male, female and strain were not different. 

 Significant differences were observed among LC50/LC10 values for hours of 

 exposure (2 h = 587/549 parts per million, 822/769 mg m-3; 4 h = 501/422 

 parts per million, 701/591 mg m-3; 6 h = 335/299 parts per million, 

 469/491 mg m-3). There was no effect of spatial position in the exposure 

 chamber on the distribution of mortality. All rats of all strains dying 

 had severe pulmonary edema. 

42 

TITLE: 

 Treatment of hydrogen sulfide intoxication: oxygen versus nitrites 

AUTHORS: 

 Ravizza AG 

 Carugo D 

 Cerchiari EL 

 Cantadore R 

 Bianchi GE 

SOURCE: 

 Vet. Hum. Toxicol.; VOL 24 ISS Aug 1982, P241-242, (REF 9) 

ABSTRACT: 

 IPA COPYRIGHT: ASHP A case report of a 34-yr-old male rendered 

 unconscious by exposure to a high concentration of hydrogen sulfide fumes 

 is presented to illustrate the advantages of oxygen therapy. Significant 

 improvement in blood gases was achieved within one h of starting oxygen. 

 At twelve h the patient was still unconscious, but responded to painful 

 stimuli. Full recovery of consciousness occurred after 20 h and the 

 patient was discharged one wk later with no sequelae. The risks of nitrite 

 therapy are discussed in contrast to the efficacy of oxygen. 

43 

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TITLE: 

 Cytotoxic effects of hydrogen sulfide on pulmonary alveolar macrophages in 

 rats. 

AUTHORS: 

 Khan AA 

 Yong S 

 Prior MG 

 Lillie LE 

SOURCE: 

 J Toxicol Environ Health. 1991, May; 33(1):57-64. [Journal of toxicology 

 and environmental health] 

ABSTRACT: 

 Respiratory rates (basal and zymosan-stimulated) and cell viability were 

 monitored in pulmonary alveolar macrophages (PAM) from rats exposed to 0, 

 70, 280, and 560 mg/m3 (0, 50, 200, and 400 ppm) hydrogen sulfide (H2S) 

 gas for 4 h. Zymosan-stimulated respiratory rates were markedly reduced in 

 PAM collected from rats exposed to 280 and 560 mg/m3 H2S; however, their 

 basal respiratory rates were not affected. Significant decrease in cell 

 viability was also observed in samples from 560 mg/m3 H2S-treated rats, 

 but it remained high and unchanged in other treatments. In vitro 

 incubation of PAM from control rats with sulfide (a precursor of H2S) and 

 its two oxidation products, sulfite and sulfate, showed that sulfide was 

 markedly more inhibitory to both respiratory rates than sulfite or 

 sulfate. These treatments did not affect cell viability. 

44 

TITLE: 

 Olfactory neuron loss in adult male CD rats following subchronic 

 inhalation exposure to hydrogen sulfide. 

AUTHORS: 

 Brenneman KA 

 James RA 

 Gross EA 

 Dorman DC 

SOURCE: 

 Toxicol Pathol. 2000 Mar-Apr; 28(2):326-33. [Toxicologic pathology] 

ABSTRACT: 

 Dysosmia and anosmia are reported to occur following human exposure to 

 hydrogen sulfide (H2S) gas. The clinical association between H2S exposure 

 and olfactory dysfunction in humans necessitates evaluation of the nasal 

 cavity and olfactory system in experimental animals used to study H2S 

 toxicity. The purpose of this study was to subchronically expose 

 10-week-old male CD rats to relatively low concentrations of H2S and to 

 histologically evaluate the nasal cavity for exposure-related lesions. 

 Rats (n = 12/group) were exposed via inhalation to 0, 10, 30, or 80 ppm 

 H2S 6 h/d and 7 d/wk for 10 weeks. Following exposure to 30 and 80 ppm 

 H2S, a significant increase in nasal lesions limited to the olfactory 

 mucosa was observed. The lesions, which consisted of olfactory neuron loss 

 and basal cell hyperplasia, were multifocal, bilaterally symmetrical, and 

 had a characteristic rostrocaudal distribution pattern. Regions of the 

 nasal cavity affected included the dorsal medial meatus and the dorsal and 

 medial portions of the ethmoid recess. The no observed adverse effect 

 level for olfactory lesions in this study was 10 ppm. For perspective, the 

 American Conference of Governmental Industrial Hygienists threshold limit 

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 value (TLV) recommendation for H2S is currently 10 ppm (proposed revision: 

 5 ppm), so the concentrations employed in the present study were 3 and 8 

 times the TLV. These findings suggest that subchronic inhalation exposure 

 to a relatively low level of H2S (30 ppm) can result in olfactory toxicity 

 in rats. However, because of differences in the breathing style and nasal 

 anatomy of rats and humans, additional research is required to determine 

 the significance of these results for human health risk assessment. 

45 

TITLE: 

 Utilizing data from multiple studies (meta-analysis) to determine 

 effective dose-duration levels. Example: rats and mice exposed to hydrogen 

 sulfide. 

AUTHORS: 

 Brown KG 

 Strickland JA 

SOURCE: 

 Regul Toxicol Pharmacol. 2003, Apr; 37(2):305-17. [Regulatory toxicology 

 and pharmacology : RTP] 

ABSTRACT: 

 The objective of this exercise was to incorporate as much data as possible 

 from multiple studies, that may differ in exposure durations, to derive a 

 chemical-specific dose-duration response curve from which to identify 

 toxicity markers (e.g., ED01, benchmark dose, and LD50). This has the 

 advantage of incorporating more information than single-study assessments 

 to improve estimates and reduce confidence intervals, and determining 

 toxicity markers as functions of exposure duration as well as dose. The 

 example used mortality for rats and mice, analyzed separately, from acute 

 exposure to hydrogen sulfide (dose refers to airborne concentration of 

 H(2)S). Statistical methods were applied to determine when data from 

 different studies could be pooled. EC01, EC10, and EC50 (doses with 

 response rates of 1, 10, and 50%) were estimated, with 95% confidence 

 intervals, at durations of 5, 10, and 30 min, and 1, 2, 4, and 6 h. A 

 single dose-duration response curve for mortality was fit to the rat data 

 for exposures of 5 min, 10 min, 30 min, and 1h, using a logistic curve 

 additive in log(dose) and log(duration). Separate fits of that model were 

 required, however, at 2, 4, and 6h, due to an increasing impact of 

 duration relative to concentration as duration increased. The curves for 

 rats fit the data exceedingly well and exhibited a threshold-like response 

 followed by a steep incline as concentration increased. There were fewer 

 data for mice but the response pattern for mortality clearly differed from 

 rats. This example demonstrates the feasibility of extending the concept 

 of single-study benchmark doses to multiple-study dose-duration 

 benchmarks, using U.S. EPA's program CatReg. Similar applications to 

 long-term animal studies could be considered. 

46 

TITLE: 

 The influence of simultaneous exposure to carbon disulfide and hydrogen 

 sulfide on the peripheral nerve toxicity and metabolism of carbon 

 disulfide in rats. 

AUTHORS: 

 Gagnaire F 

 Simon P 

 Bonnet P 

 De Ceaurriz J 

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SOURCE: 

 Toxicol Lett. 1986, Dec; 34(2-3):175-83. [Toxicology letters] 

ABSTRACT: 

 Three groups of 10 male Sprague-Dawley rats were exposed daily, 5 days a 

 week for 25 weeks, either to 500 ppm carbon disulfide (CS2), 50 ppm 

 hydrogen sulfide (H2S), or to both of them as a mixture and were 

 periodically examined for sensory and motor tail nerve conduction velocity 

 (SNCV, MNCV). A concomitant control group of 10 rats was used. In 

 addition, rats exposed to 500 ppm CS2, and those simultaneously exposed to 

 500 ppm CS2 and 50 ppm H2S, were twice examined for 24-h urine excretion 

 of 2-thio-thiazolidine-4-carboxylic acid (TTCA) in the course of the 

 experimental period. Simultaneous exposure to CS2 and H2S had no 

 significant interactive effect on nerve conduction velocities. A 

 significant time-dependent slowing down of MNCV and SNCV occurred as the 

 result of chronic exposure to CS2, including exposure to 500 ppm CS2 and 

 to the mixture of 500 ppm CS2 and 50 ppm H2S, but did not occur after 

 chronic exposure to 50 ppm H2S. With combined exposure to 500 ppm CS2 and 

 50 ppm H2S, the quantity of TTCA excreted in 24-h urine was not 

 significantly different from that occurring in response to CS2 exposure 

 alone. On the basis of these results it is suggested that chronic exposure 

 to H2S would neither influence CS2-induced peripheral nerve toxicity nor 

 obscure the interpretation of the measurement of urinary TTCA as a 

 biological indicator of CS2 exposure. 

47 

TITLE: 

 Effects of Acute Intoxication with Hydrogen Sulfide on Central Amino Acid 

 Transmitter Systems 

AUTHORS: 

 Kombian SB 

 Warenycia MW 

 Mele FG 

 Reiffenstein RJ 

SOURCE: 

 Neurotoxicology, Vol. 9, No. 4, pages 587-595, 41 references, 19881988 

ABSTRACT: 

 The effects of acute hydrogen-sulfide (7783064) intoxication on brain 

 amino acid transmitter systems were studied in rats. Adult male 

 Sprague-Dawley-rats were injected intraperitoneally with 10 or 30mg/kg 

 sodium-hydrosulfide (7775146). Rats were killed 2 minutes later and their 

 brains were removed and dissected into the cerebellum, brainstem, 

 hippocampus, striatum, and cerebral cortex. Each brain part was assayed 

 for aspartate, glycine, glutamate, glutamine, alanine, taurine, and 

 gamma-aminobutyric-acid (GABA). Sodium-hydrosulfide did not affect the 

 concentration of amino acids in the cerebral cortex, striatum, and 

 hippocampus. The 30mg/kg dose decreased the concentrations of aspartate 

 and glycine in the cerebellum. The concentrations of all seven amino 

 acids were increased in the brainstem. The increases in aspartate, 

 glycine, glutamate, alanine, taurine, and GABA concentrations were 

 constant, the increases induced by 30mg/kg sodium-hydrosulfide not being 

 significantly different from those induced by the 10mg/kg dose. The 

 30mg/kg dose decreased the concentration of glutamine to the control 

 value. The authors conclude that hydrogen-sulfide selectively affects 

 brainstem amino acid concentrations. The changes in brainstem 

 neurotransmitter amino acid concentrations may, at least in part, 

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 contribute to the acute toxicity of hydrogen-sulfide through mechanisms 

 involving respiratory arrest. 

48 

TITLE: 

 Changes in intracellular pH play a secondary role in hydrogen 

 sulfide-induced nasal cytotoxicity. 

AUTHORS: 

 Roberts ES 

 Wong VA 

 McManus BE 

 Marshall MW 

 Lancianese S 

 Dorman DC 

SOURCE: 

 Inhal Toxicol. 2006, Mar; 18(3):159-67. [Inhalation toxicology] 

ABSTRACT: 

 Hydrogen sulfide (H(2)S) is a naturally occurring gas that is also 

 associated with several industries. The potential for widespread human 

 inhalation exposure to this toxic gas is recognized as a public health 

 concern. The nasal epithelium is particularly susceptible to H(2)S-induced 

 pathology. Cytochrome oxidase inhibition is postulated as one mechanism of 

 H(2)S toxicity. Another mechanism by which the weak acid H(2)S could cause 

 nasal injury is intracellular acidification and cytotoxicity. To further 

 understand the mechanism by which H(2)S damages the nasal epithelium, 

 nasal respiratory and olfactory epithelial cell isolates and explants from 

 naive rats were loaded with the pH-sensitive intracellular chromophore 

 SNARF-1 and exposed to air or 10, 80, 200, or 400 ppm H(2)S for 90 min. 

 Intracellular pH was measured using flow cytometry or confocal microscopy. 

 Cell lysates were used to quantify total protein and cytochrome oxidase 

 activity. A modest but statistically significant decrease in intracellular 

 pH occurred following exposure of respiratory and olfactory epithelium to 

 400 ppm H(2)S. Decreased cytochrome oxidase activity was observed 

 following exposure to >10 ppm H(2)S in both respiratory and olfactory 

 epithelia. None of the treatments resulted in cytotoxicity. The 

 intracellular acidification of nasal epithelial cells by high-dose H(2)S 

 exposure and the inhibition of cytochrome oxidase at much lower H(2)S 

 concentrations suggest that changes in intracellular pH play a secondary 

 role in H(2)S-induced nasal injury. 

49 

TITLE: 

 Hydrogen Sulfide 

AUTHORS: 

 Anonymous 

SOURCE: 

 ACGIH. Documentation of the threshold limit values and biological exposure 

 indices Vol:7th Ed (2001) 3 p 

ABSTRACT: 

 A TLV-TWA of,10 ppm (14 mg/m3) and TLV-STEL of 15 ppm (21 mg/m3) are 

 recommended for occupational exposure to hydrogen sulfide. These values 

 are intended to minimize the potential for eye and respiratory tract 

 irritation, symptoms of fatigue, headache, and dizziness, and central 

 nervous system effects, the most important being paralysis of the 

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 respiratory center and sudden death. The offensive odor of hydrogen 

 sulfide is unreliable as a warning signal for hazardous exposure 

 concentrations due to the rapid onset of olfactory fatigue. The 

 recommended TLV-STEL is intended to provide an additional measure for a 

 safe exposure limit. Sufficient data were not available to recommend Skin, 

 SEN, or carcinogenicity notations. At this printing, the TLVs for hydrogen 

 sulfide are under review. 

50 

TITLE: 

 Isolation of pig colonic crypts for cytotoxic assay of luminal compounds: 

 effects of hydrogen sulfide, ammonia, and deoxycholic acid. 

AUTHORS: 

 Leschelle X 

 Robert V 

 Delpal S 

 Mouillé B 

 Mayeur C 

 Martel P 

 Blachier F 

SOURCE: 

 Cell Biol Toxicol. 2002; 18(3):193-203. [Cell biology and toxicology] 

ABSTRACT: 

 Some colonic luminal molecules resulting from bacterial metabolism of 

 alimentary or endogenous compounds are believed to exert various effects 

 on the colonic epithelial cell physiology. We isolated surface epithelial 

 cells and intact colonic crypts in order to test bacterial metabolites in 

 the pig model, which is often considered relevant for extrapolation to the 

 physiopathology of the human gastrointestinal tract. Using colonocytes 

 isolated with EDTA, we found that the initial cell viability, estimated by 

 the membrane integrity and oxidative capacity measurement, fell rapidly 

 despite several experimental attempts to preserve it such as the use of a 

 medium designed to increase the adherence of epithelial cells and of a 

 coated extracellular matrix, the presence in the culture medium of the 

 oxidative substrate butyrate, and the use of an inhibitor of the caspases 

 involved in cell apoptosis. In contrast, using dispase and collagenase as 

 proteolytic agents, we were able to obtain pig colonic crypts that 

 maintain an excellent membrane integrity after 4 h. Using this 

 preparation, we were able to test the presumably cytotoxic luminal 

 compounds hydrogen sulfide, ammonia, and deoxycholic acid on colonic crypt 

 viability. Of these, only deoxycholic acid was found to significantly 

 alter the cellular membrane integrity. It is concluded that pig colonic 

 crypts can be useful for the in vitro appraisal of the cytotoxic 

 properties of luminal compounds. 

51 

TITLE: 

 Neurotoxicological effects associated with short-term exposure of 

 Sprague-Dawley rats to hydrogen sulfide. 

AUTHORS: 

 Struve MF 

 Brisbois JN 

 James RA 

 Marshall MW 

 Dorman DC 

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SOURCE: 

 Neurotoxicology. 2001, Jun; 22(3):375-85. [Neurotoxicology] 

ABSTRACT: 

 Although hydrogen sulfide (H2S) is a known neurotoxic hazard, only a 

 limited number of experimental animal studies have examined its 

 neurochemical or behavioral effects. Our aim was to determine if 

 short-term inhalation exposure of rats to H2S would result in altered 

 brain catecholamnine levels or impaired learning and memory. Three groups 

 of adult male CD rats were tested; two groups were exposed by nose-only 

 inhalation (0, 30, 80, 200, or 400 ppm H2S) and one group was exposed by 

 whole-body inhalation (0, 10, 30, or 80 ppm H2S) for 3 h per day forfive 

 consecutive days. The first group (n = 10 rats per concentration) was 

 tested immediately following each daily nose-only H2S exposure for spatial 

 learning with a Morris water maze. Core body temperatures were also 

 monitored in these animals during and after the last H2S exposure. The 

 second group of rats (n = 10 rats per concentration) was tested for 

 spontaneous motor activity immediately following the fifth exposure. These 

 rats were then euthanized and striatal, hippocampal, and hindbrain 

 catecholamnine levels determined. A third group of rats (n = 5-7 rats per 

 concentration) was pretrained on a multiple fixed- interval (FI) schedule 

 and exposed whole-body. Daily performance on the FI schedule was compared 

 for the week pre-exposure, for the exposure week immediately following 

 daily exposures, and for the week postexposure. We observed significant 

 reductions in motor activity, water maze performance, and body temperature 

 following exposure only to high concentrations (> or = 80 ppm) of H2S. 

 Exposure to H2S did not affect regional brain catecholamine concentrations 

 or performance on the FI schedule. Additional studies using other measures 

 of behavior and longer-term exposure to H2S may be required to more 

 definitively address conditions under which H2S exposure results in 

 behavioral toxicity. 

52 

TITLE: 

 Hydrogen sulfide intoxication. A case report and discussion of treatment. 

AUTHORS: 

 Stine RJ 

 Slosberg B 

 Beacham BE 

SOURCE: 

 Ann Intern Med. 1976, Dec; 85(6):756-8. [Annals of internal medicine] 

ABSTRACT: 

 The toxicity of hydrogen sulfide is thought to be due primarily to 

 reversible inactivation of the respiratory enzyme, cytochrome oxidase, 

 with resultant inhibition of aerobic metabolism. A patient with severe 

 hydrogen sulfide poisoning and consequent profound metabolic acidosis was 

 treated successfully with nitrites and oxygen. The nitrite-induced 

 methemoglobin, by competitively binding the toxic hydrosulfide anion until 

 detoxified, presumably reactivated and protected cytochrome oxidase and 

 therby aided the patient's recovery by enhancing aerobic metabolism. His 

 rapid recovery adds clinical support to the efficacy of nitrite therapy in 

 sulfide poisoning. Therefore, we recommend that severe cases of sulfide 

 poisoning be treated with nitrite-induced methemoglobinemia in addition to 

 vigorous supportive care. 

53 

TITLE: 

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 Effects of low dissolved oxygen and hydrogen sulfide on early development 

 stages of blue crab, Portunus trituberculatus in Hiroshima Bay, Japan. 

AUTHORS: 

 KANG J-C 

 MATSUDA O 

 YAMAMOTO T 

SOURCE: 

 JOURNAL OF THE FACULTY OF APPLIED BIOLOGICAL SCIENCE HIROSHIMA UNIVERSITY; 

 32 (2). 1993. 61-70. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Acute toxicity of hydrogen sulfide to larval 

 stage of blue crab, Portunus trituberculatus was measured using a 

 continuous flow system. Survival rates of crab larvae to oxygen deficient 

 water (DO | 3.4 mg l-1) and oxygen deficient water (3.4 mg O2 l-1 and 2.6 

 mg O2 l-1) with two different levels of hydrogen sulfide (10 mug H2S l-1 

 and 5 mug H2S l-1) were also determined. Survival rate of crab larvae 

 exposed to hydrogen sulfide for 48 hours decreased at H2S \ 5.2 mug l-1, 

 H2S \ 9.5 mug l-1, H2S \ 19.7 mug l-1 levels to zoea, megalopa and crab 

 stage, respectively. Larval survival of zoea, megalopa and crab stage 

 under low oxygen was significantly affected by DO | 3.4 mg l-1, DO | 2.6 

 mg l-1, 1.5 mg l-1 levels, respectively. The combined effects of low 

 dissolved oxygen and hydrogen sulfide to the blue crab were stronger than 

 each single effect. Namely, survival rate lowered under the combined 

 exposure to | 3.4 mg O2 l-1 + \ 5 mug H2S l-1, \ 3.4 mgO2 l-1 + 10.1 mug 

 H2S l-1, 

54 

TITLE: 

 Cancer incidence, morbidity and geothermal air pollution in Rotorua, New 

 Zealand. 

AUTHORS: 

 Bates MN 

 Garrett N 

 Graham B 

 Read D 

SOURCE: 

 Int J Epidemiol. 1998, Feb; 27(1):10-4. [International journal of 

 epidemiology] 

ABSTRACT: 

 BACKGROUND: The New Zealand city of Rotorua sits on a geothermal field. 

 However, little is known about the possible health impacts of the 

 geothermal emissions. This was an ecological study that examined cancer 

 incidence and morbidity data for Rotorua. METHODS: Cancer registry and 

 hospital discharge (morbidity) data were obtained for the decade 

 1981-1990. Standardized incidence ratios (SIR) were calculated comparing 

 Rotorua residents with those living in the rest of New Zealand. Diagnostic 

 categories examined were based on known target organ systems of hydrogen 

 sulphide toxicity. RESULTS: Of the cancer sites, there was an elevated 

 rate for nasal cancers. However, this was based on only four cases. The 

 SIR for cancers of the trachea, bronchus and lung in Maori women was 1.48 

 (95% CI: 1.03-2.06). This was not explained by higher smoking rates. In 

 the hospital discharge data, a number of diseases showed elevated SIR, 

 notably diseases of the nervous system and the eye. To some extent, these 

 effects were characteristic of effects induced by hydrogen sulphide and 

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 also mercury compounds. However, there were few data with which to assess 

 whether significant mercury exposures had occurred, and other explanations 

 were possible. CONCLUSIONS: There are inadequate exposure data for Rotorua 

 to permit conclusions on likely causal associations. However, some of the 

 elevated disease rates were at least consistent with what one might expect 

 to find if sufficient exposures to hydrogen sulphide and/or mercury were 

 occurring. 

55 

TITLE: 

 The Potentiated Toxic Action of Carbon Disulfide-Hydrogen Sulfide Gas 

 Mixtures 

AUTHORS: 

 Fischer R 

SOURCE: 

 Biochemische Zeitschrift, Vol. 141, pages 540-549, 5 references, 19231923 

ABSTRACT: 

 The combined action of various concentrations of carbon-disulfide (75150) 

 and hydrogen-sulfide (7783064) gases is studied in rabbits to determine 

 whether a potentiating effect occurs. Concentrations in the inhalation 

 chamber ranged in increments from 0.240 to 0.78 parts of hydrogen-sulfide 

 per thousand parts of air and 4.81 to 14.2 milligrams of carbon-disulfide 

 per liter of air. One rabbit each was exposed to each concentration of 

 either gas or to their combination for 3 hours. At the lowest 

 concentrations of hydrogen-sulfide only irritation occurred such as 

 chewing movements, licking and some restlessness, which also occurred with 

 low carbon-disulfide concentrations in addition to sleepiness. The 

 combination of both gases produced only these effects in an additive 

 manner. The highest concentrations of hydrogen-sulfide produced the 

 initial symptoms as those of the lower concentrations and then alternating 

 strong restlessness and quiet sitting, some dyspnea, trembling and lying 

 on its side. The carbon-disulfide high concentrations produced also the 

 initial symptoms along with increasing numbness, staggering, restlessness, 

 opisthotonos and dyspnea. Again, the effects of the combination produced 

 only these effects in an additive manner. Thus, there is no potentiated 

 action of the mixture of the gases compared with the effects of the gases 

 given alone. It was shown that the two gases do not enter into a chemical 

 reaction in the mixture. It is suggested that when the two gases are 

 combined in industrial atmospheres, there is no need to assume the 

 existence of a particularly toxic action of the mixture. (German; English 

 translation available) 

56 

TITLE: 

 Hyperbaric oxygen therapy in the management of two cases of hydrogen 

 sulfide toxicity from liquid manure. 

AUTHORS: 

 Belley R 

 Bernard N 

 Côté M 

 Paquet F 

 Poitras J 

SOURCE: 

 CJEM. 2005, Jul; 7(4):257-61. [CJEM : Canadian journal of emergency 

 medical care = JCMU : journal canadien de soins medicaux d'urgence] 

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ABSTRACT: 

 Hydrogen sulfide is a potent lethal gas. Supportive care, nitrite therapy 

 and hyperbaric oxygen are the treatment modalities reported in the 

 literature in cases of hydrogen sulfide exposure. We describe an 

 industrial exposure in which 6 workers inhaled high concentrations of 

 hydrogen sulfide when they entered a closed spreader tank partially filled 

 with liquid swine manure. Five of the 6 lost consciousness, and 2 were 

 agitated and poorly responsive on arrival to the emergency department 

 despite having already received high-flow oxygen for nearly 1 hour. These 

 2 patients received nitrite therapy followed by orotracheal intubation and 

 hyperbaric oxygen. All patients were discharged home without sequelae 

 after short stays in hospital. The emergency management of hydrogen 

 sulfide exposure is briefly reviewed. 

57 

TITLE: 

 Tolerance of anoxia and hydrogen sulfide by benthic crustaceans Portunus 

 trituberculatus, Metapenaeus monoceros and Macrobrachium nipponense. 

AUTHORS: 

 KANG J-C 

 MATSUDA O 

SOURCE: 

 JOURNAL OF THE FACULTY OF APPLIED BIOLOGICAL SCIENCE HIROSHIMA UNIVERSITY; 

 32 (2). 1993. 71-78. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Both acute toxicity tests of hydrogen 

 sulfide and tolerance test to anoxia and anoxia with hydrogen sulfide on 

 Portunus trituberculatus, Metapenaeus monoceros and Macrobrachium 

 nipponense were carried out. The 96 hr-LC50 of hydrogen sulfide is 31.5 

 mug l-1 for P. trituberculatus, 35.2 mug l-1 for M. monoceros, and 51.0 

 mug l-1 for M. nipponense. In anoxia, values of median lethal time (LT50) 

 were 1.2 day (28 hr), 0.9 day (22 hr) and 1.6 day (35 hr) for P. 

 trituberculatus, M. monoceros and M. nipponense, respectively. The 

 tolerance of P. trituberculatus and M. monoceros to anoxia is lower than 

 the tolerance of M. nipponense. These results suggest that field 

 populations of P. trituberculatus and M. monoceros are easily affected by 

 natural hypoxia with hydrogen sulfide. 

58 

TITLE: 

 Hydrogen Sulfide 

AUTHORS: 

 Braker W 

 Mossman AL 

SOURCE: 

 Matheson Gas Data Book, 5th edition, Matheson Gas Products, East 

 Rutherford, New Jersey, pages 319-325, 3 references, 19711971 

ABSTRACT: 

 The Matheson Gas Data Book gives the physical constants, physical 

 characteristics, uses and toxicity of hydrogen-sulfide (7783064) besides 

 providing detailed information on precautions in handling and storage, 

 leak detection, disposal of leaking cylinders, materials of construction, 

 cylinder and valve description, and safety devices. Recommended controls 

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 include automatic pressure regulator, manual controls, flowmeters, and 

 shipping regulations. Commercial preparations, molecular structure, and 

 chemical properties of hydrogen-sulfide are discussed. Tables are given 

 for thermodynamic and detailed physical data. 

59 

TITLE: 

 Nasal lesions in rats exposed to hydrogen sulfide for four hours. 

AUTHORS: 

 Lopez A 

 Prior M 

 Yong S 

 Lillie L 

 Lefebvre M 

SOURCE: 

 Am J Vet Res. 1988, Jul; 49(7):1107-11. [American journal of veterinary 

 research] 

ABSTRACT: 

 Fischer-344 rats were exposed for 4 hours to 0, 14, 280, or 560 mg of 

 hydrogen sulfide.m-3 and killed 1, 18, or 44 hours later. We evaluated the 

 nasal epithelial cells and determined the anatomic distribution of 

 lesions. Inhalation of 560 mg of hydrogen sulfide.m-3 induced necrosis and 

 exfoliation of respiratory and olfactory mucosal cells, but not squamous 

 epithelial cells. The anatomic distribution of lesions was midway along 

 the nasal passages involving nasal and maxillary conchae, but not 

 ethmoidal conchae. Injured respiratory mucosa repaired rapidly, whereas 

 olfactory mucosa continued to exfoliate at 44 hours after exposure. 

60 

TITLE: 

 Effects of 10-ppm hydrogen sulfide inhalation on pulmonary function in 

 healthy men and women 

AUTHORS: 

 Bhambhani Y 

 Burnham R 

 Snydmiller G 

 MacLean I 

 Lovlin R 

SOURCE: 

 Journal of Occupational and Environmental Medicine Oct. 1996, Vol.38, 

 No.10, p.1012-1017. 20 ref. 

ABSTRACT: 

 A group of 9 men and 10 women inhaled medical air or 10ppm hydrogen 

 sulfide for 15min during cycle exercise at 50% of their maximal aerobic 

 power. Routine pulmonary function tests were administered at rest and 

 immediately after the two exposure conditions. No significant changes in 

 pulmonary function variables were observed and none of the subjects 

 experienced any signs or symptoms as a result of hydrogen sulfide 

 exposure. Oral inhalation of 10ppm hydrogen sulfide at an elevated 

 metabolic and ventilation rate does not significantly alter pulmonary 

 function in healthy men and women. 

61 

TITLE: 

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 Persistent cognitive and motor deficits following acute hydrogen sulphide 

 poisoning. 

AUTHORS: 

 Schneider JS 

 Tobe EH 

 Mozley PD Jr 

 Barniskis L 

 Lidsky TI 

SOURCE: 

 Occup Med (Lond). 1998, May; 48(4):255-60. [Occupational medicine (Oxford, 

 England)] 

ABSTRACT: 

 This case study describes the long-term after-effects of hydrogen sulphide 

 exposure in a previously health 27-year-old male. Upon hospital admission 

 the patient had a Glasgow Coma Score (CGS) of 3; with emergency treatment 

 including hyperbaric oxygen treatments, he progressed to a GCS of 15 on 

 day 7. Although both CT and MRI scans were unremarkable, PET using F-18 

 deoxyglucose administered 3 years after the accident showed abnormally 

 decreased metabolism bilaterally in the temporal and inferior parietal 

 lobes as well as the left thalamus. Uptake in the striatum was 

 heterogeneous and abnormal. A cerebral perfusion study using SPECT 

 performed 3.5 years after the accident revealed bilaterally decreased flow 

 in the putamen but no cortical abnormalities. Neuropsychological and 

 neurofunctional testing revealed the following impairments: microsmia, 

 psychomotor slowing, extrapyramidal signs and deficits in memory and 

 executive/planning functioning. These findings are discussed in the 

 context of hydrogen sulphide's known mechanisms of toxicity and the 

 functions of the basal ganglia. 

62 

TITLE: 

 Low dose hydrogen sulfide and its effects on the dendritic arborization of 

 developing cerebellar Purkinje cells. 

AUTHORS: 

 Hannah RS 

 Bennington R 

 Roth SH 

SOURCE: 

 Abstr Soc Neurosci 1989;15(2):1021 

ABSTRACT: 

 Hydrogen sulfide (H2S) is an environmental pollutant which can produce 

 severe effects on the adult CNS; however, little is known as to its 

 effects on the developing CNS. Pregnant rats (Sprague-Dawley) were exposed 

 to either 20 pmm or 50 pmm H2S for 7 hours per day in an environment 

 chamber from Day 7 postcoitus until Day 21 postnatal. Controls were 

 similarly treated including placement in an environmental chamber flushed 

 with room air. On Day 21 postnatal, representative pups from each litter 

 were euthanized, the cerebella removed and processed for Golgi staining. 

 Ten complete Purkinje cells were selected from each group and analysed, 

 using vertex analysis (Berry & Finn, Proc. R. Soc. Lond. B. 221:321, 

 1984). At both exposure concentrations, there was a significant increase 

 in vertex path length suggesting an increased distance between each new 

 generation of branches. New growth occurred toward the pial surface and 

 internally but was restricted laterally. The treated cells exhibited an 

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 unusually high non-random growth pattern. In summary, both treatments 

 produced significant growth changes in the dendritic arborization. 

63 

TITLE: 

 Severe hydrogen sulfide exposure in a working adolescent. 

AUTHORS: 

 Nikkanen HE 

 Burns MM 

SOURCE: 

 Pediatrics. 2004, Apr; 113(4):927-9. [Pediatrics] 

ABSTRACT: 

 We describe an occupational exposure to hydrogen sulfide gas in a 

 16-year-old boy. While cleaning the reoxygenation tank of a fish hatchery, 

 he and an adult supervisor lost consciousness. The adult died, and the 

 adolescent regained consciousness briefly when emergency medical services 

 personnel administered oxygen. At a local emergency department, he was 

 intubated for respiratory distress. He was transferred to a tertiary care 

 facility for additional management and, over the next 2 weeks, had a 

 recovery to normal function. Hydrogen sulfide is a colorless, malodorous 

 gas that results from the decay of organic material. It is a byproduct of 

 industry and agriculture. The mechanism of its toxicity is related 

 primarily to inhibition of oxidative phosphorylation, which causes a 

 decrease in available cellular energy. Although there is some anecdotal 

 evidence to suggest that the early use of hyperbaric oxygen is beneficial, 

 supportive care remains the mainstay of therapy. This report highlights 

 the sources of exposure, management, and need for more stringent 

 application of safety regulations in industries in which adolescents are 

 employed. 

64 

TITLE: 

 Pharmacokinetic-pharmacodynamic models for categorical toxicity data. 

AUTHORS: 

 Diack C 

 Bois FY 

SOURCE: 

 Regul Toxicol Pharmacol. 2005, Feb; 41(1):55-65. [Regulatory toxicology 

 and pharmacology : RTP] 

ABSTRACT: 

 We propose a pharmacokinetic-pharmacodynamic (PK/PD) model (with possibly 

 different choices for the PD link) for categorical toxicity data analysis. 

 This is extension of the one-comportment model that applies to toxic 

 endpoints categorised by grades (e.g., benign, mild, severe, and very 

 severe). The model assumes that the area under the curve (AUC) of the 

 internal quantity of the chemical substance is the critical dose-metric 

 that drives the acute toxic phenomenon. That model handles time-varying 

 concentrations and takes into account follow-up time, i.e., time at which 

 effects are observed. Moreover the model bridges mechanistically based 

 dose-response models and standard dose-response models, retaining the 

 advantages of both. We use Markov chain-Monte Carlo (MCMC) simulations to 

 fit the model to mortality data for mice exposed to chlorine, rats exposed 

 to ammonia, and categorical data (different severity levels) from acute 

 exposures of rats and humans to hydrogen sulfide. 

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65 

TITLE: 

 Physiological and biochemical effects of acute exposure of fish to 

 hydrogen sulfide. 

AUTHORS: 

 Torrans EL 

 Clemens HP 

SOURCE: 

 Comp Biochem Physiol C. 1982; 71(2):183-90. [Comparative biochemistry and 

 physiology. C, Comparative pharmacology and toxicology] 

ABSTRACT: 

 1. Exposure of channel catfish to 0.5 mg/l H2S at 20 degrees C resulted in 

 hyperpnea, followed by apnea, and finally respiratory arrest. 2. Catfish 

 brain cytochrome oxidase activity was inhibited in vitro 18% by 10(-7) M 

 H2S, 64% by 10(-6) M H2S, and 100% by 10(-4) M H2S. 3. When channel 

 catfish were exposed to 0.1 mg/l H2S at 20 degrees C for 30 min, the 

 cytochrome oxidase activity of the brain was inhibited 40% and that of the 

 gill was inhibited 74%, while blood lactate rose from 11.6 to 38.1 mg/100 

 ml. 4. Catfish with nitrite-induced methemoglobinemia showed less 

 inhibition of brain and gill cytochrome oxidase when exposed to hydrogen 

 sulfide than did control fish. 5. Sulfide-inhibited brain cytochrome 

 oxidase recovered from a 50% inhibition to control levels in channel 

 catfish after 6 hr in freshwater at 10 degrees C. 6. Management practices 

 are recommended which may help the commercial fish farmer alleviate the 

 problem of the toxicity of sulfide to fish during harvest operations. 

66 

TITLE: 

 Effects of repeated exposures of hydrogen sulphide on rat hippocampal EEG. 

AUTHORS: 

 Skrajny B 

 Reiffenstein RJ 

 Sainsbury RS 

 Roth SH 

SOURCE: 

 Toxicol Lett. 1996, Jan; 84(1):43-53. [Toxicology letters] 

ABSTRACT: 

 Exposure to high levels of hydrogen sulphide (H2S) in humans has been 

 associated with a number of respiratory and neurological symptoms. Acute 

 toxicity following exposure to high concentrations is well-documented, 

 however, there is little scientific information concerning the effects of 

 exposure to low concentrations. The effects of low levels of H2S on 

 electroencephalographic (EEG) activity in the hippocampus and neocortex 

 were investigated on the freely moving rat (Sprague-Dawley). Hippocampal 

 electrodes were implanted in the dentate gyrus (DG) and CA1 region. 

 Activity was recorded for 10 min just prior to H2S exposure in the 

 presence of air (pre-exposure). Rats were exposed to H2S (25, 50, 75, or 

 100 ppm) for 3 h/day; data was collected during the final 10 min of each 

 exposure. The total power of hippocampal theta activity increased in a 

 concentration-dependent manner in both DG and CA1; repeated exposures for 

 5 consecutive days resulted in a cumulative effect that required 2 weeks 

 for complete recovery. The effects were found to be highly significant at 

 all concentrations within subjects. Neocortical EEG and LIA (Large 

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 Amplitude Irregular Activity) were unaffected. The results demonstrate 

 that repeated exposure to low levels of H2S can produce cumulative changes 

 in hippocampal function and suggest selectivity of action of this 

 toxicant. 

67 

TITLE: 

 Peracute toxic effects of inhaled hydrogen sulfide and injected sodium 

 hydrosulfide on the lungs of rats. 

AUTHORS: 

 Lopez A 

 Prior MG 

 Reiffenstein RJ 

 Goodwin LR 

SOURCE: 

 Fundam Appl Toxicol. 1989, Feb; 12(2):367-73. [Fundamental and applied 

 toxicology : official journal of the Society of Toxicology] 

ABSTRACT: 

 This study was designed to test whether intraperitoneally injected sodium 

 hydrosulfide (NaHS) would mimic the pulmonary alterations induced by 

 lethal peracute exposure to an atmosphere containing hydrogen sulfide. 

 Groups of five Sprague-Dawley rats were exposed to an atmosphere of either 

 2317.6 +/- 547.3 mg m-3 H2S (H2S group) or no H2S (air group), or were 

 injected intraperitoneally with a solution containing 30 mg kg-1 sodium 

 hydrosulfide (NaHS group) or saline solution (vehicle control). Rats of 

 the air and saline groups were killed by cervical dislocation. All rats 

 exposed to H2S or injected with NaHS died within 3 min; however, only rats 

 exposed to H2S showed severe respiratory distress in the agonic phase 

 preceding death. In addition, rats in the H2S group had a notable 

 discharge of serous fluid from the mouth and nostrils. At necropsy, all 

 rats in the H2S group had gross and histologic evidence of pulmonary edema 

 characterized by massive extravasation of eosinophilic fluid into the 

 bronchoalveolar space. In contrast, the lungs of rats injected with NaHS 

 or saline or exposed to air were unaffected. It was concluded that the 

 edematogenic effect of H2S in the lungs cannot be reproduced by injection 

 of NaHS. The severity of lung edema induced by a peracute exposure to H2S 

 was extensive enough to account for death. 

68 

TITLE: 

 Detoxification of hydrogen sulfide and methanethiol in the cecal mucosa. 

AUTHORS: 

 Levitt MD 

 Furne J 

 Springfield J 

 Suarez F 

 DeMaster E 

SOURCE: 

 J Clin Invest. 1999, Oct; 104(8):1107-14. [The Journal of clinical 

 investigation] 

ABSTRACT: 

 Colonic bacteria liberate large quantities of the highly toxic gases 

 hydrogen sulfide (H(2)S) and methanethiol (CH(3)SH). The colonic mucosa 

 presumably has an efficient means of detoxifying these compounds, which is 

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 thought to occur through methylation of H(2)S to CH(3)SH and CH(3)SH to 

 dimethylsulfide (CH(3)SCH(3)). We investigated this detoxification pathway 

 by incubating rat cecal mucosal homogenates with gas containing H(2)S, 

 CH(3)SH, or CH(3)SCH(3). Neither CH(3)SH nor CH(3)SCH(3) was produced 

 during H(2)S catabolism, whereas catabolism of CH(3)SH liberated H(2)S but 

 not CH(3)SCH(3). Thus, H(2)S and CH(3)SH are not detoxified by methylation 

 to CH(3)SCH(3). Rather, CH(3)SH is demethylated to H(2)S, and H(2)S is 

 converted to nonvolatile metabolites. HPLC analysis of the homogenate 

 showed the metabolite to be primarily thiosulfate. Analysis of cecal 

 venous blood obtained after intracecal instillation of H(2)(35)S revealed 

 that virtually all absorbed H(2)S had been oxidized to thiosulfate. The 

 oxidation rate of H(2)S by colonic mucosa was 10,000 times greater than 

 the reported methylation rate. Conversion to thiosulfate appears to be the 

 mechanism whereby the cecal mucosa protects itself from the injurious 

 effects of H(2)S and CH(3)SH, and defects in this detoxification possibly 

 could play a role in colonic diseases such as ulcerative colitis. 

69 

TITLE: 

 Effects of hydrogen sulfide exposure on lung mitochondrial respiratory 

 chain enzymes in rats. 

AUTHORS: 

 Khan AA 

 Schuler MM 

 Prior MG 

 Yong S 

 Coppock RW 

 Florence LZ 

 Lillie LE 

SOURCE: 

 Toxicol Appl Pharmacol. 1990, May; 103(3):482-90. [Toxicology and applied 

 pharmacology] 

ABSTRACT: 

 Fischer-344 rats were exposed for 4 hr to various concentrations of 

 hydrogen sulfide (H2S) gas and killed either immediately or at 1, 24, or 

 48 hr after exposure. Mitochondrial fractions from lung tissues were 

 assayed for the activities of respiratory chain enzymes. Exposure of rats 

 to a low concentration (10 ppm) of H2S caused no significant changes in 

 the activities of lung mitochondrial enzymes. However, exposure to 

 sublethal concentrations of H2S (50-400 ppm) produced marked and highly 

 significant depressions in the activities of cytochrome c oxidase and 

 succinate oxidase complexes of the respiratory chain. The inhibition of 

 cytochrome c oxidase activity in lungs was most severe (greater than 90%) 

 in rats that died from acute exposure to greater than 500 ppm H2S. In rats 

 exposed to 200 and 400 ppm H2S, a marked recovery in cytochrome c oxidase 

 activity of lungs was observed at 24 and 48 hr postexposure. Studies in 

 vitro with rat lung mitochondria showed that low concentrations of sulfide 

 also caused a similar and selective inhibition of cytochrome c oxidase 

 activity. This effect was reversed upon removal of sulfide either by 

 washing or by oxidation with methemoglobin. The nature of sulfide 

 inhibition of cytochrome c oxidase was noncompetitive with respect to 

 ferrocytochrome c. Because the activities of NADH-cytochrome c reductase 

 and succinate-cytochrome c reductase were not significantly altered by H2S 

 exposure and in vitro treatments with low concentrations of sulfide, it is 

 concluded that under physiological conditions H2S would block the 

 respiratory chain primarily by inhibiting cytochrome c oxidase. Such a 

 biochemical impairment would lead to functional (histotoxic) hypoxia in 

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 the lung tissues. 

70 

TITLE: 

 A relationship between hydrogen sulfide exposure and taurine levels in 

 maternal rats. 

AUTHORS: 

 Hannah RS 

 Bennington R 

 Roth SH 

SOURCE: 

 Proc West Pharmacol Soc. 1990; 33:177-9. [Proceedings of the Western 

 Pharmacology Society] 

71 

TITLE: 

 Hydrogen sulfide induces direct radical-associated DNA damage. 

AUTHORS: 

 Attene-Ramos MS 

 Wagner ED 

 Gaskins HR 

 Plewa MJ 

SOURCE: 

 Mol Cancer Res. 2007, May; 5(5):455-9. [Molecular cancer research : MCR] 

ABSTRACT: 

 Hydrogen sulfide (H(2)S) is produced by indigenous sulfate-reducing 

 bacteria in the large intestine and represents an environmental insult to 

 the colonic epithelium. Clinical studies have linked the presence of 

 either sulfate-reducing bacteria or H(2)S in the colon with chronic 

 disorders such as ulcerative colitis and colorectal cancer, although at 

 this point, the evidence is circumstantial and underlying mechanisms 

 remain undefined. We showed previously that sulfide at concentrations 

 similar to those found in the human colon induced genomic DNA damage in 

 mammalian cells. The present study addressed the nature of the DNA damage 

 by determining if sulfide is directly genotoxic or if genotoxicity 

 requires cellular metabolism. We also questioned if sulfide genotoxicity 

 is mediated by free radicals and if DNA base oxidation is involved. Naked 

 nuclei from untreated Chinese hamster ovary cells were treated with 

 sulfide; DNA damage was induced by concentrations as low as 1 micromol/L. 

 This damage was effectively quenched by cotreatment with 

 butylhydroxyanisole. Furthermore, sulfide treatment increased the number 

 of oxidized bases recognized by formamidopyrimidine [fapy]-DNA 

 glycosylase. These results confirm the genotoxicity of sulfide and 

 strongly implicate that this genotoxicity is mediated by free radicals. 

 These observations highlight the possible role of sulfide as an 

 environmental insult that, given a predisposing genetic background, may 

 lead to genomic instability or the cumulative mutations characteristic of 

 colorectal cancer. 

72 

TITLE: 

 [Structural reorganization in the lining epithelium of airways and 

 respiratory areas of the lungs following exposure to hydrogen 

 sulfide-containing gas mixture] 

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AUTHORS: 

 Poliakova VS 

SOURCE: 

 Morfologiia. 2003; 124(5):20-3. [Morfologiia (Saint Petersburg, Russia)] 

ABSTRACT: 

 Structural reorganization of epithelium lining of pulmonary airways and 

 respiratory portions was studied experimentally in outbred albino rats 

 exposed to low doses (10 (g/m3) of hydrogen sulfide-containing gas mixture 

 (natural gas + air) using the methods of histoautoradiography, electron 

 microscopy and immunohistochemistry. Daily 1-hour-long exposure to gas 

 mixture for up to 14 days resulted in moderate stimulating effect on 

 specialized cells of bronchial epithelium. Following more protracted 

 exposure to gas mixture (up to 1 month), the process demonstrated the 

 involvement of protective mechanisms operating not only at the 

 subcellular, but also at the tissue level, that was revealed by activation 

 of DNA-synthesizing capacity of bronchial epithelial cells. Secretory 

 Clara cells serving as the outpost of respiratory portion, were found to 

 be significantly activated. The reversibility of the structural 

 modifications in the pulmonary epithelia was demonstrated by the study of 

 the organ 1 week following the discontinuation of a 1-month-long exposure 

 to gas mixture. 

73 

TITLE: 

 [Changes in respiration and blood circulation during the inhalation of air 

 mixtures with lethal and sublethal concentrations of hydrogen 

 sulfide-containing natural gas] 

AUTHORS: 

 Trizno NN 

 Velikanov EB 

 Tarakanov IA 

 Safonov VA 

SOURCE: 

 Biull Eksp Biol Med. 1993, Jul; 116(7):25-9. [Biulleten' eksperimental'noi 

 biologii i meditsiny] 

ABSTRACT: 

 Experiments in pentobarbital-anesthetized cats of both sexes showed that 

 upon spontaneous inhalation of hydrogen sulphide-containing gas mixtures 

 (600 mg/m3) respiratory and circulatory changes occur within 10-15 min 

 (30% of animals) and continued to 20-25 min (100% of animals) leading to 

 severe respiratory disturbances (apneusis, gasping) abrupt decrease of 

 mean systemic arterial pressure and decreased cardiac output, i.e., the 

 changes of the type of peripheral collapse. 

74 

TITLE: 

 Hydrogen sulfide poisoning: Clarification of some controversial issues 

AUTHORS: 

 Milby TH 

 Baselt RC 

SOURCE: 

 American Journal of Industrial Medicine Feb. 1999, Vol.35, No.2, 

 p.192-195. 34 ref. 

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ABSTRACT: 

 Data on the toxicity of hydrogen sulfide are reviewed. It is concluded 

 that: certain neurotoxic effects of exposure are probably due to a direct 

 toxic effect on the brain, while others are almost certainly a result of 

 hypoxia secondary to H[2]S-induced respiratory insufficiency; pulmonary 

 oedema is a common consequence of poisoning and there is suggestive 

 evidence of hyperactive airway responses in some individuals following 

 brief H[2]S-induced unconsciousness (knockdown); criteria for acceptable 

 community levels are very different than those governing occupational 

 standards; urinary thiosulfate determinations can be useful for monitoring 

 occupational exposure; and determination of sulfide ion concentrations in 

 blood or major organs can be useful in corroborating a diagnosis of fatal 

 H[2]S toxicity, but there are many pit-falls in collecting, storing, and 

 analyzing tissue and fluid samples. Topics: acute poisoning; hydrogen 

 sulfide; determination in blood; determination in urine; exposure tests; 

 hypoxia; limitation of exposure; lung diseases; neurotoxic effects; 

 pulmonary function; pulmonary oedema; thiosulfates; urine monitoring. 

75 

TITLE: 

 Physiological roles of hydrogen sulfide: synaptic modulation, 

 neuroprotection, and smooth muscle relaxation. 

AUTHORS: 

 Kimura H 

 Nagai Y 

 Umemura K 

 Kimura Y 

SOURCE: 

 Antioxid Redox Signal. 2005 May-Jun; 7(5-6):795-803. [Antioxidants & redox 

 signaling] 

ABSTRACT: 

 Nearly 300 years have passed since the first description of the toxicity 

 of hydrogen sulfide (H(2)S) in 1713. Although many studies have been 

 devoted to its toxicity, very little attention has been paid to 

 understanding its normal physiological function. Relatively high 

 concentrations of endogenous H(2)S, however, have recently been discovered 

 in animal tissues, and its possible function as a biological messenger has 

 been proposed. H(2)S enhances the activity of N-methyl-D-aspartate 

 receptors and facilitates the induction of hippocampal longterm 

 potentiation, a synaptic model for memory. H(2)S also increases 

 intracellular concentrations of Ca(2+) in glia and induces Ca(2+) waves, 

 which mediate glial signal transmission. Based on accumulating evidence 

 for the reciprocal interactions between glia and neurons, it has been 

 suggested that glia modulate synaptic transmission. Therefore, H(2)S may 

 regulate synaptic activity by modulating the activity of both neurons and 

 glia. In addition to a role in the signal transduction, H(2)S protects 

 neurons from oxidative stress and in smooth muscle it may function as a 

 relaxant. H(2)S, the toxic gas, may therefore be used as a multifunctional 

 signaling mechanism under normal physiological conditions. 

76 

TITLE: 

 Hydrogen sulfide is a novel mediator of lipopolysaccharide-induced 

 inflammation in the mouse. 

AUTHORS: 

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 Li L 

 Bhatia M 

 Zhu YZ 

 Zhu YC 

 Ramnath RD 

 Wang ZJ 

 Anuar FB 

 Whiteman M 

 Salto-Tellez M 

 Moore PK 

SOURCE: 

 FASEB J. 2005, Jul; 19(9):1196-8. [The FASEB journal : official 

 publication of the Federation of American Societies for Experimental 

 Biology] 

ABSTRACT: 

 Hydrogen sulfide (H2S) is synthesized in the body from L-cysteine by 

 several enzymes including cystathionine-gamma-lyase (CSE). To date, there 

 is little information about the potential role of H2S in inflammation. We 

 have now investigated the part played by H2S in endotoxin-induced 

 inflammation in the mouse. E. coli lipopolysaccharide (LPS) administration 

 produced a dose (10 and 20 mg/kg ip)- and time (6 and 24 h)-dependent 

 increase in plasma H2S concentration. LPS (10 mg/kg ip, 6 h) increased 

 plasma H2S concentration from 34.1 +/- 0.7 microM to 40.9 +/- 0.6 microM 

 (n=6, P < 0.05) while H2S formation from added L-cysteine was increased 

 in both liver and kidney. CSE gene expression was also increased in both 

 liver (94.2+/-2.7%, n=6, P < 0.05) and kidney (77.5+/-3.2%, n=6, 

 P < 0.05). LPS injection also elevated lung (148.2+/-2.6%, n=6, 

 P < 0.05) and kidney (78.8+/-8.2%, n=6, P < 0.05) myeloperoxidase (MPO, 

 a marker of tissue neutrophil infiltration) activity alongside 

 histological evidence of lung, liver, and kidney tissue inflammatory 

 damage. Plasma nitrate/nitrite (NOx) concentration was additionally 

 elevated in a time- and dose-dependent manner in LPS-injected animals. To 

 examine directly the possible proinflammatory effect of H2S, mice were 

 administered sodium hydrosulfide (H2S donor drug, 14 micromol/kg ip) that 

 resulted in marked histological signs of lung inflammation, increased lung 

 and liver MPO activity, and raised plasma TNF-alpha concentration 

 (4.6+/-1.4 ng/ml, n=6). In contrast, DL-propargylglycine (CSE inhibitor, 

 50 mg/kg ip), exhibited marked anti-inflammatory activity as evidenced by 

 reduced lung and liver MPO activity, and ameliorated lung and liver tissue 

 damage. In separate experiments, we also detected significantly higher 

 (150.5+/-43.7 microM c.f. 43.8+/-5.1 microM, n=5, P < 0.05) plasma H2S 

 levels in humans with septic shock. These findings suggest that H2S 

 exhibits proinflammatory activity in endotoxic shock and suggest a new 

 approach to the development of novel drugs for this condition. 

77 

TITLE: 

 Cytochrome oxidase inhibition induced by acute hydrogen sulfide 

 inhalation: correlation with tissue sulfide concentrations in the rat 

 brain, liver, lung, and nasal epithelium. 

AUTHORS: 

 Dorman DC 

 Moulin FJ 

 McManus BE 

 Mahle KC 

 James RA 

 Struve MF 

Page 45 of 245

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SOURCE: 

 Toxicol Sci. 2002, Jan; 65(1):18-25. [Toxicological sciences : an official 

 journal of the Society of Toxicology] 

ABSTRACT: 

 Hydrogen sulfide (H2S) is an important brain, lung, and nose toxicant. 

 Inhibition of cytochrome oxidase is the primary biochemical effect 

 associated with lethal H2S exposure. The objective of this study was to 

 evaluate the relationship between the concentration of sulfide and 

 cytochrome oxidase activity in target tissues following acute exposure to 

 sublethal concentrations of inhaled H2S. Hindbrain, lung, liver, and nasal 

 (olfactory and respiratory epithelial) cytochrome oxidase activity and 

 sulfide concentrations were determined in adult male CD rats immediately 

 after a 3-h exposure to H2S (10, 30, 80, 200, and 400 ppm). We also 

 determined lung sulfide and sulfide metabolite concentrations at 0, 1.5, 

 3, 3.25, 3.5, 4, 5, and 7 h after the start of a 3-h H2S exposure to 400 

 ppm. Lung sulfide concentrations increased during H2S exposure and rapidly 

 returned to endogenous levels within 15 min after the cessation of the 

 400-ppm exposure. Lung sulfide metabolite concentrations were transiently 

 increased immediately after the end of the 3-h H2S exposure. Decreased 

 cytochrome oxidase activity was observed in the olfactory epithelium 

 following exposure to > or = 30 ppm H2S. Increased olfactory epithelial 

 sulfide concentrations were observed following exposure to 400 ppm H2S. 

 Hindbrain and nasal respiratory epithelial sulfide concentrations were 

 unaffected by acute H2S exposure. Nasal respiratory epithelial cytochrome 

 oxidase activity was reduced following acute exposure to > or = 30 ppm 

 H2S. Liver sulfide concentrations were increased following exposure to > 

 or = 200 ppm H2S and cytochrome oxidase activity was increased following 

 inhalation exposure to > or = 10 ppm H2S. Our results suggest that 

 cytochrome oxidase inhibition is a sensitive biomarker of H2S exposure in 

 target tissues, and sulfide concentrations are unlikely to increase 

 postexposure in the brain, lung, or nose following a single 3-h exposure 

 to < or = 30 ppm H2S. 

78 

TITLE: 

 [Ultrastructure of the cerebral cortex after exposure to gas containing 

 hydrogen sulfide] 

AUTHORS: 

 Solnyshkova TG 

 Shakhlamov VA 

 Volodina EP 

SOURCE: 

 Morfologiia. 2002; 122(6):11-3. [Morfologiia (Saint Petersburg, Russia)] 

ABSTRACT: 

 In experimental animals exposed to hydrogen sulfide-containing gas, 

 electron microscopic study of cerebral cortex indicated the variability in 

 the reaction of layer V neurons: along with neurons demonstrating 

 irreversible damage, some cells with single signs of alteration were 

 found. The reaction of different types of glial cells was also 

 non-uniform. During initial 12 h following single exposure, 

 oligodendrocytes showed the signs of intensified endocytosis. Following 

 repeated exposures, severe destructive changes were found in myelinated 

 nerve fibers and in single neurons, in which the karyolysis and 

 cytoplasmic swelling were observed. 

Page 46 of 245

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79 

TITLE: 

 Inhibition of hydrogen sulfide generation contributes to gastric injury 

 caused by anti-inflammatory nonsteroidal drugs. 

AUTHORS: 

 Fiorucci S 

 Antonelli E 

 Distrutti E 

 Rizzo G 

 Mencarelli A 

 Orlandi S 

 Zanardo R 

 Renga B 

 Di Sante M 

 Morelli A 

 Cirino G 

 Wallace JL 

SOURCE: 

 Gastroenterology. 2005, Oct; 129(4):1210-24. [Gastroenterology] 

ABSTRACT: 

 BACKGROUND & AIMS: Hydrogen sulfide (H(2)S), an endogenous gaseous 

 mediator that causes vasodilation, is generated in mammalian tissues by 

 cystathionine beta-synthase (CBS) and cystathionine-gamma-lyase (CSE). 

 Here, we have investigated the role of H(2)S in a rodent model of 

 nonsteroidal anti-inflammatory drug (NSAID) gastropathy. METHODS: Rats 

 were given acetyl salycilic acid (ASA) or an NSAID alone or in combination 

 with NaHS, an H(2)S donor, and killed 3 hours later. Gastric blood flow 

 was measured by laser-Doppler flowmetry, whereas intravital microscopy was 

 used to quantify adhesion of leukocytes to mesenteric postcapillary 

 endothelium. RESULTS: At a dose of 100 micromol/kg, NaHS attenuated by 

 60%-70% the gastric mucosal injury, and tumor necrosis factor (TNF)-alpha, 

 intercellular adhesion molecule (ICAM)-1, and lymphocyte 

 function-associated antigen (LFA)-1 mRNA up-regulation induced by NSAIDs 

 (P < .05) NaHS administration prevented the associated reduction of 

 gastric mucosal blood flow (P < .05) and reduced ASA-induced leukocyte 

 adherence in mesenteric venules. NaHS did not affect suppression of 

 prostaglandin E(2) (PGE(2)) synthesis by NSAIDs. Glibenclamide, a K(ATP) 

 channel inhibitor, and DL-propargylglycine, a CSE inhibitor, exacerbated, 

 whereas pinacidil, a K(ATP) opener, attenuated gastric injury caused by 

 ASA. Exposure to NSAIDs reduced H(2)S formation and CSE expression (mRNA 

 and protein) and activity by 60%-70%. By promoter deletion and mutation 

 analysis, an Sp1 consensus site was identified in the CSE promoter. 

 Exposure to NSAIDs inhibits Sp1 binding to its promoter and abrogates CSE 

 expression in HEK-293 cells transfected with a vector containing the core 

 CSE promoter. Exposure to NSAIDs inhibits Sp1 and ERK phosphorylation. 

 CONCLUSIONS: These data establish a physiologic role for H(2)S in 

 regulating the gastric microcirculation and identify CSE as a novel target 

 for ASA/NSAIDs. 

80 

TITLE: 

 Olfactory mucosal necrosis in male CD rats following acute inhalation 

 exposure to hydrogen sulfide: reversibility and the possible role of 

 regional metabolism. 

AUTHORS: 

 Brenneman KA 

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 Meleason DF 

 Sar M 

 Marshall MW 

 James RA 

 Gross EA 

 Martin JT 

 Dorman DC 

SOURCE: 

 Toxicol Pathol. 2002 Mar-Apr; 30(2):200-8. [Toxicologic pathology] 

ABSTRACT: 

 Hydrogen sulfide (H2S) is a potent inhibitor of cytochrome oxidase (CO) 

 and is associated with dysosmia and anosmia in humans and nasal lesions in 

 exposed rodents. An improved understanding of the pathogenesis of these 

 lesions is needed to determine their toxicological relevance. We exposed 

 10-week-old male CD rats to 0, 30, 80, 200, or 400 ppm H2S for 3 hours/day 

 for 1 or 5 days consecutively. The nose was histologically examined 24 

 hours after H2S exposure, and lesion recovery was assessed at 2 and 6 

 weeks following the 5-day exposure. A single 3-hour exposure to > or = 80 

 ppm H2S resulted in regeneration of the respiratory mucosa and full 

 thickness necrosis of the olfactory mucosa localized to the ventral and 

 dorsal meatus, respectively. Repeated exposure to the same concentrations 

 caused necrosis of the olfactory mucosa with early mucosal regeneration 

 that extended from the dorsal medial meatus to the caudal regions of the 

 ethmoid recess. Acute exposure to 400 ppm H2S induced severe mitochondrial 

 swelling in sustentacular cells and olfactory neurons, which progressed to 

 olfactory epithelial necrosis and sloughing. CO immunoreactive cells were 

 more frequently observed in regions of the olfactory mucosa commonly 

 affected by H2S than in regions that were not. These findings demonstrate 

 that acute exposure to >80 ppm H2S resulted in reversible lesions in the 

 respiratory and olfactory mucosae of the CD rat and that CO 

 immunoreactivity may be a susceptibility factor for H2S-induced olfactory 

 toxicity in the rat. 

81 

TITLE: 

 Incorporation of tissue reaction kinetics in a computational fluid 

 dynamics model for nasal extraction of inhaled hydrogen sulfide in rats. 

AUTHORS: 

 Schroeter JD 

 Kimbell JS 

 Bonner AM 

 Roberts KC 

 Andersen ME 

 Dorman DC 

SOURCE: 

 Toxicol Sci. 2006, Mar; 90(1):198-207. [Toxicological sciences : an 

 official journal of the Society of Toxicology] 

ABSTRACT: 

 Rodents exposed to hydrogen sulfide (H2S) develop olfactory neuronal loss. 

 This lesion has been used by the risk assessment community to develop 

 occupational and environmental exposure standards. A correlation between 

 lesion locations and areas of high H2S flux to airway walls has been 

 previously demonstrated, but a quantitative dose assessment is needed to 

 extrapolate dose at lesion sites to humans. In this study, nasal 

 extraction (NE) of 10, 80, and 200 ppm H2S was measured in the isolated 

Page 48 of 245

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 upper respiratory tract of anesthetized rats under constant unidirectional 

 inspiratory flow rates of 75, 150, and 300 ml/min. NE was dependent on 

 inspired H2S concentration and air flow rate: increased NE was observed 

 when H2S exposure concentrations or inspiratory air flow rates were low. 

 An anatomically accurate, three-dimensional computational fluid dynamics 

 (CFD) model of rat nasal passages was used to predict NE of inhaled H2S. 

 To account for the observed dependence of NE on H2S exposure 

 concentration, the boundary condition used at airway walls incorporated 

 first-order and saturable kinetics in nasal tissue to govern mass flux at 

 the air:tissue interface. Since the kinetic parameters cannot be obtained 

 using the CFD model, they were estimated independently by fitting a 

 well-mixed, two-compartment pharmacokinetic (PK) model to the NE data. 

 Predicted extraction values using this PK-motivated CFD approach were in 

 good agreement with the experimental measurements. The CFD model provides 

 estimates of localized H2S flux to airway walls and can be used to 

 calibrate lesion sites by dose. 

82 

TITLE: 

 Hydrogen sulphide. 

AUTHORS: 

 Guidotti TL 

SOURCE: 

 Occup Med (Lond). 1996, Oct; 46(5):367-71. [Occupational medicine (Oxford, 

 England)] 

ABSTRACT: 

 Hydrogen sulphide (H2S) is the primary chemical hazard in natural gas 

 production in 'sour' gas fields. It is also a hazard in sewage treatment 

 and manure-containment operations, construction in wetlands, pelt 

 processing, certain types of pulp and paper production, and any situation 

 in which organic material decays or inorganic sulphides exist under 

 reducing conditions. H2S dissociates into free sulphide in the 

 circulation. Sulphide binds to many macromolecules, among them cytochrome 

 oxidase. Although this is undoubtedly an important mechanism of toxicity 

 due to H2S, there may be others H2S provides little opportunity for escape 

 at high concentrations because of the olfactory paralysis it causes, the 

 steep exposure-response relationships, and the characteristically sudden 

 loss of consciousness it can cause which is colloquially termed 

 'knockdown.' Other effects may include mucosal irritation, which is 

 associated at lower concentrations with a keratoconjunctivitis called 'gas 

 eye' and at higher concentrations with risk of pulmonary oedema. Chronic 

 central nervous system sequelae may possibly follow repeated knockdowns: 

 this is controversial and the primary effects of H2S may be confounded by 

 anoxia or head trauma. Treatment is currently empirical, with a 

 combination of nitrite and hyperbaric oxygen preferred. The treatment 

 regimen is not ideal and carries some risk. 

83 

TITLE: 

 Low concentrations of hydrogen sulphide alter monoamine levels in the 

 developing rat central nervous system. 

AUTHORS: 

 Skrajny B 

 Hannah RS 

 Roth SH 

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SOURCE: 

 Can J Physiol Pharmacol. 1992, Nov; 70(11):1515-8. [Canadian journal of 

 physiology and pharmacology] 

ABSTRACT: 

 The central nervous system is one of the primary target organs for 

 hydrogen sulphide (H2S) toxicity; however, there are limited data on the 

 neurotoxic effects of low-dose chronic exposure on the developing nervous 

 system. Levels of serotonin and norepinephrine in the developing rat 

 cerebellum and frontal cortex were determined following chronic exposure 

 to 20 and 75 ppm H2S during perinatal development. Both monoamines were 

 altered in rats exposed to 75 ppm H2S compared with controls; serotonin 

 levels were significantly increased at days 14 and 21 postnatal in both 

 brain regions, and norepinephrine levels were significantly increased at 

 days 7, 14, and 21 postnatal in cerebellum and at day 21 in the frontal 

 cortex. Exposure to 20 ppm H2S significantly increased the levels of 

 serotonin in the frontal cortex at day 21, whereas levels of 

 norepinephrine were significantly reduced in the frontal cortex at days 14 

 and 21, and at day 14 in the cerebellum. 

84 

TITLE: 

 On Relationships in Action Between Carbon Disulfide and Hydrogen Sulfide 

AUTHORS: 

 Bittersohl G 

SOURCE: 

 Medicina del Lavoro, Vol. 62, No. 12, pages 554-556, 15 references, 

 19711971 

ABSTRACT: 

 An hypothesis to explain the toxic mechanism of carbon-disulfide (75150) 

 is presented. Current theories concerning its toxic action are evaluated. 

 The increased severity of intoxication resulting from simultaneous 

 exposure to carbon-disulfide (7783064) is discussed. The autoxidation of 

 hydrogen-sulfide by a free radical mechanism is described. The toxicity 

 of carbon-disulfide is also suggested to result from a reaction with free 

 radicals produced when the carbon/sulfur bond is subjected to homolytic 

 cleavage. The free radical activity is attributed to high concentrations 

 of carbon-disulfide in the tissue or to initiation of a compound with high 

 free radical reactivity, such as hydrogen-sulfide. The subsequent attack 

 of these free radicals on membrane structural lipid is suggested as the 

 cause for carbon-disulfide neurointoxication. Possible reactions of free 

 radicals arising from carbon-disulfide cleavage with labile groups of 

 enzymes are discussed. The mechanism by which methionine bound 

 carbon-disulfide inactivates the adenosylmethionine is described. The 

 author concludes that additional studies are required to prove the 

 hypothesis that the toxicity of carbon-disulfide is a consequence of free 

 radical activity. 

85 

TITLE: 

 [Dynamics of decomposition processes in popular steamed sausage preserved 

 under different conditions] 

AUTHORS: 

 Libelt K 

SOURCE: 

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 Pol Arch Weter. 1984; 24(1):65-77. [Polskie archiwum weterynaryjne] 

ABSTRACT: 

 The studies were carried out to determine the dynamics of decomposition 

 processes of common sausage kept at three temperatures (4, 10 and 20 

 degrees C) for about 120 hr. Moreover, two different production sites and 

 two year's seasons as variation factors were taken into consideration. The 

 following decomposition indicators as durability standards were assumed: 

 pH values, quantitative level of ammonia and hydrogen sulfide and 

 organoleptic changes. Temperature and periods of sausage storing were the 

 factors of statistically significant variation of sausage pH as well as 

 ammonia and hydrogen sulfide quantitative levels. Significally higher 

 values of these indicators, however were found only for sausages kept at 

 20 degrees C, as compared with the sausages at 4 and 10 degrees C, between 

 which no significant differences occurred. In organoleptic evaluation of 

 sausages kept at 4 for 120 hr, the particular characteristics were on the 

 level of approved edibility; at 10 degrees C the sausages reached their 

 edibility limit, i.e. 3.0 points, after 96 hr, and at 20 degrees C the 

 time limit was 48 hr. 

86 

TITLE: 

 Evidence that hydrogen sulfide is a genotoxic agent. 

AUTHORS: 

 Attene-Ramos MS 

 Wagner ED 

 Plewa MJ 

 Gaskins HR 

SOURCE: 

 Mol Cancer Res. 2006, Jan; 4(1):9-14. [Molecular cancer research : MCR] 

ABSTRACT: 

 Hydrogen sulfide (H2S) produced by commensal sulfate-reducing bacteria, 

 which are often members of normal colonic microbiota, represents an 

 environmental insult to the intestinal epithelium potentially contributing 

 to chronic intestinal disorders that are dependent on gene-environment 

 interactions. For example, epidemiologic studies reveal either persistent 

 sulfate-reducing bacteria colonization or H2S in the gut or feces of 

 patients suffering from ulcerative colitis and colorectal cancer. However, 

 a mechanistic model that explains the connection between H2S and 

 ulcerative colitis or colorectal cancer development has not been 

 completely formulated. In this study, we examined the chronic cytotoxicity 

 of sulfide using a microplate assay and genotoxicity using the single-cell 

 gel electrophoresis (SCGE; comet assay) in Chinese hamster ovary (CHO) and 

 HT29-Cl.16E cells. Sulfide showed chronic cytotoxicity in CHO cells with a 

 %C1/2 of 368.57 micromol/L. Sulfide was not genotoxic in the standard SCGE 

 assay. However, in a modified SCGE assay in which DNA repair was 

 inhibited, a marked genotoxic effect was observed. A sulfide concentration 

 as low as 250 micromol/L (similar to that found in human colon) caused 

 significant genomic DNA damage. The HT29-Cl.16E colonocyte cell line also 

 exhibited increased genomic DNA damage as a function of Na2S concentration 

 when DNA repair was inhibited, although these cells were less sensitive to 

 sulfide than CHO cells. These data indicate that given a predisposing 

 genetic background that compromises DNA repair, H2S may lead to genomic 

 instability or the cumulative mutations found in adenomatous polyps 

 leading to colorectal cancer. 

87 

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TITLE: 

 [The action of industrial hydrogen sulfide-containing natural gas from the 

 Astrakhan deposit on the activity of the respiratory neurons] 

AUTHORS: 

 Velikanov EB 

 Safonov VA 

SOURCE: 

 Biull Eksp Biol Med. 1993, Jul; 116(7):32-4. [Biulleten' eksperimental'noi 

 biologii i meditsiny] 

ABSTRACT: 

 Experiments in chloral hydrate-anesthetized male Wistar rats showed that 

 upon switching of the animals to breathing of natural hydrogen 

 sulphide-containing gas rapid (starting from 10-15s), alterations of the 

 rate and depth of respiratory movements occurred which ended with sudden 

 and irreversible respiratory arrest. At this, the electrical activity of 

 the diaphragm disappeared, the burst activity of respiratory neurons first 

 became continuous and after that completely disappeared. The activity of 

 reticular neurons was the most prolonged one. 

88 

TITLE: 

 EXPOSURE TO HYDROGEN SULFIDE, MERCAPTANS, AND SULFUR DIOXIDE IN PULP 

 INDUSTRY 

AUTHORS: 

 Kangas J 

 Jappinen P 

 Savolainen H 

SOURCE: 

 American Industrial Hygiene Association Journal 45(12):787-790; 1984. 

ABSTRACT: 

 HMTC Worker exposure to high levels of hydrogen sulfide, sulfur dioxide, 

 and methyl mercaptan in pulp mills can be controlled with strict hygiene 

 practices. However, a major problem in controlling exposure is the 

 seasonal variation of hydrogen sulfide and methyl mercaptan vapor peaks. 

 Higher vapor concentrations are present in the winter when natural 

 ventilation is poor. The greatest concentrations are detected in chip 

 chutes and evaporation vacuum pumps. These toxic chemicals can inhibit 

 the cytochrome oxidase enzyme in the respiratory chain, hindering oxygen 

 utilization. One way to monitor exposure is to check workers with the red 

 blood cell protoporphyrin test. (13 ref.) 

89 

TITLE: 

 Association of excess sulfur intake and an increase in hydrogen sulfide 

 concentrations in the ruminal gas cap of recently weaned beef calves with 

 polioencephalomalacia. 

AUTHORS: 

 LONERAGAN GH 

 GOULD DH 

 CALLAN RJ 

 SIGURDSON CJ 

 HAMAR DW 

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SOURCE: 

 JOURNAL OF THE AMERICAN VETERINARY MEDICAL ASSOCIATION; 213 (11). 1998. 

 1599-1604. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Polioencephalomalacia (PEM) is an important 

 neurologic disease of ruminants. Pathologic concentrations of ruminal 

 hydrogen sulfide appear to be a central component in the pathogenesis of 

 sulfur-associated PEM. High concentrations of hydrogen sulfide in the 

 ruminal gas cap provide evidence for excessive sulfur intake. Thiamine 

 deficiency, lead toxicosis, and salt toxicity/water deprivation should be 

 ruled out as potential causes of PEM. All feedstuffs and water should be 

 analyzed to determine sources of excessive sulfur. 

90 

TITLE: 

 Sediment contaminants and Microtox toxicity tested in a direct contact 

 exposure test. 

AUTHORS: 

 SVENSON A 

 EDSHOLT E 

 RICKING M 

 REMBERGER M 

 ROTTORP J 

SOURCE: 

 ENVIRONMENTAL TOXICOLOGY AND WATER QUALITY; 11 (4). 1996. 293-300. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Limnic and brackish water sediments were 

 tested in a modified contact exposure bioluminescence test, the Microtox 

 test. A variety of chemical constituents were analyzed in the sediments 

 such as metals, chlorinated pesticides, and polychlorinated biphenyls. 

 Sulfur in the common elemental form and pore water hydrogen sulfide were 

 also analyzed. The measured effect in the Microtox toxicity test was 

 correlated with the various chemical parameters to determine the origin of 

 the toxic effect. Based on multivariate data analysis, a group of metals 

 including Cu, Zn, Pb, and Cd were correlated positively with the Microtox 

 toxicity tested in the direct contact test. Similarly, but to a lesser 

 extent sulfur, hydrogen sulfide, and the pesticides p,p'-DDT and p,p'-DDD 

 were also correlated. Other pesticides and all the analyzed 

 polychlorinated biphenyls were poorly, if at all, correlated with the 

 toxicity of the samples. In a comparison with the Microtox toxicity of the 

 pure compound 

91 

TITLE: 

 Acute and subchronic toxicity studies of rats exposed to vapors of methyl 

 mercaptan and other reduced-sulfur compounds. 

AUTHORS: 

 Tansy MF 

 Kendall FM 

 Fantasia J 

 Landin WE 

 Oberly R 

 Sherman W 

SOURCE: 

Page 53 of 245

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 J Toxicol Environ Health. 1981 Jul-Aug; 8(1-2):71-88. [Journal of 

 toxicology and environmental health] 

ABSTRACT: 

 Acute inhalation experiments were conducted to determine 24-h LC50 values 

 for adult Sprague-Dawley rats of both sexes exposed to vapors of methyl 

 mercaptan and other reduced-S compounds for 4 h periods. Using calculated 

 gas concentrations, the following LC50 value for each gas and combination 

 was determined: metyhl mercaptan, 675 ppm; dimethyl sulfide, 40,250 ppm; 

 dimethyl disulfide, 805 ppm; hydrogen sulfide, 444 ppm; and an equimolar 

 mixture of methyl mercaptan, dimethyl sulfide, and dimethyl disulfide, 550 

 ppm. The effects of body and tissue weights, gross metabolic performance, 

 O2 consumption, systolic blood pressure, various blood parameters, and 

 intestinal transit time associated with 3-mo exposures of young adult male 

 rats to chemically verified concentrations of 2, 17, and 57 ppm methyl 

 mercaptan vapor are summarized in this report. No mortality was 

 experienced by any group. Histopathological findings were essentially nil 

 except for microscopic suggestions of liver damage. The most readily 

 apparent phenomenon was the decrease in body weight. Average values of 

 terminal body weights for all exposed groups were lower than that for the 

 sham control group. This difference was significant in the 57 ppm group 

 and followed a statistically significant dose-related trend. 

92 

TITLE: 

 Chemical suitability of substrates for walleye egg development in the 

 lower Fox River, Wisconsin (USA). 

AUTHORS: 

 AUER MT 

 AUER NA 

SOURCE: 

 TRANS AM FISH SOC; 119 (5). 1990. 871-876. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Site suitability for egg development was 

 assessed for walleyes Stizostedion vitreum in the Fox River, Wisconsin. 

 Water chemistry at the sediment-water interface was compared with criteria 

 for walleye egg hatch success (oxygen and hydrogen sulfide) and chronci 

 toxicity (free ammonia). Reduced concentrations of dissolved oxygen and 

 elevated concentrations of ammonia-nitrogen and hydrogen sulfide occurred 

 above some sand and all soft muck substrates. The chemical oxygen demand 

 (COD) of the surficial sediments was a useful surrogate variable for 

 identifying the chemical suitability of spawning sites; locations with a 

 surficial sediment COD less than 40 mg O2/g dry weight were considered 

 suitable. A comprehensive surficial sediment survey of the lower Fox River 

 below the DePere Dam showed that optimal walleye spawning habitat 

 (gravel-cobble substrate) is rare (less than 3% of the area) and that 75% 

 of the suboptimal (sand and muck) substrate is chemically unsuitable for 

 walle 

93 

TITLE: 

 [The main principles of improving working and environmental conditions in 

 gas-processing industry] 

AUTHORS: 

 Boĭko VI 

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SOURCE: 

 Gig Tr Prof Zabol. 1990(11):5-8. [Gigiena truda i professional'nye 

 zabolevaniia] 

ABSTRACT: 

 The major hygienically unfavourable factors in gas extraction industry 

 include air contamination with natural gas components and its processing 

 products, noise overload, exceedingly high (in summer) and low (in winter) 

 temperatures at working sites. Primary health and environment related 

 preventive measures should include the introduction of the most advanced 

 techniques of purification of raw gas, exhausts into the atmosphere 

 including hydrogen sulfide, sulphur dioxide and hydrocarbons, as well as 

 further modernization of the technological equipment used with particular 

 emphasis on the hermetic properties of separate devices and pipelines. 

94 

TITLE: 

 H2S cytotoxicity mechanism involves reactive oxygen species formation and 

 mitochondrial depolarisation. 

AUTHORS: 

 Eghbal MA 

 Pennefather PS 

 O'Brien PJ 

SOURCE: 

 Toxicology. 2004, Oct 15; 203(1-3):69-76. [Toxicology] 

ABSTRACT: 

 A number of scavengers of reactive oxygen species (ROS) were found to be 

 protective against cell death induced by hydrogen sulfide (H2S) in 

 isolated hepatocytes. The H2O2 scavengers alpha-ketoglutarate and 

 pyruvate, which also act as energy substrate metabolites, were more 

 protective against H2S toxicity than lactate which is only an energy 

 substrate metabolite. All of these results suggest that H2S toxicity is 

 dependent on ROS production. We measured ROS formation directly in 

 hepatocytes using the fluorogenic dichlorofluorescin method. H2S-induced 

 ROS formation was dose dependent and pyruvate inhibited this ROS 

 production. Non-toxic concentrations of H2S enhanced the cytotoxicity of 

 H2O2 generated by glucose/glucose oxidase, which was inhibited by CYP450 

 inibitors. Furthermore, hepatocyte ROS formation induced by H2S was 

 decreased by CYP450 inhibitors cimetidine and benzylimidazole. These 

 results suggest that CYP450-dependant metabolism of H2S is responsible for 

 inducing ROS production. H2S-induced cytotoxicity was preceded by 

 mitochondrial depolarization as measured by rhodamine 123 fluorescence. 

 Mitochondrial depolarization induced by H2S was prevented by zinc, 

 methionine and pyruvate all of which decreased H2S-induced cell death. 

 Treatment of H2S poisoning may benefit from interventions aimed at 

 minimizing ROS-induced damage and reducing mitochondrial damage. 

95 

TITLE: 

 Cerebral cortex ultrastructure during exposure to hydrogen sulfide gas. 

AUTHORS: 

 Solnyshkova TG 

 Shakhlamov VA 

 Volodina EP 

SOURCE: 

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 Neurosci Behav Physiol. 2004, May; 34(4):343-5. [Neuroscience and 

 behavioral physiology] 

96 

TITLE: 

 Toxicity of Ammonia, Chlorine, Hydrogen Cyanide, Hydrogen Sulphide, and 

 Sulphur Dioxide Gases V. Animals 

AUTHORS: 

 Weedon FR 

 Hartzell A 

 Setterstrom C 

SOURCE: 

 Contributions from the Boyce Thompson Institute, Vol. 11, pages 365-385, 

 17 references, 19401940 

ABSTRACT: 

 Toxicity of ammonia (7664417), chlorine (7782505), hydrogen cyanide 

 (74908), hydrogen-sulfide (7783064), and sulfur-dioxide (7446095) gases is 

 investigated in house flies, rats, and mice exposed to 16-1000 ppm for up 

 to 16 hours. Ammonia shows greatest toxicity to all species tested, 

 followed by sulfur-dioxide, chlorine, hydrogen-sulfide, and 

 hydrogen-cyanide. Toxicity curves, symptoms of intoxication, and autopsy 

 findings are presented. 

97 

TITLE: 

 MECHANISMS OF SULFIDE TOXICITY 

AUTHORS: 

 ARP A 

SOURCE: 

 Crisp Data Base National Institutes of Health 

ABSTRACT: 

 Hydrogen sulfide is a well-known and potent metabolic toxin that poisons 

 mitochondrial oxidative phosphorylation at micromolar concentrations. An 

 accumulating body of evidence, however, suggests that sulfide may exert 

 other toxic effects in humans, and that chronic exposure to sulfide 

 concentrations that are currently considered safe may actually have long- 

 term effects on central nervous system functions. For the past decade, we 

 have been studying invertebrates that are evolutionarily adapted to 

 sulfide concentrations that would be lethal to other animals. Recently, 

 this research has uncovered a number of toxic sulfide effects that are 

 independent of oxidative phosphorylation and that likely have parallels 

 with the pathological effects of sulfide in animals. With this foundation, 

 we will now expand our research scope to focus on the effects of sulfide 

 across a broad range of animals. The objective of the research program of 

 this application for competing continuation of MBRS funding is to 

 characterize the cellular and molecular mechanisms of hydrogen sulfide 

 toxicity, with a long-term objective of identifying the pathology of 

 sulfide toxicity, with a long-term objective of identifying the pathology 

 of sulfide toxicity in humans. We propose to 1) define the mechanism by 

 which sulfide inhibits muscle contraction, 2) determine whether sulfide is 

 produced endogenously in animal tissue and has synergistic interactions 

 with nitric oxide, 3) investigate the long-term effects of sulfide 

 emphasizing induction of apoptosis and degenerative changes in cell and 

 tissue ultrastructure, and 4) initiate investigations of the toxic effects 

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 of sulfide on nerve function. In achieving these objectives, we will 

 provide information essential for understanding the effects of sulfide 

 exposure on humans, for developing treatment strategies for sulfide 

 poisoning, and for redefining occupational and public health exposure 

 limits. Our research effort has consistently involved underrepresented 

 minority undergraduate and graduate students, and numerous aspects of this 

 project will provide excellent opportunities for MBRS students to 

 formulate hypotheses and realize their research goals while training on 

 modern equipment. This hands-on training, followed by publication and 

 presentation of their research results will encourage and enable them to 

 successfully pursue a career in the biomedical sciences. 

98 

TITLE: 

 Molecular mechanisms of hydrogen sulfide toxicity. 

AUTHORS: 

 Truong DH 

 Eghbal MA 

 Hindmarsh W 

 Roth SH 

 O'Brien PJ 

SOURCE: 

 Drug Metab Rev. 2006; 38(4):733-44. [Drug metabolism reviews] 

ABSTRACT: 

 RATIONALE: The toxicity of H2S has been attributed to its ability to 

 inhibit cytochrome c oxidase in a similar manner to HCN. However, the 

 successful use of methemoglobin for the treatment of HCN poisoning was not 

 successful for H2S poisonings even though the ferric heme group of 

 methemoglobin scavenges H2S. Thus, we speculated that other mechanisms 

 contribute to H2S induced cytotoxicity. Experimental procedure. Hepatocyte 

 isolation and viability and enzyme activities were measured as described 

 by Moldeus et al. (1978), and Steen et al. (2001). RESULTS: Incubation of 

 isolated hepatocytes with NaHS solutions (a H2S source) resulted in 

 glutathione (GSH) depletion. Moreover, GSH depletion was also observed in 

 TRIS-HCl buffer (pH 6.0) treated with NaHS. Several ferric chelators 

 (desferoxamime and DETAPAC) and antioxidant enzymes (superoxide dismutase 

 [SOD] and catalase) prevented cell-free and hepatocyte GSH depletion. 

 GSH-depleted hepatocytes were very susceptible to NaHS cytotoxicity, 

 indicating that GSH detoxified NaHS or H2S in cells. Cytotoxicity was also 

 partly prevented by desferoxamine and DETAPC, but it was increased by 

 ferric EDTA or EDTA. Cell-free oxygen consumption experiments in TRIS-HCl 

 buffer showed that NaHS autoxidation formed hydrogen peroxide and was 

 prevented by DETAPC but increased by EDTA. We hypothesize that H2S can 

 reduce intracellular bound ferric iron to form unbound ferrous iron, which 

 activates iron. Additionally, H2S can increase the hepatocyte formation of 

 reactive oxygen species (ROS) (known to occur with electron transport 

 chain). H2S cytotoxicity therefore also involves a reactive sulfur 

 species, which depletes GSH and activates oxygen to form ROS. 

99 

TITLE: 

 Sulfide as a confounding factor in toxicity tests with the sea urchin 

 Paracentrotus lividus: comparisons with chemical analysis data. 

AUTHORS: 

 Losso C 

 Arizzi Novelli A 

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 Picone M 

 Volpi Ghirardini A 

 Ghetti PF 

 Rudello D 

 Ugo P 

SOURCE: 

 Environ Toxicol Chem. 2004, Feb; 23(2):396-401. [Environmental toxicology 

 and chemistry / SETAC] 

ABSTRACT: 

 Sperm cell and embryo toxicity tests with the sea urchin Paracentrotus 

 lividus were performed to assess the toxicity of sulfide, which is 

 considered a confounding factor in toxicity tests. For improved 

 information on the sensitivity of these methods to sulfide, experiments 

 were performed in the same aerobic conditions used for testing 

 environmental samples, with sulfide concentrations being monitored at the 

 same time by cathodic stripping voltammetry. New toxicity data for sulfide 

 expressed as median effective concentration (EC50) and no-observed-effect 

 concentration (NOEC) are reported. The EC50 value for the embryo toxicity 

 test (total sulfide at 0.43 mg/L) was three times lower than for the sperm 

 cell test (total sulfide at 1.20 mg/L), and the NOEC values were similar 

 (on the order of total sulfide at 10(-1) mg/L) for both tests. The 

 decrease in sulfide concentration during the bioassay as a consequence of 

 possible oxidation of sulfide by dissolved oxygen was determined by 

 voltammetric analysis, indicating a half-life of about 50 min in the 

 presence of gametes. To check the influence of sulfide concentrations on 

 toxicity effects in real samples, toxicity (with the sperm cell toxicity 

 test) and chemical analyses also were performed in pore-water samples 

 collected with an in situ sampler in sediments of the Lagoon of Venice 

 (Italy). A highly positive correlation between increased acute toxicity 

 and increased sulfide concentration was found. Examination of data 

 revealed that sulfide is a real confounding factor in toxicity testing in 

 anoxic environmental samples containing concentrations above the 

 sensitivity limit of the method. 

100 

TITLE: 

 Alteration of the morphology and neurochemistry of the developing 

 mammalian nervous system by hydrogen sulphide. 

AUTHORS: 

 Roth SH 

 Skrajny B 

 Reiffenstein RJ 

SOURCE: 

 Clin Exp Pharmacol Physiol. 1995, May; 22(5):379-80. [Clinical and 

 experimental pharmacology & physiology] 

ABSTRACT: 

 1. Hydrogen sulphide (H2S) is a broad spectrum toxicant that occurs widely 

 in nature and is also released by a variety of industrial activities and 

 processes. 2. The central nervous system (CNS) appears to be the major 

 target organ. 3. There is great potential for insult or injury to the 

 developing or immature CNS. 4. The risk of chronic or repeated exposures 

 to low concentrations have not been well defined. 5. Exposure to low 

 concentrations of H2S to time-pregnant rats from day 5 postcoitus until 

 day 21 postnatal results in architectural modification of cerebellar 

 Purkinje cells, alteration of putative amino acid neurotransmitters and 

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 changes in monoamine levels in the developing rat brain up to day 21 

 postnatal. 6. H2S-induced alterations in monoamine tissue levels observed 

 in the developing rat brain return to control values if exposure is 

 discontinued during development, that is, at day 21 postnatal. 

101 

TITLE: 

 [Interaction between endogenous nitric oxide and hydrogen sulfide in 

 pathogenesis of hypoxic pulmonary hypertension] 

AUTHORS: 

 Zhang QY 

 Du JB 

 Shi L 

 Zhang CY 

 Yan H 

 Tang CS 

SOURCE: 

 Beijing Da Xue Xue Bao. 2004, Feb; 36(1):52-6. [Beijing da xue xue bao. Yi 

 xue ban = Journal of Peking University. Health sciences] 

ABSTRACT: 

 OBJECTIVE: To investigate the interaction between nitric (NO) / nitric 

 oxygenase (NOS) and hydrogen sulfide (H(2)S)/ cystathionine-gamma-lyase 

 (CSE) system in the pathogenesis of hypoxic pulmonary hypertension. 

 METHODS: 25 rats were randomly divided into four groups: hypoxic group 

 (n=7 ), hypoxic + L-NAME group (n=6 ), hypoxic + PPG group (n=6) and 

 control group (n=6 ). After 21 days, pulmonary artery mean pressure (mPAP) 

 of each rat was evaluated, and the plasma concentration of H(2)S and NO 

 was measured. Meanwhile, the activities of CSE in pulmonary tissue in 

 hypoxic, hypoxic + L-NAME and control groups were detected, respectively, 

 and expressions of NOS in pulmonary arteries in hypoxic, hypoxic + PPG and 

 control groups were also detected by immunohistochemistry technique. 

 RESULTS: mPAP was significantly increased in hypoxic rats as compared with 

 normal controls. Meanwhile, compared with controls, the production of NO 

 and H(2)S in plasma, the activity of CSE in pulmonary tissue and 

 expression of NOS in pulmonary arteries were markedly decreased in hypoxic 

 rats. However, mPAP was significantly increased in hyopxic + L-NAME group 

 as compared with hypoxic groups, and at the same time, the plasma 

 concentration of NO was markedly decreased. However, the plasma 

 concentration of H(2)S and the activity of CSE in pulmonary tissue in 

 hyopxic+L-NAME group were increased significantly as compared with those 

 of hypoxic group. PPG also worsened pulmonary hypertension of hypoxic 

 rats, however,it increased endogenous production of NO and the expression 

 of NOS of pulmonary arteries obviously. CONCLUSION: There is a negative 

 feed back effect between NO/NOS system and H(2)S/CSE system in development 

 of hypoxic pulmonary hypertension. They might interact with each other and 

 therefore play an important regulating role in hypoxic pulmonary 

 hypertension. 

102 

TITLE: 

 Tobacco plants transformed with the O-acetylserine (thiol) lyase gene of 

 wheat are resistant to toxic levels of hydrogen sulphide gas. 

AUTHORS: 

 Youssefian S 

 Nakamura M 

 Sano H 

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SOURCE: 

 Plant J. 1993, Nov; 4(5):759-69. [The Plant journal : for cell and 

 molecular biology] 

ABSTRACT: 

 O-acetylserine (thiol) lyase (EC4.2.99.8) is the key enzyme in the 

 cysteine biosynthetic pathway of plants and prokaryotes. The gene, cys1, 

 encoding this enzyme was isolated from a wheat (Triticum aestivum L.) cDNA 

 library, and its deduced amino acid sequence found to show 53% sequence 

 identity with the O-acetyl-serine (thiol) lyase of Escherichia coli and 

 Salmonella typhimurium. The deduced peptide consists of 325 amino acids 

 (34.1 kDa), contains a conserved motif for the binding of pyridoxal 

 phosphate, a co-factor required for enzymatic activity, and an N-terminal 

 region of 37 amino acid residues resembling chloroplast transit peptides. 

 The identity of cys1 was further demonstrated through complementation of 

 an E. coli cysteine auxotroph, which lacks O-acetylserine (thiol) lyase, 

 by expression of the wheat gene. Northern blot analysis showed that cys1 

 is highly expressed in green vegetative and reproductive tissues and in 

 the roots of wheat, as well as in the leaves of several plant species. 

 Southern blot analysis demonstrated that the gene exists as a single copy 

 in the wheat genome. Tobacco plants transformed with cys1 in the sense 

 orientation (sense plants) or antisense orientation (antisense plants), 

 under the control of the CaMV 35S promoter, showed high levels of 

 transcripts. The O-acetylserine (thiol) lyase activity in transgenic 

 plants was determined, and found to be three- to fivefold higher in sense 

 plants than in control plants, but unaffected in antisense transformants. 

 Fumigation experiments with toxic levels of hydrogen sulphide (H2S) gas 

 showed that while sense transformants were highly resistant, control and 

 antisense plants were severely damaged by the treatment. 

103 

TITLE: 

 Chromatographic separation and identification of products from the 

 reaction of dimethylarsinic acid with hydrogen sulfide. 

AUTHORS: 

 Fricke MW 

 Zeller M 

 Sun H 

 Lai VW 

 Cullen WR 

 Shoemaker JA 

 Witkowski MR 

 Creed JT 

SOURCE: 

 Chem Res Toxicol. 2005, Dec; 18(12):1821-9. [Chemical research in 

 toxicology] 

ABSTRACT: 

 The reaction of dimethylarsinic acid (DMAV) with hydrogen sulfide (H2S) is 

 of biological significance and may be implicated in the overall toxicity 

 and carcinogenicity of arsenic. The course of the reaction in aqueous 

 phase was monitored, and an initial product, dimethylthioarsinic acid, was 

 observed by using LC-ICP-MS and LC-ESI-MS. Dimethylarsinous acid was 

 observed as a minor product. A second slower-forming product was 

 identified, and the electrospray mass chromatograms for this species 

 produced ions at m/z 275, 171, and 137 in positive mode. To aid in the 

 identification of this slower-forming product, crystalline standards of 

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 sodium dimethyldithioarsinate and dimethylarsino dimethyldithioarsinate 

 were prepared and re-characterized by using improved spectroscopic and 

 structural analysis techniques. An aqueous solution of sodium 

 dimethyldithioarsinate produced a single major chromatographic peak that 

 matched the retention time (7.6 min) of the slower-forming product and 

 contained similar molecular ions at m/z 275, 171, and 137 via LC-ESI-MS. 

 The dimethylarsino dimethyldithioarsinate standard produced four aqueous 

 phase species one of which coeluted with the slower forming product. This 

 coeluting peak also produced the identical ESI-MS ions as the 

 slower-forming product of DMAV + H2S. ESI-MS/MS experiments conducted on 

 sodium dimethyldithioarsinate in deuterated water produced molecular ions 

 at m/z 276, 173, and 137. Subsequent collisionally activated dissociation 

 (CAD) experiments on m/z 276 did not produce a product ion at m/z 173. 

 These data indicate that two different species are present in solution, 

 while NMR data indicate that only dimethyldithioarsinic acid exists in 

 aqueous solutions. This discrepancy was investigated by conducting NMR 

 studies on the acidic solution of sodium dimethyldithioarsinate after 

 taking this solution to dryness. The resolubilized solution produced a 

 proton NMR signal characteristic of dimethylarsino dimethyldithioarsinate. 

 Therefore, it was concluded that the ESI-MS ion at m/z 275 associated with 

 the slowly forming second reaction product and the sodium 

 dimethyldithioarsinate compound is a product of the ESI desolvation 

 process. 

104 

TITLE: 

 The actions of hydrogen sulfide on dorsal raphe serotonergic neurons in 

 vitro. 

AUTHORS: 

 Kombian SB 

 Reiffenstein RJ 

 Colmers WF 

SOURCE: 

 J Neurophysiol. 1993, Jul; 70(1):81-96. [Journal of neurophysiology] 

ABSTRACT: 

 1. The actions of hydrogen sulfide (HS-) on membrane and synaptic 

 properties of dorsal raphe (DR) serotonergic cells were studied in the in 

 vitro brain stem slice preparation, using intracellular sharp 

 microelectrode and whole-cell recording techniques. 2. Sulfide produced 

 two reversible, concentration-dependent effects on resting membrane 

 properties of DR cells: (1) 14% responded to HS- with a slow onset 

 hyperpolarization or an outward current accompanied by an conductance 

 increase in voltage clamp (holding potential = -60 mV; monophasic outward 

 cell) or (2) 39% responded with a rapid-onset depolarization corresponding 

 to a weakly voltage-dependent inward current showing little or no change 

 in conductance between -115 and -40 mV (monophasic inward cell). In 

 addition, 29.5% showed both the above effects, responding first with a 

 rapid-onset depolarization and then a sustained hyperpolarization. Such 

 cells had membrane currents very similar to those seen in the monophasic 

 inward and outward cells (biphasic cells). Finally, 17.5% of DR cells had 

 no measurable postsynaptic membrane response to HS-. 3. The outward 

 current induced in the presence of HS- had a reversal potential of about 

 -90 mV when recorded either with 2 M KCl or 145 mM potassium gluconate in 

 the pipette and was accompanied by an increase in conductance, suggesting 

 that it is caused by an elevated conductance to K+. 4. This current was 

 sensitive to the removal of external Ca2+ and blockade by Cd2+, suggesting 

 that it is activated by an elevation in internal [Ca2+]. It was also 

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 blocked by apamin or Ba2+ and Cs+, both of which revealed an underlying 

 inward current. The outward current was insensitive to the application of 

 a large variety of antagonists to other known voltage- and 

 calcium-dependent K+ channels. Elevation of intracellular ATP using a 

 patch pipette did not prevent the activation of the outward current. 5. 

 HS- reversibly suppressed a voltage-dependent outward current activated in 

 the voltage range of -50 to -40 mV. This current was also blocked by 10 mM 

 tetraethylammonium, suggesting that HS- suppresses the delayed rectifier 

 in DR cells. 6. The inward current could be observed in the presence of 

 HS- not only in monophasic inward cells but also in monophasic outward or 

 biphasic cells whose outward current was selectively blocked. This inward 

 current was sensitive to the removal of extracellular Ca2+, or the the 

 application of relatively low concentrations of Cd2+, suggesting that it 

 is carried by Ca2+. Both these manipulations also blocked the outward 

 current in monophasic outward or biphasic cells.(ABSTRACT TRUNCATED AT 400 

 WORDS) 

105 

TITLE: 

 Fertility and developmental neurotoxicity effects of inhaled hydrogen 

 sulfide in Sprague-Dawley rats. 

AUTHORS: 

 Dorman DC 

 Brenneman KA 

 Struve MF 

 Miller KL 

 James RA 

 Marshall MW 

 Foster PM 

SOURCE: 

 Neurotoxicol Teratol. 2000 Jan-Feb; 22(1):71-84. [Neurotoxicology and 

 teratology] 

ABSTRACT: 

 In this study, we examined whether perinatal exposure by inhalation to 

 hydrogen sulfide (H2S) had an adverse impact on pregnancy outcomes, 

 offspring prenatal and postnatal development, or offspring behavior. 

 Virgin male and female Sprague-Dawley rats (12 rats/sex/concentration) 

 were exposed (0, 10, 30, or 80 ppm H2S; 6 h/day, 7 days/week) for 2 weeks 

 prior to breeding. Exposures continued during a 2-week mating period 

 (evidence of copulation = gestation day 0 = GD 0) and then from GD 0 

 through GD 19. Exposure of dams and their pups (eight rats/litter after 

 culling) resumed between postnatal day (PND) 5 and 18. Adult male rats 

 were exposed for 70 consecutive days. Offspring were evaluated using motor 

 activity (PND 13, 17, 21, and 60+/-2), passive avoidance (PND 22+/-1 and 

 62+/-3), functional observation battery (PND 60+/-2), acoustic startle 

 response (PND 21 and 62+/-3), and neuropathology (PND 23+/-2 and 61+/-2). 

 There were no deaths and no adverse physical signs observed in F0 male or 

 female rats during the study. A statistically significant decrease in feed 

 consumption was observed in F0 male rats from the 80-ppm H2S exposure 

 group during the first week of exposure. There were no statistically 

 significant effects on the reproductive performance of the F0 rats as 

 assessed by the number of females with live pups, litter size, average 

 length of gestation, and the average number of implants per pregnant 

 female. Exposure to H2S did not affect pup growth, development, or 

 performance on any of the behavioral tests. The results of our study 

 suggest that H2S is neither a reproductive toxicant nor a behavioral 

 developmental neurotoxicant in the rat at occupationally relevant exposure 

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 concentrations ( < or =10 ppm). 

106 

TITLE: 

 Testing Toxic Atmospheres 

AUTHORS: 

 Bernz NR 

SOURCE: 

 Heating, Piping and Air Conditioning, Vol. 15, pages 482-484, 1 reference, 

 19431943 

ABSTRACT: 

 The importance of reducing the occupational disease hazards in war 

 industries is stressed. The toxicity of a number of gases is discussed, 

 and methods for their detection and quantitative determination are 

 presented. The gases include carbon-monoxide, hydrogen-sulfide (7783064), 

 hydrogen-cyanide, sulfur-dioxide, nitrogen-oxides, ammonia, phosgene, 

 radon and thoron. Hydrogen-sulfide is encountered primarily in the 

 artificial silk, chemical, and petroleum industries. Safe limits between 

 20-50ppm have been suggested. Hydrogen-sulfide can be determined 

 quantitatively by iodometric titration, or by the length of discoloration 

 in a tube containing a reactive chemical. 

107 

TITLE: 

 Hydrogen sulfide inhibits nitric oxide production and nuclear 

 factor-kappaB via heme oxygenase-1 expression in RAW264.7 macrophages 

 stimulated with lipopolysaccharide. 

AUTHORS: 

 Oh GS 

 Pae HO 

 Lee BS 

 Kim BN 

 Kim JM 

 Kim HR 

 Jeon SB 

 Jeon WK 

 Chae HJ 

 Chung HT 

SOURCE: 

 Free Radic Biol Med. 2006, Jul 1; 41(1):106-19. [Free radical biology & 

 medicine] 

ABSTRACT: 

 Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is 

 endogenously synthesized by cystathionine gamma-lyase (CSE) and/or 

 cystathionine beta-synthase (CBS) from L-cysteine (L-Cys) metabolism, is a 

 putative vasodilator, and its role in nitric oxide (NO) production is 

 unexplored. Here, we show that at noncytotoxic concentrations, H(2)S was 

 able to inhibit NO production and inducible NO synthase (iNOS) expression 

 via heme oxygenase (HO-1) expression in RAW264.7 macrophages stimulated 

 with lipopolysaccharide (LPS). Both H(2)S solution prepared by bubbling 

 pure H(2)S gas and NaSH, a H(2)S donor, dose dependently induced HO-1 

 expression through the activation of the extracellular signal-regulated 

 kinase (ERK). Pretreatment with H(2)S or NaHS significantly inhibited 

 LPS-induced iNOS expression and NO production. Moreover, NO production in 

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 LPS-stimulated macrophages that are expressing CSE mRNA was significantly 

 reduced by the addition of L-Cys, a substrate for H(2)S, but enhanced by 

 the selective CSE inhibitor beta-cyano-L-alanine but not by the CBS 

 inhibitor aminooxyacetic acid. While either blockage of HO activity by the 

 HO inhibitor, tin protoporphyrin IX, or down-regulation of HO-1 expression 

 by HO-1 small interfering RNA (siRNA) reversed the inhibitory effects of 

 H(2)S on iNOS expression and NO production, HO-1 overexpression produced 

 the same inhibitory effects of H(2)S. In addition, LPS-induced nuclear 

 factor (NF)-kappaB activation was diminished in RAW264.7 macrophages 

 preincubated with H(2)S. Interestingly, the inhibitory effect of H(2)S on 

 NF-kappaB activation was reversed by the transient transfection with HO-1 

 siRNA, but was mimicked by either HO-1 gene transfection or treatment with 

 carbon monoxide (CO), an end product of HO-1. CO treatment also inhibited 

 LPS-induced NO production and iNOS expression via its inactivation of 

 NF-kappaB. Collectively, our results suggest that H(2)S can inhibit NO 

 production and NF-kappaB activation in LPS-stimulated macrophages through 

 a mechanism that involves the action of HO-1/CO. 

108 

TITLE: 

 Chemiluminescent Light Generating. 

AUTHORS: 

 Anon 

SOURCE: 

 Govt Reports Announcements &amp; Index (GRA&I), Issue 03, 1990 

ABSTRACT: 

 TD3: This citation summarizes a one-page announcement of technology 

 available for utilization. Hydrogen sulfide is often emitted into the 

 atmosphere during the industrial production of methanol, methane, glycols 

 and other hydrocarbons. The toxicity of this gas makes it critically 

 important to be able to continuously monitor its presence in the 

 atmosphere. Amounts as small as one part per million can also poison 

 costly catalysts used to produce petrochemicals. Continuous monitoring by 

 present methods is difficult and requires long collection times, 

 concentration of the hydrogen sulfide and time-consuming chemical 

 preparation. Thus, truly continuous monitoring cannot be achieved. Ames 

 Laboratory researchers have addressed this problem by developing a way to 

 continuously monitor hydrogen sulfide and methyl mercaptan at levels as 

 low as one part per billion, and with high sensitivity. The method is 

 based on a new reaction that involves chemiluminescent technology for 

 detection. Chemiluminescence refers t 

109 

TITLE: 

 Changes in arterial hydrogen sulfide (H(2)S) content during septic shock 

 and endotoxin shock in rats. 

AUTHORS: 

 Hui Y 

 Du J 

 Tang C 

 Bin G 

 Jiang H 

SOURCE: 

 J Infect. 2003, Aug; 47(2):155-60. [The Journal of infection] 

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ABSTRACT: 

 OBJECTIVES: To explore the changes of hydrogen sulfide (H(2)S) in vascular 

 tissues of rats with septic shock and endotoxin shock and its possible 

 pathophysiological implication. METHODS: Rat models of septic shock 

 induced by cecal ligation and puncture and of endotoxic shock induced by 

 injection of endotoxin were used in this study. The authors measured 

 hymodynamic variations, metabolic data, H(2)S and nitric oxide (NO) 

 contents of different arteries in rats with septic shock and endotoxic 

 shock. RESULTS: The results showed that hemodynamic parameters including 

 the heart rate (HR), the mean arterial pressure (BP), and the +dP/dt max 

 decreased markedly, while the left ventricular end-diastolic pressure 

 (LVEDP) increased significantly and the rats developed hypoglycemia and 

 lactic acidosis. Arterial H(2)S contents were significantly increased 

 (P < 0.01) in both septic and endotoxic shock (P < 0.01). Endogenous 

 H(2)S and NO contents all negatively correlated with BP, cardiac function 

 and the degree of hypoglycemia (P < 0.01). CONCLUSIONS: The results of 

 our study demonstrated that endogenous vascular H(2)S increased in rats 

 with septic shock and endotoxic shock. It was suggested that endogenous 

 H(2)S was involved in physiological and pathophysiological process during 

 shock. 

110 

TITLE: 

 Effect of hydrogen sulfide on growth of sulfate reducing bacteria. 

AUTHORS: 

 REIS M AM 

 ALMEIDA JS 

 LEMOS PC 

 CARRONDO M JT 

SOURCE: 

 BIOTECHNOL BIOENG; 40 (5). 1992. 593-600. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. A culture of sulfate reducing bacteria (SRB) 

 growing on lactate and sulfate was incubated at different pH values in the 

 range of 5.8-7.0. The effect of pH on growth rate was determined in this 

 pH range; the highest growth rate was observed at pH 6.7. Hydrogen sulfide 

 produced from sulfate reduction was found to have a direct and reversible 

 toxicity effect on the SRB. A hydrogen sulfide concentration of 547 mg 

 (16.1 mM) completely inhibited the culture growth. Comparison between 

 acetic acid and hydrogen sulfide inhibition is presented and the 

 concomitant inhibition kinetics are mathematically described. 

111 

TITLE: 

 Exposure to low levels of hydrogen sulfide elevates circulating glucose in 

 maternal rats. 

AUTHORS: 

 Hayden LJ 

 Goeden H 

 Roth SH 

SOURCE: 

 J Toxicol Environ Health. 1990, Sep; 31(1):45-52. [Journal of toxicology 

 and environmental health] 

ABSTRACT: 

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 Although the lethal effect of hydrogen sulfide (H2S) has long been known, 

 the results of exposure to low levels of H2S have not been well 

 documented. Rat dams and pups were exposed to low levels of H2S (less than 

 or equal to 75 ppm) from d 1 of gestation until d 21 postpartum and 

 analyzed for changes in circulating enzymatic activity and metabolites. 

 Blood glucose was significantly elevated in maternal blood on d 21 

 postpartum at all exposure levels. This increase in glucose was 

 accompanied by a possible decrease in serum triglyceride in the pups and 

 in the dams on d 21 postpartum. There was no evidence of alterations in 

 serum alkaline phosphatase, lactate dehydrogenase, or serum glutamate 

 oxaloacetate transaminase. 

112 

TITLE: 

 Gases in agricultural slurry stores. 

AUTHORS: 

 Groves JA 

 Ellwood PA 

SOURCE: 

 Ann Occup Hyg. 1991, Apr; 35(2):139-51. [The Annals of occupational 

 hygiene] 

ABSTRACT: 

 The evolution of gases during the handling of animal slurry was 

 investigated at five sites. Particular attention was paid to the mixing 

 and emptying operations since it is when performing these that personnel 

 are most likely to be at risk of exposure. The main hazard was found to be 

 high transient concentrations of hydrogen sulphide presenting in some 

 cases a serious acute toxicity problem. Time-weighted average exposures 

 did not generally indicate any long-term exposure risk. Other features 

 noted were the evolution of ammonia and methane, although not at high 

 levels, and some increase in the carbon dioxide concentration. Some 

 reduction in oxygen concentration was measured, but generally the risk of 

 poisoning by hydrogen sulphide was more serious than the risk of 

 asphyxiation. 

113 

TITLE: 

 Growth and development in the rat during sub-chronic exposure to low 

 levels of hydrogen sulfide. 

AUTHORS: 

 Hayden LJ 

 Goeden H 

 Roth SH 

SOURCE: 

 Toxicol Ind Health. 1990 May-Jul; 6(3-4):389-401. [Toxicology and 

 industrial health] 

ABSTRACT: 

 The effects of low levels of hydrogen sulfide (H2S) on mammalian growth 

 and development are unknown although it has long been postulated that H2S 

 can inhibit critical developmental functions through the cleavage of 

 disulfide bonds and chelation of essential metal ions. Gravid rat dams 

 exposed to H2S (less than or equal to 75 PPM) from day 6 of gestation 

 until day 21 postpartum (PP) demonstrated normal reproductive parameters 

 until parturition. At parturition, however, delivery time was extended in 

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 a dose dependent manner with a maximum increase of 42% at 75 PPM. Maternal 

 liver cholesterol content was elevated significantly on day 21 postpartum 

 following exposure to 75 PPM H2S each day for 6 weeks. Pups which were 

 exposed in utero and neonatally to day 21 postpartum developed with a 

 subtle decrease in time of ear detachment and hair development and with no 

 other observed change in growth and development through day 21 postpartum. 

114 

TITLE: 

 Hydrogen sulfide: clandestine microbial messenger? 

AUTHORS: 

 Lloyd D 

SOURCE: 

 Trends Microbiol. 2006, Oct; 14(10):456-62. [Trends in microbiology] 

ABSTRACT: 

 Although the toxicity of hydrogen sulfide (H(2)S) has been substantiated 

 for almost 230 years, its pivotal roles in both aerobic and anaerobic 

 organisms have only recently become evident. In low oxygen environments 

 with millimolar concentrations of H(2)S, it functions as an electron donor 

 and as an energy source in some systems. At micromolar levels, 

 intracellular H(2)S in aerobic organisms has a vital role in redox 

 balancing. At even lower concentrations, H(2)S provides essential signals 

 in yeast, in the brain and in smooth and cardiac muscles. Here, other 

 possible coordinating roles within and between microorganisms are 

 suggested, including the possibility that H(2)S functions as a signalling 

 mediator in prokaryotes. It is expected that future research will uncover 

 a host of novel functions, not only in eukaryotes but also in prokaryotic 

 species. 

115 

TITLE: 

 Effect of hydrogen sulphide on liver somatic index and Fulton's condition 

 factor in Mystus nemurus. 

AUTHORS: 

 HOQUE MT 

 YUSOFF FM 

 LAW AT 

 SYED MA 

SOURCE: 

 JOURNAL OF FISH BIOLOGY; 52 (1). 1998. 23-30. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. The growth rate and liver somatic index were 

 significantly (P < 0.05) lower in Mystus nemurus exposed to hydrogen 

 sulphide compared to controls. These differences increased with 

 corresponding increases in hydrogen sulphide concentrations. No 

 significant differences (P > 0.05) in Fulton's condition factor were 

 detected between the exposed fish and the controls. The results revealed 

 that liver somatic index is a more sensitive indicator of hydrogen 

 sulphide toxicity compared to Fulton's condition factor. 

116 

TITLE: 

 Effects of acute intoxication with hydrogen sulfide on central amino acid 

 transmitter systems. 

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AUTHORS: 

 Kombian SB 

 Warenycia MW 

 Mele FG 

 Reiffenstein RJ 

SOURCE: 

 Neurotoxicology. 1988 (Winter); 9(4):587-95. [Neurotoxicology] 

ABSTRACT: 

 The acute effects of hydrogen sulfide (H2S) on brain amino acid levels 

 were examined in five regions of the rat brain following administration of 

 either saline (controls), or 10 or 30 mg/kg i.p. of sodium hydrosulfide 

 (NaHS). These doses represented sublethal (0.66 x LD50) as well as lethal 

 (2 x LD50) amounts. No significant changes in amino acid levels were found 

 in the cerebral cortex, striatum or hippocampus. In the cerebellum, 

 aspartate and glycine levels declined at 10 mg/kg NaHS. The region showing 

 the greatest change was the brainstem where aspartate, glutamate, 

 glutamine, GABA, glycine and taurine and alanine all increased. It would 

 appear then, that acute intoxication results in substantial changes in 

 brainstem amino acid levels. As some of these amino acids have been 

 implicated in the neuronal control of breathing, one of the underlying 

 causes of death following H2S may be the alteration of amino acid 

 neurotransmitter levels and metabolism resulting in the arrest of central 

 respiratory drive. 

117 

TITLE: 

 Acute hydrogen sulfide poisoning. Demonstration of selective uptake of 

 sulfide by the brainstem by measurement of brain sulfide levels. 

AUTHORS: 

 Warenycia MW 

 Goodwin LR 

 Benishin CG 

 Reiffenstein RJ 

 Francom DM 

 Taylor JD 

 Dieken FP 

SOURCE: 

 Biochem Pharmacol. 1989, Mar 15; 38(6):973-81. [Biochemical pharmacology] 

ABSTRACT: 

 The possibility of measuring sulfide levels in the central nervous system 

 (CNS) opens up many avenues for exploration. In acute hydrogen sulfide 

 (H2S) poisoning, death results from loss of central respiratory drive. To 

 date, however, measurement of brain sulfide has not been possible. By 

 employing gas dialysis and ion chromatography coupled to electrochemical 

 detection, rat brain sulfide levels could be measured either following 

 inhalation of H2S or after injection of sodium hydrosulfide (median lethal 

 dose, [LD50] = 14.6 +/- 1.00 mg/kg). Accumulation of brain sulfide was 

 linearly proportional to the dose over the range 0.50 LD50 to 3.33 LD50 

 units, and was strongly correlated with mortality data (R = 0.947). 

 Furthermore, analysis of untreated (control) brain showed an endogenous 

 sulfide level of 1.57 +/- 0.04 micrograms/g (mean +/- SE; N = 16). Studies 

 on various rat brain regions (brainstem, cerebellum, hippocampus, striatum 

 and cortex) showed that the endogenous sulfide level of brainstem, 1.23 

 +/- 0.06 micrograms/g, was significantly lower than that of the other 

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 brain regions. Net uptake of sulfide was greatest in the brainstem (3.02 

 micrograms/g) compared to the other regions as was the selective 

 accumulation of sulfide as calculated from normalized blood flow rates. 

 The results of subcellular fractionation demonstrated that sulfide was 

 detectable in fractions enriched in myelin, synaptosomes and mitochondria. 

 Approximately one-quarter of the endogenous sulfide content of whole rat 

 brain was found in the mitochondrial fraction. The sulfide content of 

 these fractions increased 2- to 3-fold after 50 mg/kg NaHS, the greatest 

 increases occurring in myelin- and mitochondrial-enriched fractions. 

118 

TITLE: 

 Sewer Fume Poisoning 

AUTHORS: 

 McCormack MF 

SOURCE: 

 Journal of the American College of Emergency Physicians, Vol. 4, No. 2, 

 pages 141-142, 4 references, 19751975 

ABSTRACT: 

 Treatment of sewer fume poisoning was reported. Two sewer workers 

 (SIC-7699) exposed to sewer fumes were admitted for emergency treatment; 

 one worker was dead on hospital arrival. The survivor was cyanotic and 

 unconscious, but breathing vigorously. Oxygen was administered, along 

 with valium and decadron. Methane (74828) intoxication was suspected at 

 this point. Amyl-nitrate (1002160) and sodium-nitrate (7631994) were 

 administered. The patient also received morphine (57272) and Lasix 

 (54319) for pulmonary edema evident in chest X-rays. He was discharged 

 after 5 days. The deleterious central nervous system effects were 

 produced from direct toxicity of hydrogen-sulfide (7783064), and secondary 

 effects from anoxia. The key to determining hydrogen-sulfide as the 

 poison in this instance was the blackened coins in the subjects' pockets 

 which was caused by the presence of hydrogen-sulfide. The antidote was 

 the induction of methemoglobinemia with nitrites. The authors conclude 

 that hydrogen-sulfide inhibits cytochrome-oxidase. Sewer fume poisoning 

 is rare and therefore may not be recognized. 

119 

TITLE: 

 Hydrogen sulfide as a neuromodulator. 

AUTHORS: 

 Kimura H 

SOURCE: 

 Mol Neurobiol. 2002, Aug; 26(1):13-9. [Molecular neurobiology] 

ABSTRACT: 

 Hydrogen sulfide (H2S) is a well-known toxic gas with the smell of rotten 

 eggs. Since the first description of the toxicity of H2S in 1713, most 

 studies about H2S have been devoted to its toxic effects. Recently, H2S 

 has been proposed as a physiologically active messenger. Three groups 

 discovered that the brain contains relatively high concentrations of 

 endogenous H2S. This discovery accelerated the identification of an 

 H2S-producing enzyme, cystathionine beta-synthase (CBS) in the brain. In 

 addition to the well-known regulators for CBS, S-adenosyl-L-methionine 

 (SAM) and pyridoxal-5'-phosphate, it was recently found that 

 Ca2+/calmodulin-mediated pathways are involved in the regulation of CBS 

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 activity. H2S is produced in response to neuronal excitation, and alters 

 hippocampal long-term potentiation (LTP), a synaptic model for memory. can 

 also regulate the release of corticotropin-releasing hormone (CRH) from 

 hypothalamus. Another H2S producing enzyme, cystathionine gamma-lyase 

 (CSE), has been identified in smooth muscle, and H2S relaxes smooth muscle 

 in synergy with nitric oxide (NO). Recent progress in the study of H2S as 

 a novel neuromodulator/transmitter in the brain is briefly reviewed. 

120 

TITLE: 

 Hydrogen sulfide protects neurons from oxidative stress. 

AUTHORS: 

 Kimura Y 

 Kimura H 

SOURCE: 

 FASEB J. 2004, Jul; 18(10):1165-7. [The FASEB journal : official 

 publication of the Federation of American Societies for Experimental 

 Biology] 

ABSTRACT: 

 Hydrogen sulfide (H2S), which is a well-known toxic gas, is found in 

 relatively high concentrations in the brain. Although a neuromodulatory 

 role of H2S has been demonstrated, little is known of its other biological 

 functions. Here we show that H2S protects primary cultures of neurons from 

 death in a well-studied model of oxidative stress caused by glutamate, a 

 process called oxidative glutamate toxicity--or oxytosis. We found that 

 H2S increases the glutathione levels, which normally decrease during the 

 cell death cascade, by enhancing the activity of gamma-glutamylcysteine 

 synthetase and up-regulating cystine transport. Cystine (cysteine) is the 

 rate-limiting substrate of glutathione synthesis. These observations 

 reveal that H2S protects neurons from oxytosis by increasing the 

 production of the antioxidant glutathione. 

121 

TITLE: 

 Acute Exposure Guideline Levels (AEGLs) For Hydrogen Sulfide. 

AUTHORS: 

 Bast C 

 Barbee SJ 

SOURCE: 

 Toxicol Sci 2005 Mar;84(1-S):302 

ABSTRACT: 

 AEGL values represent one-time exposures for increasingly severe effects 

 with AEGL-1 being least and AEGL-3 being most severe. Hydrogen sulfide is 

 a colorless, flammable gas at ambient temperature and pressure. It has an 

 odor similar to that of rotten eggs and is both an irritant and 

 asphyxiant. It acts similarly to cyanide by interrupting the electron 

 transport chain through inhibition of cytochrome oxidase. AEGL-1 values 

 (0.75 ppm, 0.60 ppm, 0.51 ppm, 0.36 ppm, and 0.33 ppm, for 10-min, 30-min, 

 1-hr, 4-hr, and 8-hr, respectively) were based on headache in asthmatic 

 humans exposed to 2 ppm H2S for 30 minutes. AEGL-1 values were adjusted by 

 a modifying factor of 3. AEGL-2 values (41 ppm, 32 ppm, 27 ppm, 29 ppm, 

 and 17 ppm, for 10-min, 30-min, 1-hr, 4-hr, and 8-hr, respectively) were 

 based on perivascular edema in rats exposed to 200 ppm H2S for 4 hours. 

 The AEGL-3 values (76 ppm, 59 ppm, 50 ppm, 37 ppm, and 31 ppm, for 10-min, 

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 30- min, 1-hr, 4-hr, and 8-hr, respectively) were based on a 1-hour 

 lethality threshold in rats of 504 ppm H2S. Interspecies and intraspecies 

 uncertainty factors of 3 each were applied to AEGL-2 and AEGL-3 values. 

 AEGL-2 and AEGL-3 values were scaled across time using the 

 exposure-concentration duration relationship, c(4.4) x t = k, shown to be 

 valid for lethality in rats for H2S exposures ranging from 10-minutes to 

 6-hours. 

122 

TITLE: 

 Effects of repeated hydrogen sulphide (H2S) exposure on learning and 

 memory in the adult rat. 

AUTHORS: 

 Partlo LA 

 Sainsbury RS 

 Roth SH 

SOURCE: 

 Neurotoxicology. 2001, Apr; 22(2):177-89. [Neurotoxicology] 

ABSTRACT: 

 The effects of repeated exposure (125 ppm) of hydrogen sulphide (H2S) on 

 learning and memory in the rat were investigated. A 16-arm radial arm maze 

 (RAM) was used to examine neurobehavioural functioning in a series of 

 three experiments. Experiment 1 involved training animals on a complex 

 spatial maze task, prior to a 5-week period of exposure to H2S or a 

 control gas mixture. Rats were tested for maze retention after each 5-day 

 exposure period. It was determined that repeated H2S exposure had no 

 effect on memory for a previously learned spatial task. Experiment 2 was 

 conducted to determine whether H2S interferes with the acquisition of a 

 novel spatial task. Naïve animals received daily maze training and 

 exposure (H2S or control) sessions over an extended 11-week period (48 

 sessions). The results indicated that the groups were comparable on four 

 of five measures of maze performance. H2S animals were impaired in their 

 ability to find all of the reinforcers prior to the end of a trial, 

 suggesting that H2S had an effect on performance rate, but not acquisition 

 of the maze task. Finally, Experiment 3 was conducted to determine what 

 role proactive interference might play in H2S-related brain impairment. 

 Animals from the preceding experiment were trained on a new reversed 

 contingency maze task. H2S animals made more overall arm entries than 

 controls, suggesting that H2S may impair learning by increasing the 

 animals' susceptibility to interference from irrelevant stimuli. The 

 prefrontal cortex was discussed as a potential target site of H2S. The 

 pathophysiological mechanisms underlying the effect of H2S on normal brain 

 function have yet to be identified. 

123 

TITLE: 

 Neuromuscular sensitivity to hydrogen sulfide in the marine invertebrate 

 Urechis caupo. 

AUTHORS: 

 Julian D 

 Dalia WE 

 Arp AJ 

SOURCE: 

 J Exp Biol. 1998, May; 201(Pt 9):1393-403. [The Journal of experimental 

 biology] 

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ABSTRACT: 

 Hydrogen sulfide (HS) is a well-known inhibitor of aerobic respiration via 

 its reversible binding of mitochondrial cytochrome c oxidase, but recent 

 studies have suggested that HS may have other non-respiratory actions. We 

 have studied the effects of HS on spontaneous and evoked contractions in 

 vitro under hypoxic and anoxic conditions in nerve-muscle preparations 

 from the echiuran worm Urechis caupo. Contraction amplitude in response to 

 electric field stimulation under anoxic conditions was completely 

 abolished by HS within minutes in a classic dose-response relationship 

 (Kd=31 mmol l-1, r2=0.86). Exposure of body wall and esophagus to HS in 

 vitro for up to 6 h demonstrated that the contraction amplitude and 

 frequency of spontaneous activity were relatively insensitive to anoxia, 

 but that the sensitivity to HS was similar to that seen in 

 field-stimulated muscle (Kd=2.7-32 mmol l-1). The toxic effects of HS were 

 reversible, with almost complete recovery under anoxic conditions within 

 the first hour. These data indicate that HS at millimolar concentrations 

 can directly inhibit muscle contraction. Although the mechanism of this 

 action is unknown, it does not appear to involve metabolic pathways or 

 oxygen transport. 

124 

TITLE: 

 Hydrogen sulfide protects HT22 neuronal cells from oxidative stress. 

AUTHORS: 

 Kimura Y 

 Dargusch R 

 Schubert D 

 Kimura H 

SOURCE: 

 Antioxid Redox Signal. 2006 Mar-Apr; 8(3-4):661-70. [Antioxidants & redox 

 signaling] 

ABSTRACT: 

 Hydrogen sulfide (H2S) is a neuromodulator in the brain and a relaxant for 

 smooth muscle. H2S protects primary cortical neurons from oxidative stress 

 by increasing the intracellular concentrations of glutathione, the major 

 antioxidant in cells. However, changes in glutathione alone are not 

 sufficient to account for full protection in all types of nerve cells. H2S 

 is here shown to protect an immortalized mouse hippocampal cell line from 

 oxidative glutamate toxicity by activating ATP-dependent K+ (KATP) and Cl- 

 channels, in addition to increasing the levels of glutathione. The present 

 study therefore identifies a novel pathway for H2S protection from 

 oxidative stress. 

125 

TITLE: 

 Effect of the Mixture of Carbon Disulfide and Hydrogen Sulfide in Air on 

 White Rats under Conditions of Continuous Exposure for Several Months 

AUTHORS: 

 Misiakiewicz Z 

 Szulinska G 

 Chyba A 

SOURCE: 

 Roczniki Panstwowego Zakladu Higieny, Vol. 23, No. 4, pages 465-475, 23 

 references, 19721972 

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ABSTRACT: 

 Investigations were performed on rats in five biological chambers with 

 continuous air flow. In the chambers constant levels of the following 

 gases were maintained: 0.1 milligram per cubic meter of carbon-disulfide 

 (75150); 0.01 milligram per cubic meter of carbon-disulfide 0.1 milligram 

 per cubic meter of hydrogen-sulfide (7783064); 1.0 milligram per cubic 

 meter of carbon-disulfide and 1.0 milligram per cubic meter of 

 hydrogen-sulfide. The following variables were measured periodically in 

 all the groups of experimental animals: weight increments, coproporphyrin 

 levels in the urine, cholinesterase blood activity, and asparate 

 aminotransferase serum activity. At the end of the experiment 

 histopathologic investigations were also carried out. Weight increases 

 were reduced, coproporphyrin excretion and the enzyme activities were 

 increased. The results show that the toxic effect of carbon-disulfide is 

 more severe when hydrogen-sulfide is also present in the air. (Polish; 

 English translation available) 

126 

TITLE: 

 Biochemical and cytologic alterations in the respiratory tract of rats 

 exposed for 4 hours to hydrogen sulfide. 

AUTHORS: 

 Lopez A 

 Prior M 

 Yong S 

 Albassam M 

 Lillie LE 

SOURCE: 

 Fundam Appl Toxicol. 1987, Nov; 9(4):753-62. [Fundamental and applied 

 toxicology : official journal of the Society of Toxicology] 

ABSTRACT: 

 Fischer-344 rats were killed by exsanguination 1, 20, and 44 hr after a 

 single 4-hr exposure to an atmosphere of 0, 10, 200, and 400 ppm of 

 hydrogen sulfide (H2S). Alterations in the activities of lactate 

 dehydrogenase and alkaline phosphatase, and cytomorphology of epithelial 

 cells in fluids obtained by nasal and bronchoalveolar lavage were used as 

 indicators of cell injury. Changes in the number of leukocytes were used 

 as indicators of inflammatory response, and changes in the concentration 

 of protein were used as indicators of altered vascular permeability. 

 Inhalation of H2S resulted in 139, 483, and 817% increased cellularity in 

 the nasal cavity of rats exposed to 10, 200, and 400 ppm, respectively. 

 This was due to marked exfoliation of degenerated epithelial cells and 

 exudation of neutrophils. The high dose of H2S resulted in a moderate 

 increase in lactate dehydrogenase and protein in nasal passages; values 

 returned to baseline levels 20 hr later. Bronchoalveolar cell counts were 

 decreased in rats exposed to 400 ppm and unchanged in those exposed to 10 

 and 200 ppm. Enzymatic activities in lung lavage fluid were moderately 

 elevated (up to 90%), yet protein concentrations were increased by more 

 than 3000% and remained significantly elevated up to 44 hr after exposure 

 to 400 ppm. It was concluded that inhalation of H2S has a severe cytotoxic 

 effect on the nasal epithelium and a severe edematogenic effect on lung 

 parenchyma. These results are in agreement with autopsy findings of 

 individuals killed by accidental exposure to H2S-containing sour gas. 

127 

TITLE: 

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 Nitrite as antidote for acute hydrogen sulfide intoxication? 

AUTHORS: 

 Beck JF 

 Bradbury CM 

 Connors AJ 

 Donini JC 

SOURCE: 

 Am Ind Hyg Assoc J. 1981, Nov; 42(11):805-9. [American Industrial Hygiene 

 Association journal] 

ABSTRACT: 

 The detoxification of hydrogen sulfide (H2S) by a heme catalyzed oxidation 

 was examined as part of an on-going study of H2S toxicity. Interlocking O2 

 absorption and sulfide depletion data indicate that both oxyhemoglobin and 

 methemoglobin are effective catalytic agents. Although the latter is more 

 efficacious, the life time of excess sulfide in the presence of oxygen and 

 either of the above is of the order of minutes. It has also been 

 established that the formation of methemoglobin following nitrite 

 administration occurs preferentially under oxygen poor conditions. Under 

 an atmospheric or oxygen enriched environment, which favors sulfide 

 depletion, the nitrite retards sulfide oxidation. Thus nitrite as an 

 antidote for acute H2S intoxication can only be effective within the first 

 few minutes after the exposure, at which time resuscitation and/or 

 ventilation of the victim is likely to produce conditions in which the 

 nitrite actually slows sulfide removal. 

128 

TITLE: 

 Method of Generating Chemiluminescent Light. 

AUTHORS: 

 Anon 

SOURCE: 

 Govt Reports Announcements &amp; Index (GRA&I), Issue 17, 1989 

ABSTRACT: 

 TD3: This citation summarizes a one-page announcement of technology 

 available for utilization. Hydrogen sulfide is often emitted into the 

 atmosphere during the industrial production of methanol, methane, glycols 

 and other hydrocarbons. The toxicity of this gas makes it critically 

 important to be able to continuously monitor its presence in the 

 atmosphere. Amounts as small as one part per million can also poison 

 costly catalysts used to produce petrochemicals. Continuous monitoring by 

 present methods is difficult and requires long collection times, 

 concentration of the hydrogen sulfide, and time-consuming chemical 

 preparation. Thus, truly continuous monitoring cannot be achieved. Ames 

 Laboratory researchers have addressed this problem by developing a way to 

 continuously monitor hydrogen sulfide and methyl mercaptan (another 

 sulfur-containing compound) at levels as low as one part per billion, and 

 with high sensitivity. The method is based on a new reaction that involves 

 chemiluminescent technology for 

129 

TITLE: 

 Monoamine oxidase inhibition as a sequel of hydrogen sulfide intoxication: 

 increases in brain catecholamine and 5-hydroxytryptamine levels. 

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AUTHORS: 

 Warenycia MW 

 Smith KA 

 Blashko CS 

 Kombian SB 

 Reiffenstein RJ 

SOURCE: 

 Arch Toxicol. 1989; 63(2):131-6. [Archives of toxicology] 

ABSTRACT: 

 Administration of sodium hydrosulfide (NaHS), an alkali salt of hydrogen 

 sulfide (H2S) at doses of 10 and 30 mg/kg, corresponding to sublethal and 

 lethal doses (0.66 and 2.0 X LD50) resulted in significant increases in 

 regional catecholamine levels of the rat brain only after the dose of 2.0 

 x LD50 of NaHS. Whereas the cortex and the cerebellum showed little or no 

 change in catecholamine content, the hippocampus, striatum and brainstem 

 all showed increases in noradrenaline and adrenaline. Additional analysis 

 also showed that brainstem dopamine and 5-hydroxytryptamine levels (5-HT) 

 increased as well. In vitro testing of sulfide for inhibition of monoamine 

 oxidase (MAO) activity showed the anion to be inhibitory with an IC50 of 

 39.1 +/- 3.6 microM. Inhibition of MAO activity ex vivo could be 

 demonstrated at a dose of 100 mg/kg but not at the lower dose of 30 mg/kg 

 NaHS. Inhibition of enzyme activity could not be demonstrated at this 

 lower dose, possibly due to the well known rapid intramitochondrial 

 metabolism of sulfide. Correlation of synaptosomal and mitochondrial 

 sulfide levels with enzyme inhibition data suggests that inhibition of MAO 

 may be an important contributing factor to the mechanism(s) underlying 

 loss of central respiratory drive after fatal intoxication with H2S. 

130 

TITLE: 

 Hydrogen sulfide - Safe handling in ports 

SOURCE: 

 Postbus 69, 2270 MA Voorburg, Netherlands, 2nd edition 1982. 10p. 

ABSTRACT: 

 Contents of this data sheet: physical and chemical properties; hazards 

 (toxicity and health damage, symptoms, risk of leakage, fire and 

 overpressure if temperature increases rapidly); rules for transport and 

 containers; declaration on docking and preparations for unloading; safety 

 measures (tanks, cylinders, etc. containing hydrogen sulfide under 

 pressure should be kept well away from any source of heat); testing for 

 leakage and repairing leaks; prevention of poisoning incidents, use of 

 respirators, storage of hydrogen sulfide under pressure; slinging of 

 cylinders; first aid in case of contact with skin or eyes, or inhalation); 

 marking of containers. 

131 

TITLE: 

 [Hyperbaric oxygen for hydrogen sulfide poisoning] 

AUTHORS: 

 Goldenberg I 

 Shoshani O 

 Mushkat Y 

 Bentur Y 

 Melamed Y 

 Shupak A 

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SOURCE: 

 Harefuah. 1994, Nov 1; 127(9):300-2, 360. [Harefuah] 

ABSTRACT: 

 Hydrogen sulfide (H2S) is a toxic gas produced in decaying substances 

 containing organic sulfur. Exposure to the gas causes severe disturbances 

 in the central nervous and respiratory systems. The mechanism of toxicity 

 is disruption of the electron transport chain in mitochondria, resulting 

 in intracellular hypoxia. Treatment of H2S poisoning includes mechanical 

 ventilation with 100% oxygen and immediate administration of sodium 

 nitrate. Treatment with hyperbaric oxygen (HBO) has been studied in animal 

 models, and has also been used in a number of patients. However, the 

 clinical effectiveness of this mode of therapy has not been clearly 

 proven. Having recently treated a case of H2S poisoning, we suggest HBO to 

 reduce mortality. 

132 

TITLE: 

 Nitric oxide-releasing flurbiprofen reduces formation of proinflammatory 

 hydrogen sulfide in lipopolysaccharide-treated rat. 

AUTHORS: 

 Anuar F 

 Whiteman M 

 Siau JL 

 Kwong SE 

 Bhatia M 

 Moore PK 

SOURCE: 

 Br J Pharmacol. 2006, Apr; 147(8):966-74. [British journal of 

 pharmacology] 

ABSTRACT: 

 The biosynthesis of both nitric oxide (NO) and hydrogen sulfide (H2S) is 

 increased in lipopolysaccharide (LPS)-injected mice and rats but their 

 interaction in these models is not known. In this study we examined the 

 effect of the NO donor, nitroflurbiprofen (and the parent molecule 

 flurbiprofen) on NO and H2S metabolism in tissues from LPS-pretreated 

 rats. Administration of LPS (10 mg kg(-1), i.p.; 6 h) resulted in an 

 increase (P < 0.05) in plasma TNF-alpha, IL-1beta and nitrate/nitrite 

 (NO(x)) concentrations, liver H2S synthesis (from added cysteine), CSE 

 mRNA, inducible nitric oxide synthase (iNOS), myeloperoxidase (MPO) 

 activity (marker for neutrophil infiltration) and nuclear factor-kappa B 

 (NF-kappaB) activation. Nitroflurbiprofen (3-30 mg kg(-1), i.p.) 

 administration resulted in a dose-dependent inhibition of the LPS-mediated 

 increase in plasma TNF-alpha, IL-1beta and NO(x) concentration, liver H2S 

 synthesis (55.00+/-0.95 nmole mg protein(-1), c.f. 62.38+/-0.47 nmole mg 

 protein(-1), n = 5, P < 0.05), CSE mRNA, iNOS, MPO activity and NF-kappaB 

 activation. Flurbiprofen (21 mg kg(-1), i.p.) was without effect. These 

 results show for the first time that nitroflurbiprofen downregulates the 

 biosynthesis of proinflammatory H2S and suggest that such an effect may 

 contribute to the augmented anti-inflammatory activity of this compound. 

 These data also highlight the existence of 'crosstalk' between NO and H2S 

 in this model of endotoxic shock. 

133 

TITLE: 

 Histologic and ultrastructural alterations in lungs of rats exposed to 

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 sub-lethal concentrations of hydrogen sulfide. 

AUTHORS: 

 Lopez A 

 Prior M 

 Lillie LE 

 Gulayets C 

 Atwal OS 

SOURCE: 

 Vet Pathol. 1988, Sep; 25(5):376-84. [Veterinary pathology] 

ABSTRACT: 

 Fischer-344 rats were killed 1, 18, and 42 hr after a single 4-hr exposure 

 to an atmosphere of 0, 116, or 615 mg m-3 of hydrogen sulfide (H2S). 

 Lungs, fixed by the intratracheal route, were examined by light and 

 electron microscopy. Histologic changes were transient and mainly present 

 in rats exposed to 615 mg m-3 H2S. Lesions included severe but transitory 

 pulmonary edema and fibrinocellular alveolitis which was restricted to the 

 proximal alveolar region of the lung. Electron microscopically, ciliated 

 bronchiolar cells were the only cells that developed necrosis; they were 

 rapidly replaced by mitosis. Alveolar endothelium had cytoplasmic blebs, 

 but alveolar epithelium had minor changes. No mast cell degranulation was 

 detected in lungs with edema. A 4-hr exposure to 615 mg m-3 is markedly 

 edematogenic for the lung but only moderately cytotoxic for pulmonary 

 cells. 

134 

TITLE: 

 Learning and memory in Lymnaea are negatively altered by acute low-level 

 concentrations of hydrogen sulphide. 

AUTHORS: 

 Rosenegger D 

 Roth S 

 Lukowiak K 

SOURCE: 

 J Exp Biol. 2004, Jul; 207(Pt 15):2621-30. [The Journal of experimental 

 biology] 

ABSTRACT: 

 Hydrogen sulphide (H(2)S) is a common industrial pollutant as well as an 

 endogenous neural transmitter/neural modulator. Experiments were performed 

 on the pond snail Lymnaea stagnalis to determine the acute effects of 

 low-level exposure to H(2)S (50-100 micromol l(-1)) on aerial respiratory 

 behaviour, associative learning, and its subsequent consolidation into 

 long-term memory (LTM). A 3-neuron network whose sufficiency and necessity 

 have been demonstrated drives aerial respiratory behaviour in Lymnaea. In 

 the presence of 100 micromol l(-1) H(2)S the number of bouts of aerial 

 respiration and the total breathing time were significantly increased 

 compared to the control hypoxic situation, but were equivalent to those 

 observed in snails that had been subjected to a 'more intense hypoxic 

 challenge'. In addition, at a concentration of 100 micromol l(-1) H(2)S 

 neither associative learning nor long-term memory (LTM) were observed. 

 However, snails subjected to a 'more intense hypoxic challenge' still had 

 the capacity to learn and form LTM. These snails, in fact, showed 

 statistically the best learning and memory performance of any group. While 

 learning and memory were observed at 50 and 75 micromol l(-1) H(2)S, 

 respectively, they were statistically poorer than the learning and memory 

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 exhibited by snails in the standard hypoxia condition. Hence the ability 

 to learn and form memory was compromised by H(2)S. Thus an invertebrate 

 model system with a well-defined neural network can be used to study of 

 the effects of H(2)S on the processes of learning and memory. 

135 

TITLE: 

 Hydrogen sulfide poisoning: clarification of some controversial issues. 

AUTHORS: 

 Milby TH 

 Baselt RC 

SOURCE: 

 Am J Ind Med. 1999, Feb; 35(2):192-5. [American journal of industrial 

 medicine] 

ABSTRACT: 

 BACKGROUND: Hydrogen sulfide is a toxic gas about which much has been 

 written. We discuss here several issues we believe would benefit from 

 further clarification. CONCLUSIONS: We conclude that: 1) Certain 

 neurotoxic effects of exposure are probably due to a direct toxic effect 

 on the brain, while others are almost certainly a result of hypoxia 

 secondary to H2S-induced respiratory insufficiency; 2) pulmonary edema is 

 a common consequence of poisoning and there is suggestive evidence of 

 hyperactive airway responses in some individuals following brief 

 H2S-induced unconsciousness (knockdown); 3) criteria for acceptable 

 community levels are very different than those governing occupational 

 standards; 4) urinary thiosulfate determinations can be useful for 

 monitoring occupational exposure; and 5) determination of sulfide ion 

 concentrations in blood or major organs can be useful in corroborating a 

 diagnosis of fatal H2S toxicity, but there are many pitfalls in 

 collecting, storing, and analyzing tissue and fluid samples. 

136 

TITLE: 

 Impaired detoxication of hydrogen sulfide in ulcerative colitis? 

AUTHORS: 

 Picton R 

 Eggo MC 

 Langman MJ 

 Singh S 

SOURCE: 

 Dig Dis Sci. 2007, Feb; 52(2):373-8. [Digestive diseases and sciences] 

ABSTRACT: 

 Impaired butyrate oxidation and raised counts of sulfate-reducing bacteria 

 in the colon of patients with ulcerative colitis (UC) indicate that the 

 disease may be induced or aggravated by hydrogen sulfide toxicity. We 

 aimed to examine enzymatic removal of H(2)S in erythrocytes and colonic 

 mucosa from controls and patients with UC and Crohn's disease (CD). 

 Rhodanese (RHOD) and thiol methyltransferase (TMT) activities were 

 measured in rectal mucosa and erythrocytes, and plasma thiocyanate was 

 determined. Four groups were analyzed: patients with UC, patients with CD, 

 hospital controls (patients with dyspepsia or IBS), and a group of healthy 

 volunteers. RHOD and TMT activity in rectal biopsies did not differ 

 significantly between controls and patients with UC or CD (n=56). Control 

 levels of RHOD were significantly higher in men than in women (212+/-25 

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 and 132+/-14 nmol/mg/min, respectively; P < 0.01). In erythrocytes 

 (n=128) RHOD activity was significantly higher in UC patients than in 

 hospital or volunteer controls (1.15+/-0.12 compared with 0.88+/-0.12 and 

 0.66+/-0.02 nmol/mg/min; P < 0.05 and P < 0.02, respectively). TMT 

 activity was also significantly higher in erythrocytes from UC patients 

 and hospital controls than volunteer controls (2.02+/-0.13 pmol/mg/min 

 [P < 0.001], 1.51+/-0.21 pmol/mg/min [P < 0.05], and 1.17+/-0.18 

 pmol/mg/min, respectively). We found no evidence of defective enzymic 

 detoxication of sulfide by RHOD or TMT in patients with UC or CD. 

137 

TITLE: 

 Chronic exposure to low concentrations of hydrogen sulfide produces 

 abnormal growth in developing cerebellar Purkinje cells. 

AUTHORS: 

 Hannah RS 

 Roth SH 

SOURCE: 

 Neurosci Lett. 1991, Jan 28; 122(2):225-8. [Neuroscience letters] 

ABSTRACT: 

 Hydrogen sulfide (H2S) may produce deleterious effects on the developing 

 central nervous system. The dendritic fields of developing cerebellar 

 Purkinje cells were analyzed to determine the effects of chronic exposure 

 to low concentrations of H2S during perinatal development. Treatment with 

 two concentrations (20 and 50 ppm) of H2S produced severe alterations in 

 the architecture and growth characteristics of the Purkinjec cell 

 dendritic fields. The architectural modifications included longer 

 branches, an increase in the vertex path length and variations in the 

 number of branches in particular areas of the dendritic field. The treated 

 cells also exhibited a nonsymmetrical growth pattern at a time when random 

 terminal branching is normally occurring. These findings suggest that 

 developing neurons exposed to low concentrations of H2S are at risk of 

 severe deficits. 

138 

TITLE: 

 Neurobehavioral evaluation for a community with chronic exposure to 

 hydrogen sulfide gas. 

AUTHORS: 

 Inserra SG 

 Phifer BL 

 Anger WK 

 Lewin M 

 Hilsdon R 

 White MC 

SOURCE: 

 Environ Res. 2004, May; 95(1):53-61. [Environmental research] 

ABSTRACT: 

 In May 2000, the Agency for Toxic Substances and Disease Registry of the 

 US government conducted a health investigation in response to community 

 concerns regarding ambient and indoor hydrogen sulfide (H(2)S), odor, and 

 health symptoms in Dakota City, Nebraska. The objective was to determine 

 whether adult residents in an area with repeated exposure to H(2)S showed 

 poorer performance on neurobehavioral tests than unexposed residents. 

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 Study participants were required to meet age (#10878;16 years of age) and 

 length of residency (2 years) eligibility requirements. A battery of 

 computer-assisted standardized neurobehavioral tests was administered in 

 English or Spanish. A questionnaire was used to collect information about 

 participants, demographic and health status. Three hundred forty-five 

 people agreed to participate. After the exclusion of 10 persons, analyses 

 were conducted on 335 participants; 171 residents in the target area and 

 164 residents in the comparison area. The two groups were comparable in 

 demographic characteristics and various health conditions. Overall, 

 neurobehavioral test results for the target and comparison groups were 

 similar. Residence in the H(2)S-exposed area was associated with 

 marginally poorer performance on a test of memory, namely, match to sample 

 score, and a test of grip strength. However, these differences were not 

 significant. Deficits in overall neurobehavioral performance were not 

 associated with exposure to H(2)S in this study. 

139 

TITLE: 

 A large-scale categorization of sites in San Francisco Bay, USA, based on 

 the sediment quality triad, toxicity identification evaluations, and 

 gradient studies. 

AUTHORS: 

 Hunt JW 

 Anderson BS 

 Phillips BM 

 Tjeerdema RS 

 Taberski KM 

 Wilson CJ 

 Puckett HM 

 Stephenson M 

 Fairey R 

 Oakden J 

SOURCE: 

 Environ Toxicol Chem. 2001, Jun; 20(6):1252-65. [Environmental toxicology 

 and chemistry / SETAC] 

ABSTRACT: 

 Sediment quality was assessed in San Francisco Bay, California, USA, using 

 a two-tiered approach in which 111 sites were initially screened for 

 sediment toxicity. Sites exhibiting toxicity were then resampled and 

 analyzed for chemical contamination, recurrent toxicity, and, in some 

 cases, benthic community impacts. Resulting data were compared with newly 

 derived threshold values for each of the metrics in a triad-based 

 weight-of-evidence evaluation. Sediment toxicity test results were 

 compared with tolerance limits derived from reference site data, benthic 

 community data were compared with threshold values for a relative benthic 

 index based on the presence and abundance of pollution-tolerant and 

 -sensitive taxa, and concentrations of chemicals and chemical mixtures 

 were compared with sediment quality guideline-based thresholds. A total of 

 57 sites exceeded threshold values for at least one metric, and each site 

 was categorized based on triad inferences. Nine sites were found to 

 exhibit recurrent sediment toxicity associated with elevated contaminant 

 concentrations, conditions that met program criteria for regulatory 

 attention. Benthic community impacts were also observed at three of these 

 sites, providing triad evidence of pollution-induced degradation. Multi- 

 and univariate correlations indicated that chemical mixtures, heavy 

 metals, chlordanes, and other organic compounds were associated with 

 measured biological impacts in the Bay. Toxicity identification 

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 evaluations indicated that metals were responsible for pore-water toxicity 

 to sea urchin larvae at two sites. Gradient studies indicated that the 

 toxicity tests and benthic community metrics employed in the study 

 predictably tracked concentrations of chemical mixtures in Bay sediments. 

140 

TITLE: 

 Hematological changes due to chronic exposure to natural gas leakage in 

 polluted areas of Masjid-i-Sulaiman (Khozestan province, Iran). 

AUTHORS: 

 Saadat M 

 Bahaoddini A 

SOURCE: 

 Ecotoxicol Environ Saf. 2004, Jun; 58(2):273-6. [Ecotoxicology and 

 environmental safety] 

ABSTRACT: 

 An overwhelming number of studies have given consistent findings that 

 environmental or occupational exposure to oil products results in a 

 significant decrease in circulating erythrocytes, hemoglobin, platelets, 

 total white blood cells, and absolute numbers of lymphocytes and 

 neutrophils. Some parts of Masjid-i-Sulaiman (located in the southwest of 

 Iran) are contaminated by subsurface leakage of natural gas, which 

 contains a high level of hydrogen sulfide. The amount of all reactive 

 sulfur compounds in air of contaminated areas of MIS was estimated as 

 equal to 0.023+/-0.002 ppm of SO(2). In the present report the 

 hematological findings of 99 persons from polluted areas of MIS were 

 compared with those of 396 individuals from the general population of MIS 

 matched by age (+/-3 years) and sex. The CBC test and the WBC differential 

 were analyzed in one central laboratory according to standard 

 hematological methods, by Coulter S (Biomedical). The multiple linear 

 regression method was applied in order to detect differences among exposed 

 and unexposed groups for hematological markers. The absolute mean number 

 of red blood cells, percentages of hematocrit, level of hemoglobin, and 

 absolute number of platelets were significantly higher among the exposed 

 subjects compared with the control group. However, the absolute mean 

 numbers of white blood cells, lymphocytes, and neutrophils were 

 significantly decreased in the exposed group compared with the control. 

141 

TITLE: 

 Demyelination of nerve fibers in the central nervous system caused by 

 chronic exposure to natural hydrogen sulfide-containing gas. 

AUTHORS: 

 Solnyshkova TG 

SOURCE: 

 Bull Exp Biol Med. 2003, Oct; 136(4):328-32. [Bulletin of experimental 

 biology and medicine] 

ABSTRACT: 

 We studied the effect of natural gas from Astrakhan' gas field on rat 

 brain. The study revealed a specific effect of natural H(2)S-containing 

 gas on myelin sheaths in the brain, which determines its neurotoxicity 

 even at low concentrations in the inspired air. 

142 

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TITLE: 

 Probabilistic Consequence Assessment of Hydrogen Sulphide Releases from a 

 Heavy Water Plant. Sensitivity Study of Sulphur Dioxide Toxicity. 

AUTHORS: 

 Baynes CJ 

SOURCE: 

 Govt Reports Announcements &amp; Index (GRA&I), Issue 12, 1989 

ABSTRACT: 

 TD3: This study investigates the sensitivity of the probabilistic 

 consequences projected by the computer code GASPROB to changes in the 

 assumed toxicity of sulfur dioxide gas (SO2). GASPROB simulates the 

 consequences of accidental releases to the atmosphere of hydrogen sulfide 

 (H2S) at a heavy water plant. Five combinations of different LC50 and LC10 

 functions (lethal concentration versus exposure time) were tested, each 

 varying over 3 orders of magnitude. The results indicate a distinct 

 sensitivity to both the LC50 and LC10 functions. (Atomindex citation 

 20:008454) I. 

143 

TITLE: 

 Toxicity of hydrogen sulfide on hard clam, Meretrix lusoria. 

AUTHORS: 

 KUO CH 

 CHOW ST 

SOURCE: 

 J CHIN SOC VET SCI; 16 (3). 1990. 237-244. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. The toxic effects of hydrogen sulfide on 

 hard clam, Meretrix lusoria under varying acidity, dissolved oxygen 

 contents, temperatures and salinities, were examined in order to clarify 

 the causes of mass mortality of this species. The results are summarized 

 as followings: Under the optimal conditions, 24 hr -LC 50, 48 hr-Lc 50, 72 

 hr-Lc 50 and 96 hr-LC 50 H2S was 4.70, 3.83, 2.81 and 2.51 mg/l, 

 respectively. The toxicity of hydrogen sulfide to the hard clam was 

 maximal under 15-20 ppt in salinity, 7.5-8.5 in acidity (pH) and at the 

 temperature higher than 25ê C. The toxicity effect was found decrease as 

 the physical conditions were deviated from the range of the parameters 

 mentioned and related to the metabolic rate of the clam. 

144 

TITLE: 

 [Current aspects of mechanisms underlying effects of multi-component 

 natural gas, its toxicity and selectivity] 

AUTHORS: 

 Setko NP 

SOURCE: 

 Med Tr Prom Ekol. 1996(1):12-6. [Meditsina truda i promyshlennaia 

 ekologiia] 

ABSTRACT: 

 Experiments on animals included acute, subacute and chronic inhalation of 

 natural gas containing hydrogen sulfide. The multi-component natural gas 

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 was proved to induce more intensive toxic effects, than its components do. 

 When inhaled in concentrations equal to the MACs for its components, the 

 gas induces higher permeability of cellular membranes, compromised 

 biocatalysis systems, 2 times increased lipid peroxidation, disturbed 

 thiol disulfide balance. Mechanism underlying primary effect of the 

 natural gas is associated mostly with activated free radicals, methylation 

 and oxidation of sulfur compounds and their interaction with proteins 

 containing sulfides and metals. 

145 

TITLE: 

 [Problems of occupational hygiene in present-day processing of hydrogen 

 sulfide-containing gases and hydrocarbon condensates] 

AUTHORS: 

 Zebzeev VV 

 Setko NP 

 Zheludeva GN 

SOURCE: 

 Gig Tr Prof Zabol. 1989(5):32-4. [Gigiena truda i professional'nye 

 zabolevaniia] 

146 

TITLE: 

 Anaerobic treatability of waste water from pulp and paper industries. 

AUTHORS: 

 Norrman J 

 Narbuvold R 

 Nyström L 

SOURCE: 

 Biotechnol Adv. 1984; 2(2):329-45. [Biotechnology advances] 

ABSTRACT: 

 A black liquor evaporator condensate from a Kraft mill and a waste water 

 from production of corrugating medium were anaerobically treated on a 

 laboratory scale. The composition of the waste waters was determined 

 before and after treatment in fixed bed reactors.Toxicity studies by the 

 Microtox-method showed that both waste waters were highly toxic and a 

 slight decrease in toxicity was achieved by anaerobic treatment. Despite 

 the toxicity efficient anaerobic treatment was obtained.Major components 

 of the condensate were methanol, ethanol, acetone, guaiacol, hydrogen 

 sulfide and dimethyl disulfide. Anaerobic treatment reduced the 

 concentration of the major components considerably with one exception. The 

 concentration of hydrogen sulfide was unchanged.Organic overloading of the 

 fixed bed reactor or a temperature drop resulted in an accumulation of 

 acetone, although methanol and ethanol were degraded. Major components of 

 the waste water from the production of corrugating medium were: 

 Klason-lignin, acid-soluble lignin, carbohydrates, extractives and ash. 

 When the fixed bed reactor was operated at a volumetric load of 1.6 kg 

 COD/m(3).d the following reductions were obtained: Klason - lignin (solids 

 fraction 84%; soluble and colloidal fraction 76%), acid-soluble lignin 

 (solids fraction 56%; soluble and colloidal fraction 7%), carbohydrates 

 (100%), extractives (71%), total-S (80%), COD (73%) and BOD(7) (78%). 

 Kinetic studies showed that condensate was more easily degraded 

 anaerobically than corrugating medium waste water. 

147 

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TITLE: 

 Mutagenicity of the L-rhamnose-ammonia-hydrogen sulfide Browning reaction 

 mixture. 

AUTHORS: 

 Toda H 

 Sekizawa J 

 Shibamoto T 

SOURCE: 

 J Agric Food Chem. 1981 Mar-Apr; 29(2):381-4. [Journal of agricultural and 

 food chemistry] 

148 

TITLE: 

 Ninety Day Vapor Inhalation Toxicity Study of Hydrogen Sulfide using 

 Fischer 344 Rats, Sprague-Dawley Rats, and B6C3F1 Mice. 

SOURCE: 

 Govt Reports Announcements & Index (GRA&I), Issue 01, 2007 

ABSTRACT: 

 The quality of the documents listed in the Office of Toxic Substances 

 database may not meet usual NTIS standards but are included to further the 

 opportunity for the scientific and technical community to locate materials 

 which may not be available elsewhere. The content is the responsibility of 

 OTS. Prepared in cooperation with Chemical Industry Inst. of Toxicology, 

 Research Triangle Park, NC. Sponsored by Environmental Protection Agency, 

 Washington, DC. Office of Toxic Substances. 

 A 90-day inhalation toxicity study using Fischer 344 rats, Sprague-Dawley 

 rats and B(sub 6)C(sub 3)F(Sub 1) mice (exposed simultaneously in the same 

 chambers) was conducted with hydrogen sulfide vapor and carbon disulfide 

 vapor. 

149 

TITLE: 

 Toxicology of sulfur in ruminants: review. 

AUTHORS: 

 Kandylis K 

SOURCE: 

 J Dairy Sci. 1984, Oct; 67(10):2179-87. [Journal of dairy science] 

ABSTRACT: 

 This review deals with the toxicology of sulfur in ruminants including 

 toxicity, neurotoxic effects, and mechanism of toxic action of hydrogen 

 sulfide, clinical signs, and treatment. It will report effects of 

 excessive intake of sulfur by ruminants on feed intake, animal 

 performance, ruminal digestion and motility, rumination, and other 

 physiological functions. Poisoning of animals with sulfur from industrial 

 emissions (sulfur dioxide) also is discussed. Excessive quantities of 

 dietary sulfur (above .3 to .4%) as sulfate or elemental sulfur may cause 

 toxic effects and in extreme cases can be fatal. The means is discussed 

 whereby consumption of excessive amounts of sulfur leads to toxic effects. 

150 

TITLE: 

 Carbonic anhydrase metabolism is a key factor in the toxicity of CO2 and 

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 COS but not CS2 toward the flour beetle Tribolium castaneum [Coleoptera: 

 Tenebrionidae]. 

AUTHORS: 

 Haritos VS 

 Dojchinov G 

SOURCE: 

 Comp Biochem Physiol C Toxicol Pharmacol. 2005, Jan; 140(1):139-47. 

 [Comparative biochemistry and physiology. Toxicology & pharmacology : CBP] 

ABSTRACT: 

 The analogues carbon dioxide (CO(2)), carbonyl sulfide (COS) and carbon 

 disulfide (CS(2)) have been useful as substrate probes for enzyme 

 activities. Here we explored the affinity of the enzyme carbonic anhydrase 

 for its natural substrate CO(2), as well as COS and CS(2) (1) by in vitro 

 kinetic metabolism studies using pure enzyme and (2) through mortality 

 bioassay of insects exposed to toxic levels of each of the gases during 

 carbonic anhydrase inhibition. Hydrolysis of COS to form hydrogen sulfide 

 was catalysed rapidly showing parameters K(m) 1.86 mM and K(cat) 41 s(-1) 

 at 25 degrees C; however, the specificity constant (K(cat)/K(m)) was 

 4000-fold lower than the reported value for carbonic anhydrase-catalysed 

 hydration of CO(2). Carbonic anhydrase-mediated CS(2) metabolism was a 

 further 65,000-fold lower than COS. Both results demonstrate the 

 deactivating effect toward the enzyme of sulfur substitution for oxygen in 

 the molecule. We also investigated the role of carbonic anhydrases in 

 CO(2), COS and CS(2) toxicity using a specific inhibitor, acetazolamide, 

 administered to Tribolium castaneum (Herbst) larvae via the diet. CO(2) 

 toxicity was greatly enhanced by up to seven-fold in acetazolamide-treated 

 larvae indicating that carbonic anhydrases are a key protective enzyme in 

 elevated CO(2) concentrations. Conversely, mortality was reduced by up to 

 12-fold in acetazolamide-treated larvae exposed to COS due to reduced 

 formation of toxic hydrogen sulfide. CS(2) toxicity was unaffected by 

 acetazolamide. These results show that carbonic anhydrase has a key role 

 in toxicity of the substrates CO(2) and COS but not CS(2), despite minor 

 differences in chemical formulae. 

151 

TITLE: 

 Pathologic response of the lung to irritant gases. 

AUTHORS: 

 Robinson FR 

 Runnels LJ 

 Conrad DA 

 Teclaw RF 

 Thacker HL 

SOURCE: 

 Vet Hum Toxicol. 1990, Dec; 32(6):569-72. [Veterinary and human 

 toxicology] 

ABSTRACT: 

 The pathologic response of the lung to irritant gases ranges from the 

 acute exudative phase through the subacute proliferative phase to the 

 chronic fibrosing phase. These responses are based on damage to the Type I 

 cells, and possibly endothelial cells, and the subsequent proliferative 

 and repair processes in the surviving animals. Responses to high dose 

 exposures appear at the microscopic level as exudation of protein rich 

 fluids into alveoli (alveolar edema) and subsequent death due to anoxia. 

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 Physiologically, this could be described as a mismatch of ventilation with 

 perfusion, resulting in impaired gas exchange. Animals surviving this 

 acute exudative phase resolve the alveolar edema to fibrin, and Type II 

 cells become hypertrophic and hyperplastic in the process of replacing the 

 damaged Type I cells. The acute and subacute responses also elicit 

 inflammatory changes in the interstitium of the lung that may progress to 

 fibrosis in the chronic stage of a survivable exposure. Diagnostic cases 

 in livestock involving irritant gases reflect similar toxic injuries to 

 the lung. 

152 

TITLE: 

 [The effect on respiration and blood circulation of a hydrogen 

 sulfide-containing natural gas] 

AUTHORS: 

 Velikanov EB 

 Trizno NN 

 Tarakanov IA 

 Safonov VA 

SOURCE: 

 Biull Eksp Biol Med. 1993, Jul; 116(7):35-8. [Biulleten' eksperimental'noi 

 biologii i meditsiny] 

153 

TITLE: 

 Mitochondrial depolarization following hydrogen sulfide exposure in 

 erythrocytes from a sulfide-tolerant marine invertebrate. 

AUTHORS: 

 Julian D 

 April KL 

 Patel S 

 Stein JR 

 Wohlgemuth SE 

SOURCE: 

 J Exp Biol. 2005, Nov; 208(Pt 21):4109-22. [The Journal of experimental 

 biology] 

ABSTRACT: 

 Sulfide-tolerant marine invertebrates employ a variety of mechanisms to 

 detoxify sulfide once it has entered their bodies, but their 

 integumentary, respiratory epithelium and circulatory cells may still be 

 exposed to toxic sulfide concentrations. To investigate whether sulfide 

 exposure is toxic to mitochondria of a sulfide-tolerant invertebrate, we 

 used the fluorescent dyes JC-1 and TMRM to determine the effect of sulfide 

 exposure on mitochondrial depolarization in erythrocytes from the annelid 

 Glycera dibranchiata. In erythrocytes exposed to 0.11-1.9 mmol l-1 sulfide 

 for 1 h, the dyes showed fluorescence changes consistent with 

 sulfide-induced mitochondrial depolarization. At the highest sulfide 

 concentration, the extent of depolarization was equivalent to that caused 

 by the mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone 

 (CCCP). Even when induced by as little as 0.3 mmol l-1 sulfide, the 

 depolarization was not reversible over a subsequent 5 h recovery period. 

 The mechanism of toxicity was likely not via inhibition of cytochrome c 

 oxidase (COX), since other COX inhibitors and other mitochondrial electron 

 transport chain inhibitors did not produce similar effects. Furthermore, 

 pharmacological inhibition of the mitochondrial permeability transition 

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 pore failed to prevent sulfide-induced depolarization. Finally, increased 

 oxidation of the free radical indicators H2DCFDA and MitoSOX in 

 erythrocytes exposed to sulfide suggests that sulfide oxidation increased 

 oxidative stress and superoxide production, respectively. Together, these 

 results indicate that sulfide exposure causes mitochondrial depolarization 

 in cells of a sulfide-tolerant annelid, and that this effect, which 

 differs from the actions of other COX inhibitors, may be via increased 

 free radical damage. 

154 

TITLE: 

 Aspects of life development at deep sea hydrothermal vents. 

AUTHORS: 

 Gaill F 

SOURCE: 

 FASEB J. 1993, Apr 1; 7(6):558-65. [The FASEB journal : official 

 publication of the Federation of American Societies for Experimental 

 Biology] 

ABSTRACT: 

 Hydrothermal vent organisms are living in an unexpected deep-sea 

 environment, several thousand meters below the surface, where the earth's 

 crustal plates are spreading apart. The vent fluids are usually hot (350 

 degrees C), anoxic, and contain high concentrations of hydrogen sulfide. 

 This environment may be considered as extreme given the pressure, the high 

 temperature, the chemical toxicity of the fluids, and the total lack of 

 photosynthetic production for animal nutrition. The recent discovery of 

 the unique fauna of the hydrothermal vent communities has brought an 

 unexpected mode of animal nutrition in which chemoautotrophic bacterial 

 symbionts are maintained within specialized cells of the host animal. The 

 bacterial symbionts obtain energy by oxidizing reduced sulfur compounds 

 from the environment. A portion of this fixed carbon is used by the 

 eukaryotic host. The present review will focus on four of the main topics 

 studied on the paradigmatic vent organism Riftia pachyptila, a giant 

 gutless tube worm: 1) the chemoautotrophic symbiosis, 2) the toxicity of 

 hydrogen sulfide, 3) the characteristics of the extracellular matrices of 

 the worms, especially data obtained on collagens, and 4) the influence of 

 temperature and pressure on worm biology. 

155 

TITLE: 

 Hydrogen sulfide exposure on Rhode Island's shoreline. 

AUTHORS: 

 Fulton JP 

 Vanderslice R 

 Marshall RJ 

 Dundulis W 

SOURCE: 

 Med Health R I. 2003, Nov; 86(11):365-6. [Medicine and health, Rhode 

 Island] 

156 

TITLE: 

 Mortality and cancer morbidity in a cohort of Canadian petroleum workers. 

AUTHORS: 

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 Lewis RJ 

 Schnatter AR 

 Drummond I 

 Murray N 

 Thompson FS 

 Katz AM 

 Jorgensen G 

 Nicolich MJ 

 Dahlman D 

 Thériault G 

SOURCE: 

 Occup Environ Med. 2003, Dec; 60(12):918-28. [Occupational and 

 environmental medicine] 

ABSTRACT: 

 AIMS: To assess mortality and cancer morbidity in Canadian petroleum 

 workers and explore exposure-response relations for specific petroleum 

 agents. METHODS: A total of 25 292 employees hired between 1964 and 1994 

 were linked to the Canadian tumour registry and national mortality 

 database. Exposure-response trends were assessed for hydrocarbon 

 solvents/fuels, hydrocarbon lubricants, petroleum coke/spent catalyst, and 

 hydrogen sulphide (H2S). RESULTS: External comparison analyses (mortality 

 and incidence) showed deficits for all causes and all malignant neoplasms 

 combined and were consistent with expectation for most malignant and 

 non-malignant sites analysed. Gall bladder cancer mortality was increased 

 among males based on four deaths, but cases had no common job assignments 

 and the increase was focused in workers employed < 10 years. 

 Mesothelioma incidence was increased. Most exposure-specific analyses were 

 compromised by small numbers. Statistically significant increases were 

 observed for H2S exposure and a subgroup of accidental deaths as well as 

 for petroleum coke/spent catalyst exposure and lung cancer. While both 

 findings have a degree of biologic plausibility, the H2S association, 

 which exhibited a clearer exposure-response pattern, could be subject to 

 unmeasured confounders. Additionally, interpretation was complicated by 

 the high correlation between hydrocarbon and H2S exposures. With regard to 

 lung cancer, the analysis could not adequately control for smoking, was 

 based on small numbers, and exhibited a tenuous exposure-response pattern. 

 CONCLUSION: The findings for mesothelioma suggest the need for continued 

 attention to asbestos in the petroleum industry. The relation between 

 accidental deaths and H2S exposure deserves closer scrutiny in similarly 

 exposed populations. Further analyses of lung cancer are underway and will 

 be reported separately. 

157 

TITLE: 

 Criteria for a Recommended Standard... Occupational Exposure to 

 Hydrogen-Sulfide 

AUTHORS: 

 Anonymous 

SOURCE: 

 Division of Criteria Documentation and Standards Development, NIOSH, 

 Cincinnati, Ohio, Contract No. 099-74-0031, DHEW (NIOSH) Publication No. 

 77-158, 159 pages, 171 references, 19771977 

ABSTRACT: 

 The recommended standard is given limiting employee exposure to less than 

 15 milligrams of hydrogen-sulfide (7783064) per cubic meter of air (10ppm) 

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 during a 10 minute sampling period for up to a 10-hour work shift in a 

 40-hour workweek with evacuation of the area if the concentration equals 

 or exceeds 70 milligrams per cubic meter. In addition, standards are 

 given for medical surveillance, labeling and posting, personal protective 

 equipment, work practices, sanitation, and monitoring and recordkeeping. 

 The criteria for the standards are also given, including extent of 

 exposure in the United States, historical reports of exposure, effects on 

 humans, epidemiological studies, animal toxicity, correlation of exposure 

 and effect, carcinogenicity, mutagenicity, teratogenicity, effects on 

 reproduction, environmental concentrations to which workers have been 

 exposed, various attempts at controlling exposure, environmental sampling 

 and analytical methods, biological monitoring, work practices and safety 

 precautions for handling carbon-disulfide, the bases upon which previous 

 and the present standards are recommended, and research needs. Appendices 

 give the recommended air sampling method, analytical method, 

 specifications for monitors, material safety data sheet, and NIOSH interim 

 work practice recommendations for the gas and oil industry issued in 

 August, 1976. Tables give physical and chemical properties, occupations 

 with potential exposure, and calibration setup for personal sampling pump. 

 (Contract No. 099-74-0031) 

158 

TITLE: 

 Neurotoxicity of hydrogen sulfide may result from inhibition of 

 respiratory enzymes. 

AUTHORS: 

 Roth SH 

 Skrajny B 

 Bennington R 

 Brookes J 

SOURCE: 

 Proc West Pharmacol Soc. 1997; 40:41-3. [Proceedings of the Western 

 Pharmacology Society] 

159 

TITLE: 

 Simultaneous gas chromatographic determination of four toxic gases 

 generally present in combustion atmospheres. 

AUTHORS: 

 Endecott BR 

 Sanders DC 

 Chaturvedi AK 

SOURCE: 

 J Anal Toxicol. 1996 May-Jun; 20(3):189-94. [Journal of analytical 

 toxicology] 

ABSTRACT: 

 The measurement of combustion gases produced by burning aircraft cabin 

 materials poses a continuing limitation for smoke toxicity research. 

 Because toxic effects of gases depend on both their concentrations and the 

 duration of exposure, frequent atmosphere sampling is necessary to define 

 the gas concentration-exposure time curve. A gas chromatographic (GC) 

 method was developed for the simultaneous analyses of carbon monoxide 

 (CO), hydrogen sulfide (H2S), sulfur dioxide (SO2), and hydrogen cyanide 

 (HCN). The method used an MTI M200 dual-column gas chromatograph equipped 

 with 4-m molecular sieve-5A and 8-m PoraPlot-U wall-coated capillary 

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 columns and two low-volume, high-sensitivity thermal conductivity 

 detectors. Detectability (in parts per million [ppm]) and retention times 

 (in seconds) for the gases were as follows: CO, 100 ppm, 28 s; H2S, 50 

 ppm, 26 s; SO2, 125 ppm, 76 s; and HCN, 60 ppm, 108 s. The method was 

 effective for determining these gases in mixtures and in the combustion 

 atmospheres generated by burning wool (CO, HCN, and H2S) and modacrylic 

 fabrics (CO and HCN). Common atmospheric gaseous or combustion products 

 (oxygen, carbon dioxide, nitrogen, water vapor, and other volatiles) did 

 not interfere with the analyses. However, filtration of the combustion 

 atmospheres was necessary to prevent restriction of the GC sampling inlet 

 by smoke particulates. The speed, sensitivity, and selectivity of this 

 method make it suitable for smoke toxicity research and for evaluating 

 performance of passenger protective breathing equipment. Also, this method 

 can potentially be modified to analyze these gases when they are liberated 

 from biosamples. 

160 

TITLE: 

 Hydrogen sulfide: UK occupational exposure limits. 

AUTHORS: 

 Costigan MG 

SOURCE: 

 Occup Environ Med. 2003, Apr; 60(4):308-12. [Occupational and 

 environmental medicine] 

161 

TITLE: 

 Concentration-time-response modeling for acute and short-term exposures. 

AUTHORS: 

 Brown KG 

 Foureman GL 

SOURCE: 

 Regul Toxicol Pharmacol. 2005, Oct; 43(1):45-54. [Regulatory toxicology 

 and pharmacology : RTP] 

ABSTRACT: 

 Risk of health effects from acute and short-term exposure depends on 

 exposure time as well as exposure concentration. A general approach to 

 extending a concentration-response model to include time as a variable is 

 described using mortality of rats exposed to hydrogen sulfide (H(2)S) as 

 an example. This particular example resulted in a logit model with 

 concentration-time (c-t) relationship linear in time and 

 log-concentration. It provided an improved statistical fit, based on the 

 Akaike information criterion in the observed time range, 30 m-360 m, over 

 implementing the c-t relationship of [ten Berge, W.F., Zwart, A., 

 Appelman, L.M., 1986. Concentration-time mortality response relationship 

 of irritant and systemically acting vapours and gases. J. Hazard. Mater. 

 13, 301--309] as a default in the logit model. This approach also 

 indicated that there might be a fundamental difference in the relationship 

 between concentration, time, and response at short exposure times, 

 somewhere less than 30 m, a hypothesis for further consideration from a 

 biological perspective. In general, the proposed approach provides 

 flexibility to develop a concentration-time-response model, and the 

 associated concentration-time relationship, from the data. Interpretation 

 and potential implications, however, need to be considered within the 

 context of biological plausibility as well. Implementation of the proposed 

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 approach requires adequate data for separate concentration-response 

 modeling at each of several exposure durations. 

162 

TITLE: 

 US EPA's acute reference exposure methodology for acute inhalation 

 exposures. 

AUTHORS: 

 Strickland JA 

 Foureman GL 

SOURCE: 

 Sci Total Environ. 2002, Apr 8; 288(1-2):51-63. [The Science of the total 

 environment] 

ABSTRACT: 

 The US Environmental Protection Agency (EPA) National Center for 

 Environmental Assessment is engaged in the development of a methodology 

 for Agency use to perform risk assessments for non-cancer effects due to 

 acute inhalation exposures. The methodology will provide general guidance 

 for deriving chemical-specific acute exposure benchmarks called acute 

 reference exposures (AREs). Chemical-specific AREs are analogous to 

 reference concentra tions (RfCs) for chronic non-cancer effects and will 

 be incorporated in chemical-specific files in the US EPA's Integrated Risk 

 Information System (IRIS) as they are developed and reviewed. AREs will 

 have wide applicability in assessing the potential health risks of 

 accidental and routine acute releases of chemicals to the environment. The 

 proposed methodology for ARE development provides a framework for choosing 

 an optimal derivation approach, depending on the type of data available, 

 from the no-observed-adverse-effect level (NOAEL), benchmark concentration 

 (BMC), or categorical regression approaches. Uncertainty factors are 

 applied to the point of departure, determined by one of the recommended 

 approaches, to derive the ARE. Due to the capability to use more 

 exposure-response information than the NOAEL approach allows, 

 exposure-response analyses such as BMC and categorical regression are 

 favored as methods to develop the point of departure when the available 

 database will support such analyses. The NOAEL approach is suitable when 

 the data are insufficient to support exposure-response modeling. 

 Applications of the proposed ARE methodology are illustrated by the 

 derivation of example AREs for hydrogen sulfide and 

 hexachlorocyclopentadiene, which showcase the categorical regression and 

 NOAEL approaches, respectively. In addition, a recent review of the 

 proposed ARE methodology by the US EPA Risk Assessment Forum is discussed. 

163 

TITLE: 

 [Hygienic assessment of physical and psychophysiologic development of 

 children residing in the area of emissions of Orenburg gas-producing 

 plants] 

AUTHORS: 

 Karpenko IL 

 Utenina VV 

 Ochadchaia ND 

 Perepelkin SV 

 Shkunov VV 

SOURCE: 

 Gig Sanit. 1998 Nov-Dec(6):40-3. [Gigiena i sanitariia] 

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ABSTRACT: 

 The children and adolescents residing in rural settlements located in the 

 vicinity of sites of industrial extraction and processing of hydrogen 

 sulphide-containing gas were studied. The drinking water and ambient air 

 in these settlements were shown to be polluted. Low indices of the 

 children's mental, physiological, and physical development were revealed. 

164 

TITLE: 

 [Effect of hydrogen sulphide containing gas condensate on the humoral 

 immune reaction] 

AUTHORS: 

 Popkov KV 

 Boev VM 

 Frolov BA 

SOURCE: 

 Gig Sanit. 1992 Nov-Dec(11-12):67-8. [Gigiena i sanitariia] 

165 

TITLE: 

 Massive emissions of toxic gas in the Atlantic. 

AUTHORS: 

 Weeks SJ 

 Currie B 

 Bakun A 

SOURCE: 

 Nature. 2002, Jan 31; 415(6871):493-4. [Nature] 

ABSTRACT: 

 Recurrent eruptions of toxic hydrogen sulphide gas in the waters along the 

 Namibian coast off southwestern Africa have been considered to be local 

 features with only limited ecosystem-scale consequences. But satellite 

 remote sensing has revealed that these naturally occurring events are much 

 more extensive and longer-lasting than previously suspected, and that the 

 resultant hypoxia may last for much longer. The effects on the marine 

 ecology and valuable coastal fisheries of this region are likely to be 

 important. 

166 

TITLE: 

 Respiratory responses of the air-breathing fish Hoplosternum littorale to 

 hypoxia and hydrogen sulfide. 

AUTHORS: 

 Affonso EG 

 Rantin FT 

SOURCE: 

 Comp Biochem Physiol C Toxicol Pharmacol. 2005, Jul; 141(3):275-80. 

 [Comparative biochemistry and physiology. Toxicology & pharmacology : CBP] 

ABSTRACT: 

 The present study analyzes the respiratory responses of the neotropical 

 air-breathing fish Hoplosternum littorale to graded hypoxia and increased 

 sulfide concentrations. The oxygen uptake (VO2), critical O2 tension 

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 (PcO2), respiratory (fR) and air-breathing (fRA) frequencies in response 

 to graded hypoxia were determined for fish acclimated to 28 degrees C. H. 

 littorale was able to maintain a constant VO2 down to a PcO2 of 50 mm Hg, 

 below which fish became dependent on the environmental O2 even with 

 significant increases in fR. The fRA was kept constant around 1 breath 

 h(-1) above 50 mm Hg and increased significantly below 40 mm Hg, reaching 

 maximum values (about 4.5 breaths h(-1)) at 10 mm Hg. The lethality to 

 sulfide concentrations under normoxic and hypoxic conditions were also 

 determined along with the fRA. For the normoxic fish the sulfide lethal 

 limit was about 70 microM, while in the hypoxic ones this limit increased 

 to 87 muM. The high sulfide tolerance of H. littorale may be attributed to 

 the air-breathing capability, which is stimulated by this compound. 

167 

TITLE: 

 Effect of hydrogen sulphide on two species of penaeid prawns Penaeus 

 indicus (H. Milne Edwards) and Metapenaeus dobsoni (Miers). 

AUTHORS: 

 Gopakumar G 

 Kuttyamma VJ 

SOURCE: 

 Bull Environ Contam Toxicol. 1996, Nov; 57(5):824-8. [Bulletin of 

 environmental contamination and toxicology] 

168 

TITLE: 

 [Behavioral studies on toxicity of hydrogen sulfide by means of 

 conditioned avoidance responses in rats (author's transl)] 

AUTHORS: 

 Higuchi Y 

SOURCE: 

 Nippon Yakurigaku Zasshi. 1977, Apr; 73(3):307-19. [Nippon yakurigaku 

 zasshi. Folia pharmacologica Japonica] 

169 

TITLE: 

 Hydrogen sulfide poisoning 

AUTHORS: 

 Downie A 

SOURCE: 

 Lancet; VOL 1 ISS Jan 28 1978, P219, (REF 1) 

ABSTRACT: 

 IPA COPYRIGHT: ASHP A treatment regimen for hydrogen sulfide poisoning, 

 if no medical help is available, using a capsule of amyl nitrite broken 

 into a cloth, or 10 ml of 3% sodium nitrite IV over 2 to 3 min is 

 described. 

170 

TITLE: 

 Effect of polycyclic aromatic hydrocarbons on somatic chromosomes of coal 

 tar workers. 

AUTHORS: 

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 Yadav JS 

 Seth N 

SOURCE: 

 Cytobios. 1998; 93(374):165-73. [Cytobios] 

ABSTRACT: 

 The genotoxic effect of polycyclic aromatic hydrocarbons (PAHs) on somatic 

 human chromosomes obtained from lymphocytes of 49 coal tar workers exposed 

 to 26 micrograms/m3 benzo(a)pyrene, 16 mg/m3 benzene and 0.04 mg/m3 H2S in 

 the ambient air, compared to equal numbers of matched controls breathing 

 air containing 1 microgram/m3 benzo(a)pyrene, 1.5 mg/m3 benzene and 0.02 

 mg/m3 H2S, was investigated. The mitotic index (MI), chromosome 

 aberrations (CAs), sister chromatid exchanges (SCEs) and satellite 

 associations (SAs) were analysed. All the parameters showed a significant 

 increase (p < 0.01 and 0.05) in the exposed individuals compared with 

 the controls: viz MI, 4.59-7.92; CAs, 0.77-3.0; SCEs, 5.89-6.80; and SAs, 

 8.18-14.26. The occurrence of the DG type of satellite associations were 

 highest and the 3D type lowest. The frequency of SCEs was highest in coal 

 tar workers with an exposure period of 6-10 years. It is suggested that 

 these results show PAH is genotoxic for humans. 

171 

TITLE: 

 [Experimental substantiation of the maximum permissible exposure levels of 

 gases discharged from polymer materials with reference to their olfactory 

 effect] 

AUTHORS: 

 Mondoev GL 

 Bogachuk GP 

 Barkova NP 

SOURCE: 

 Gig Sanit. 1991, Jan(1):14-7. [Gigiena i sanitariia] 

172 

TITLE: 

 127. Hydrogen Sulphide 

AUTHORS: 

 Nordic expert group; The Dutch expert committee on occupational standards; 

 Svendsen K 

SOURCE: 

 Arbete och Hälsa Vol:14 (2001) 31 p 

ABSTRACT: 

 Hydrogen sulphide (H2S) is a gas that can be generated in nature whenever 

 organic material containing sulphur is present and oxygen is depleted. In 

 addition it can be generated in several industrial settings. It is 

 difficult to predict the rate of gas emission from biological processes, 

 but evidently H2S, when generated, may rapidly reach lethal levels. There 

 is an additional risk in that the unpleasant smell of the gas disappears 

 before harmful levels are reached. H2S must therefore be regarded as a 

 dangerous gas whenever it may occur, with a potential to entail a 

 significant risk of health injury or death in various occupational 

 settings. The main and most quoted effect of H2S is on the nervous system, 

 as the gas, when absorbed into cells, inhibits enzymes of the respiratory 

 chain. The acute toxicity of H2S on the nervous system has been 

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 extensively documented. Furthermore, the direct local action on mucous 

 membranes results in irritation and inflammation of the eyes and 

 respiratory tract. Eye irritation is reported at exposure levels of 0.7-4 

 ppm (1-5 mg/m3) of H2S with concomitant exposure to CS2. Acute exposure at 

 nonfatal levels can result in long-lasting or permanent injury of the 

 nervous system, and in pulmonary oedema. In this context, toxic 

 encephalopathy has also been described in persons accidentally exposed to 

 H2S without losing their consciousness. Exposure levels as low as 2 ppm (3 

 mg/m3) has caused respiratory effects in asthmatic persons, and an 

 increased mortality of coronary heart diseases has been demonstrated in 

 workers exposed to H2S levels below 20 ppm (28 mg/m3). Results from animal 

 studies and an epidemiological study have given reason to take precautions 

 against any exposure of pregnant women. 

173 

TITLE: 

 Inhalation Toxicity Of Combustion Products Of Perchlorate-Fuel Propellants 

 

AUTHORS: 

 Feinsilver L 

 MacNamee JK 

 McGrath FP 

 Oberst FW 

SOURCE: 

 Chemical Corps, Army Chemical Center, Maryland, Medical Division Research 

 Report No. 20, 33 pages, 4 references, 19501950 

ABSTRACT: 

 Toxic combustion products of solid propellant containing perchlorate fuel 

 mixtures were investigated in mice and rats. Adult white-mice and 

 white-rats were exposed to four different combustion products from 

 propellants in an inhalation chamber. The toxic components from 

 propellants were JPL-126, JPL-100-L, JPL-118, and AN-509. The rats and 

 mice were exposed to the smoke and gases discharged at doses from 50 to 

 400 grams for various periods of time. The mortality rate was determined. 

 The general behavior of the surviving animals was also observed. 

 Pathological examination was made on live and dead animals. Continuous 

 sampling from the chamber was made for gaseous components such as 

 hydrogen-sulfide (7783064), sulfur-dioxide (7446095), hydrogen-chloride 

 (7647010), and carbon-monoxide (630080). In some experiments smoke was 

 filtered from the gas and animals were exposed to the filtered product and 

 mortality rate was determined. The apparent order of decreasing toxicity 

 of the combustion gases were JPL-126, JPL-100-L, JPL-118, and AN-509. In 

 general, mice were more susceptible to the toxic action of these gases 

 than rats. Mortality in mice due to toxicity of JPL-126 was 90 percent 

 while the mortality rate due to JPL-100-L, JPL-118, and AN-509, were 20, 

 10, and 10 percent, respectively. No striking differences were seen in 

 mortality between filtered and unfiltered gases. Pathological examination 

 revealed severe respiratory damage, particularly edema and hemorrhage. 

 Observation of general behavior revealed eye irritation and lacrimal 

 secretion in each eye. Sampling and analysis showed that JPL-126, 

 JPL-100-L, and JPL-118 contained mixtures of hydrogen-sulfide, 

 sulfur-dioxide, hydrogen-chloride, and carbon-monoxide, while AN-509 

 consisted of hydrogen-chloride and carbon-monoxide. The authors conclude 

 that discharge gases from the propellants contain toxic components. 

174 

TITLE: 

 Exposure to toxic agents: the heme biosynthetic pathway and hemoproteins 

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 as indicator. 

AUTHORS: 

 Marks GS 

SOURCE: 

 Crit Rev Toxicol. 1985; 15(2):151-79. [Critical reviews in toxicology] 

ABSTRACT: 

 The heme biosynthetic pathway is closely controlled by levels of the end 

 product of the pathway, namely, heme, and porphyrins are normally formed 

 in only trace amounts. When control mechanisms are disturbed by 

 xenobiotics, porphyrins accumulate and serve as a signal of the 

 interaction between a xenobiotic and the heme biosynthetic pathway. For 

 example, an increase in erythrocyte protoporphyrin is a useful measurement 

 for early detection of exposure to lead and porphyrinuria was an early 

 manifestation of a hexachlorobenzene-induced porphyria in Turkey. In 

 recent years a variety of additional xenobiotics has been shown to 

 interact with the heme biosynthetic pathway, namely, halogenated aromatic 

 hydrocarbons, pesticides, sulfides, and a variety of metals. Moreover, 

 different xenobiotics (e.g., dihydropyridines and compounds containing 

 unsaturated carbon-carbon bonds) interact with the prosthetic heme of 

 cytochrome P-450 forming novel N-alkylporphyrins. 

175 

TITLE: 

 The avian respiratory system: a unique model for studies of respiratory 

 toxicosis and for monitoring air quality. 

AUTHORS: 

 Brown RE 

 Brain JD 

 Wang N 

SOURCE: 

 Environ Health Perspect. 1997, Feb; 105(2):188-200. [Environmental health 

 perspectives] 

ABSTRACT: 

 There are many distinct differences (morphologic, physiologic, and 

 mechanical) between the bird's lung-air-sac respiratory system and the 

 mammalian bronchoalveolar lung. In this paper, we review the physiology of 

 the avian respiratory system with attention to those mechanisms that may 

 lead to significantly different results, relative to those in mammals, 

 following exposure to toxic gases and airborne particulates. We suggest 

 that these differences can be productively exploited to further our 

 understanding of the basic mechanisms of inhalant toxicology (gases and 

 particulates). The large mass-specific gas uptake by the avian respiratory 

 system, at rest and especially during exercise, could be exploited as a 

 sensitive monitor of air quality. Birds have much to offer in our 

 understanding of respiratory toxicology, but that expectation can only be 

 realized by investigating, in a wide variety of avian taxa, the 

 pathophysiologic interactions of a broad range of inhaled toxicants on the 

 bird's unique respiratory system. 

176 

TITLE: 

 [Hygienic evaluation of hydrogen sulfide-containing thermal waters used in 

 hot water supply systems] 

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AUTHORS: 

 Beruashvili TsA 

SOURCE: 

 Gig Sanit. 1980, Jun(6):11-3. [Gigiena i sanitariia] 

177 

TITLE: 

 Three-dimensional brain metabolic imaging in patients with toxic 

 encephalopathy. 

AUTHORS: 

 Callender TJ 

 Morrow L 

 Subramanian K 

 Duhon D 

 Ristovv M 

SOURCE: 

 Environ Res. 1993, Feb; 60(2):295-319. [Environmental research] 

ABSTRACT: 

 Thirty-three workers, ages 24 to 63, developed clinical toxic 

 encephalopathy after exposure to neurotoxins and were studied by SPECT 

 brain scans. Five were exposed to pesticides, 13 were acutely exposed to 

 mixtures of solvents, 8 were chronically exposed to mixtures of hazardous 

 wastes that contained organic solvents, 2 were acutely exposed to phosgene 

 and other toxins, and 5 had exposures to hydrogen sulfide. Twenty-nine had 

 neuropsychological testing and all had a medical history and physical. Of 

 the workers who had a clinical diagnosis of toxic encephalopathy, 31 

 (93.9%) had abnormal SPECT brain scans with the most frequent areas of 

 abnormality being temporal lobes (67.7%), frontal lobes (61.3%), basal 

 ganglia (45.2%), thalamus (29.0%), parietal lobes (12.9%), motorstrip 

 (9.68%), cerebral hemisphere (6.45%), occipital lobes (3.23%), and caudate 

 nucleus (3.23%). Twenty-three out of 29 (79.3%) neuropsychological 

 evaluations were abnormal. Other modalities when performed included the 

 following percentages of abnormals: NCV, 33.3%; CPT sensory nerve testing, 

 91.3%; vestibular function testing, 71.4%; olfactory testing, 89.2%; sleep 

 EEG analysis, 85.7%; EEG, 8.33%; CT, 7.14%; and MRI brain scans, 28.6%. 

 The complex of symptoms seen in toxic encephalopathy implies dysfunction 

 involving several CNS regions. This series of patients adds to the 

 previous experience of brain metabolic imaging and demonstrates that 

 certain areas of the brain are typically affected despite differences in 

 toxin structure, that these lesions can be globally defined by SPECT/PET 

 brain scans, that these lesion correlate well with clinical and 

 neuropsychological testing, and that such testing is a useful adjunct to 

 previous methods. EEG and structural brain imaging such as CT and MRI are 

 observed to have poor sensitivity in this type of patient. Additional 

 metabolic imaging studies need to be done to explore dose, time, and 

 specific toxin effects as well as mechanisms of toxicity and olfactory 

 migration. 

178 

TITLE: 

 Toxicology of hydrogen sulfide. 

AUTHORS: 

 Reiffenstein RJ 

 Hulbert WC 

 Roth SH 

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SOURCE: 

 Annu Rev Pharmacol Toxicol. 1992; 32:109-34. [Annual review of 

 pharmacology and toxicology] 

ABSTRACT: 

 Significant progress has been made in determining the action of sulfide on 

 the primary target organs. It is reasonably clear that sulfide causes both 

 K(+)-channel-mediated hyperpolarization of neurons and potentiation of 

 other inhibitory mechanisms. It is not clear whether these processes are 

 similar to those that occur in anoxia. Changes in perinatal and adult 

 brain neurotransmitter content and release may be related to clinical 

 impairment of cognition. H2S exposures at concentrations below the current 

 occupational limits cause physiological changes in pulmonary function, 

 thus suggesting that asthmatics are at risk. Studies of fetal and neonatal 

 brain tissue have shown an abnormal development, and the long-term 

 consequences of these neuronal changes have not yet been assessed. 

 Finally, new approaches to therapy are required, such as the use of agents 

 that actively remove sulfide from its sites of action. This may prove more 

 useful in preventing some of the long-term adverse sequelae than the use 

 of nitrites and hyperbaric O2, although the latter should be used in cases 

 of pulmonary edema. 

179 

TITLE: 

 Toxicity of hydrogen sulphide to juveniles of Macrobrachium rosenbergii. 

AUTHORS: 

 JAYAMANNE SC 

SOURCE: 

 J NATL SCI COUNC SRI LANKA; 20 (2). 1992. 191-198. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Static bio-assays were performed for 96 h to 

 determine the mean lethal concentrations (LC50) of hydrogen sulphide for 

 juveniles of Macrobrachium rosenbergii De Man. Broods of two size classes 

 were tested and LC50 values were determined for 24, 48, 72 and 96 h. The 

 LC50 values were 6.36, 4.25, 3.09 and 2.57 mg/l H2S for brood 1 (7.26 | 

 0.85 mm) and 5.57, 4.79, 4.25 and 4.20 for brood 2 (15.08 | 1.08 mm) 

 respectively, for 24, 48, 72 and 96 h. The safe concentration of hydrogen 

 sulphide for juveniles of M. rosenbergii was determined to be 0.26 mg/l. 

180 

TITLE: 

 Toxicological Profile for Hydrogen Sulfide. 

AUTHORS: 

 Anon 

SOURCE: 

 Govt Reports Announcements &amp; Index (GRA&I), Issue 25, 1999 

ABSTRACT: 

 TD3: This public health statement tells you about hydrogen sulfide and the 

 effects of exposure. Prepared in cooperation with Sciences International, 

 Inc., Alexandria, VA. Sponsored by Agency for Toxic Substances and Disease 

 Registry, Atlanta, GA. 

181 

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TITLE: 

 Pulmonary edema of environmental origin--newer concepts. 

AUTHORS: 

 Cordasco EM 

 Demeter SR 

 Kester L 

 Cordasco MA 

 Lammert G 

 Beerel F 

SOURCE: 

 Angiology. 1986, Jun; 37(6):440-7. [Angiology] 

ABSTRACT: 

 Pulmonary edema of non-cardiac origin is usually an urgent clinical 

 problem, which has recently increased in frequency throughout the world in 

 the past few years. This is partly due to sociological factors and to 

 pre-eminent advances in industrial technology. Recent severe massive toxic 

 gas explosions have had national and worldwide implications. Therefore, 

 urgent and appropriate therapy is of utmost importance in most of these 

 patients. The use of high flow oxygen with Constant Positive Pressure 

 Breathing are the main inhalational therapeutic approaches. Newer 

 modalities of treatment include: (1) earlier Fiberoptic bronchoscopy in 

 those individuals afflicted with aspiration problems and (2) certain 

 specific chemical blocking agents for the management of phosgene 

 intoxication and hydrogen sulfide toxicity. Preventive environmental 

 measures are also important. 

182 

TITLE: 

 Thiosulfate elimination and permeability in a sulfide-adapted marine 

 invertebrate. 

AUTHORS: 

 Julian D 

 Wieting SL 

 Seto SL 

 Bogan MR 

 Arp AJ 

SOURCE: 

 Physiol Biochem Zool. 1999 Jul-Aug; 72(4):416-25. [Physiological and 

 biochemical zoology : PBZ] 

ABSTRACT: 

 Oxidation of hydrogen sulfide to thiosulfate is one of the 

 best-characterized mechanisms by which animals adapted to sulfide minimize 

 its toxicity, but the mechanism of thiosulfate elimination in these 

 animals has remained unclear. In this study, we examined the accumulation 

 and elimination of thiosulfate in the sulfide-adapted marine worm Urechis 

 caupo. The coelomic fluid of U. caupo exposed to 50-100 micromol L-1 

 sulfide in hypoxic seawater (Po2 ca. 10 kPa) accumulated (mean+/-SD) 

 132+/-41 micromol L-1 thiosulfate after 2 h, reaching 227+/-113 micromol 

 L-1 after an additional 4 h in aerated, sulfide-free seawater. In 

 whole-animal thiosulfate clearance studies, the rate of thiosulfate 

 elimination from the coelomic fluid followed a single exponential time 

 course with a half-life of 6 h. The thiosulfate permeability coefficient 

 of isolated preparations mounted in diffusion chambers was 7.6x10-5+/-7. 

 7x10-5 cm s-1 for the hindgut and 5.5x10-7+/-2.7x10-7 cm s-1 for the body 

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 wall. These rates were independent of the direction of net efflux 

 (mucosal-to-serosal or serosal-to-mucosal). Using a simple mathematical 

 model of U. caupo that incorporates the thiosulfate permeability 

 coefficients, the thiosulfate half-life was calculated to be 23 h without 

 hindgut ventilation but less than 1 h with normal hindgut ventilation. 

 Based on this information, we propose that passive thiosulfate diffusion 

 across the hindgut is adequate to explain the observed rates of 

 thiosulfate elimination. 

183 

TITLE: 

 Hydrogen sulfide intoxication: A case report and discussion of treatment. 

AUTHORS: 

 STINE RJ 

 SLOSBERG B 

 BEACHAM BE 

SOURCE: 

 ANN INTERN MED; 85 (6). 1976 756-758 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. The toxicity of hydrogen sulfide is thought to 

 be due primarily to reversible inactivation of the respiratory enzyme, 

 cytochrome oxidase, with resultant inhibition of aerobic metabolism. A 

 patient with severe hydrogen sulfide poisoning and consequent profound 

 metabolic acidosis was treated successfully with nitrites and oxygen. The 

 nitrite-induced methemoglobin, by competititively binding the toxic 

 hydrosulfide anion until detoxified, presumably reactivated and protected 

 cytochrome oxidase and thereby aided the patient's recovery by enhancing 

 aerobic metabolism. His rapid recovery adds clinical support to the 

 efficacy of nitrite therapy in sulfide poisoning. Severe cases of sulfide 

 poisoning should be treated with nitrite-induced methemoglobinemia in 

 addition to vigorous supportive care. 

184 

TITLE: 

 General evaluation of risk associated with the use of pesticides and other 

 chemical substances on animal breeding and plant production farms. 

AUTHORS: 

 Pomorska K 

SOURCE: 

 Int J Occup Saf Ergon. 1999; 5(3):449-57. [International journal of 

 occupational safety and ergonomics : JOSE] 

ABSTRACT: 

 A general characteristic of chemical risk on plant production farms in 

 Poland is presented. The paper describes risk associated with the natural 

 occurrence of chemical substances (such as ammonium and hydrogen sulfide) 

 in the process of animal breeding and risk connected with the use of 

 artificial fertilizers and pesticides. Pesticides are briefly described 

 taking into consideration toxicity classes and the toxic effect of 

 individual compounds. Exposure to pesticides is presented for individual 

 methods and related activities. Finally, the author discusses pesticide 

 risk on fruit-growing farms and in greenhouses. 

185 

TITLE: 

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 [Hydrogen sulfide intoxication--toxicity and therapy] 

AUTHORS: 

 Benson F 

 Karlsson T 

SOURCE: 

 Lakartidningen. 1972, Feb 2; 69(6):627-31. [Lakartidningen] 

186 

TITLE: 

 H2S induces a suspended animation-like state in mice. 

AUTHORS: 

 Blackstone E 

 Morrison M 

 Roth MB 

SOURCE: 

 Science. 2005, Apr 22; 308(5721):518. [Science] 

ABSTRACT: 

 Mammals normally maintain their core body temperature (CBT) despite 

 changes in environmental temperature. Exceptions to this norm include 

 suspended animation-like states such as hibernation, torpor, and 

 estivation. These states are all characterized by marked decreases in 

 metabolic rate, followed by a loss of homeothermic control in which the 

 animal's CBT approaches that of the environment. We report that hydrogen 

 sulfide can induce a suspended animation-like state in a nonhibernating 

 species, the house mouse (Mus musculus). This state is readily reversible 

 and does not appear to harm the animal. This suggests the possibility of 

 inducing suspended animation-like states for medical applications. 

187 

TITLE: 

 HYDROGEN SULFIDE-INDUCED CHANGES IN COIN APPEARANCE 

AUTHORS: 

 GRAEME KA 

 WALLACE KL 

 CURRY SC 

 TANEN DA 

 HIGGINS TJ 

SOURCE: 

 ANNUAL MEETING OF THE NORTH AMERICAN CONGRESS OF CLINICAL TOXICOLOGY, 

 ORLANDO, FLORIDA, USA, SEPTEMBER 9-15, 1998. JOURNAL OF TOXICOLOGY 

 CLINICAL TOXICOLOGY; 36 (5). 1998. 469-470. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM MEETING ABSTRACT MEETING POSTER HUMAN 

 SEWER WORKERS TOXICOLOGY HYDROGEN SULFIDE TOXICITY HYDROGEN SULFIDE 

 EXPOSURE COIN APPEARANCE HYDROGE SULFIDE-INDUCED CHANGES 

188 

TITLE: 

 [Toxicity of chronic dermatoses using hydrogen sulfide baths from 

 Sokolovogorskiĭ spring] 

AUTHORS: 

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 Dvoriantseva MV 

SOURCE: 

 Vopr Kurortol Fizioter Lech Fiz Kult. 1973 May-Jun; 38(3):252-4. [Voprosy 

 kurortologii, fizioterapii, i lechebnoi fizicheskoi kultury] 

189 

TITLE: 

 Poisoning from Hydrogen Sulphide 

AUTHORS: 

 Fowler HC 

SOURCE: 

 Oil and Gas Journal, pages 170/173-174, 17 references, 19281928 

ABSTRACT: 

 Hazards associated with the presence of hydrogen-sulfide (7783064) (H2S) 

 gas in the petroleum industry are reviewed. General characteristics, 

 solubility, and toxicity are discussed. There are three general phases of 

 the hydrogen-sulfide problem: health and safety (the human phase); 

 corrosion (the equipment phase); and treatment (the process phase). The 

 need to control these phases is emphasized. Possible sources of 

 contamination around producing wells, pipe lines, refineries, and gasoline 

 factories are described. Cases of accidental poisoning by H2S in a work 

 situation where rescuers were also overcome are described. Symptoms of 

 poisoning by low concentrations of H2S over a period of time are 

 discussed. These include eye irritation, dry cough, a feeling of fullness 

 in the chest, and lung irritation. At high concentrations, 

 unconsciousness often occurs. The author suggests there is a need for all 

 workers in the vicinity of H2S to learn of its highly toxic effects and to 

 wear suitable breathing equipment. 

190 

TITLE: 

 Inhibition of respiratory and bioenergetic mechanisms by hydrogen sulfide 

 in mammalian brain. 

AUTHORS: 

 Nicholson RA 

 Roth SH 

 Zhang A 

 Zheng J 

 Brookes J 

 Skrajny B 

 Bennington R 

SOURCE: 

 J Toxicol Environ Health A. 1998, Jul 24; 54(6):491-507. [Journal of 

 toxicology and environmental health. Part A] 

ABSTRACT: 

 The biochemical effects of hydrogen sulfide were investigated by treating 

 enzyme homogenates and synaptosomes prepared from mammalian brain with 

 sodium sulfide. Brain cytochrome c oxidase activity was highly sensitive 

 to inhibition by sodium sulfide, as demonstrated by an IC50 of 0.13 

 microM. Sodium sulfide was also found to inhibit carbonic anhydrase 

 activity in cerebellum, frontal cortex, and hippocampus. Synaptosomal 

 oxygen consumption was significantly reduced as the concentration of 

 sodium sulfide was increased from 20 to 100 microM; this was accompanied 

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 by a concentration-dependent depolarization of the synaptosomal 

 mitochondrial membrane in situ and a reduction in synaptosomal ATP 

 concentration. In other experiments using synaptosomes, sodium sulfide 

 caused a significant calcium-independent increase in the extracellular 

 accumulation of L-glutamate, inhibited Na+-dependent uptake of 

 [3H]glutamate, but was unable to influence intrasynaptosomal free ionic 

 Ca2+. Parallel studies conducted in vivo showed that rats exposed over a 

 5-d period to hydrogen sulfide (100 ppm for 3 h/d) had significantly 

 higher concentrations of L-glutamate in the hippocampus compared to 

 control animals. In summary, our results indicate that sulfide causes 

 extensive disruption to respiratory and related mitochondrial functions in 

 mammalian brain in vitro. The reduced capacity of nerve endings to take up 

 L-glutamate may contribute to the raised L-glutamate levels observed in 

 vivo. 

191 

TITLE: 

 Effect of in vitro exposure to hydrogen sulfide on rabbit alveolar 

 macrophages cultured on gas-permeable membranes. 

AUTHORS: 

 Robinson AV 

SOURCE: 

 Environ Res. 1982, Apr; 27(2):491-500. [Environmental research] 

192 

TITLE: 

 Preliminary Air Pollution Survey of Hydrogen Sulfide 

AUTHORS: 

 Miner S 

SOURCE: 

 U. S. Department of Health, Education, and Welfare, Public Health Service, 

 Consumer Protection and Environmental Health Service, National Air 

 Pollution Control Administration, Publication No. APTD 69-37,, 19691969 

 91 pages, 148 references 

ABSTRACT: 

 Review of the literature revealing that hydrogen-sulfide (7783064) in 

 concentrations higher than the million micrograms per cubic meter of air 

 causes human death by respiratory paralysis, while lower concentrations 

 induce respiratory, cardiovascular, psychic, and nervous alterations. Wet 

 scrubbers and incineration are used in various industries to reduce 

 emissions of the gas. Analytical techniques for measuring 

 hydrogen-sulfide are reviewed. 

193 

TITLE: 

 Experimental Studies on CS2 and H2-S Poisoning: The Histological Changes 

 in Hematopoietic Organs and Other Main Internal Organs 

AUTHORS: 

 Tsuyoshi W 

SOURCE: 

 Shikoku Igaku Zasshi, Vol. 14, pages 549-554, 32 references, 19591959 

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ABSTRACT: 

 Rabbits exposed for 140 days to carbon-disulfide (75150) (300ppm) or 

 hydrogen-sulfide (7783064) (100ppm), at the rate of 30 minutes per day, 

 failed to present any significant histopathological alterations except for 

 slight alterations of the liver, kidneys and testes in the 

 hydrogen-sulfide exposed group. Animals exposed to a mixture of 

 carbon-disulfide and hydrogen-sulfide presented significant histological 

 alterations in the bone marrow, liver, spleen, kidneys, testes, ovaries, 

 etc. The results indicate that the association of the two agents has a 

 synergistic effect manifested by significant damage to the body. 

 (Japanese; English translation available) 

194 

TITLE: 

 [Role of preventive examinations of workers administering hydrogen sulfide 

 (Matsest) baths] 

AUTHORS: 

 Putiatina TI 

SOURCE: 

 Oftalmol Zh. 1981; 36(5):314. [Oftalmologicheskii zhurnal] 

195 

TITLE: 

 Commensal bacteria, redox stress, and colorectal cancer: mechanisms and 

 models. 

AUTHORS: 

 Huycke MM 

 Gaskins HR 

SOURCE: 

 Exp Biol Med (Maywood). 2004, Jul; 229(7):586-97. [Experimental biology 

 and medicine (Maywood, N.J.)] 

ABSTRACT: 

 The potential role for commensal bacteria in colorectal carcinogenesis is 

 explored in this review. Most colorectal cancers (CRCs) occur sporadically 

 and arise from the gradual accumulation of mutations in genes regulating 

 cell growth and DNA repair. Genetic mutations followed by clonal selection 

 result in the transformation of normal cells into malignant derivatives. 

 Numerous toxicological effects of colonic bacteria have been reported. 

 However, those recognized as damaging epithelial cell DNA are most easily 

 reconciled with the currently understood genetic basis for sporadic CRC. 

 Thus, we focus on mechanisms by which particular commensal bacteria may 

 convert dietary procarcinogens into DNA damaging agents (e.g., ethanol and 

 heterocyclic amines) or directly generate carcinogens (e.g., 

 fecapentaenes). Although these and other metabolic activities have yet to 

 be linked directly to sporadic CRC, several lines of investigation are 

 reviewed to highlight difficulties and progress in the area. Particular 

 focus is given to commensal bacteria that alter the epithelial redox 

 environment, such as production of oxygen radicals by Enterococcus 

 faecalis or production of hydrogen sulfide by sulfate-reducing bacteria 

 (SRB). Super-oxide-producing E. faecalis has conclusively been shown to 

 cause colonic epithelial cell DNA damage. Though SRB-derived hydrogen 

 sulfide (H(2)S) has not been reported thus far to induce DNA damage or 

 function as a carcinogen, recent data demonstrate that this reductant 

 activates molecular pathways implicated in CRC. These observations 

 combined with evidence that SRB carriage may be genetically encoded evoke 

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 a working model that incorporates multifactorial gene-environment 

 interactions that appear to underlie the development of sporadic CRC. 

196 

TITLE: 

 Cumulative biochemical effects of repeated subclinical hydrogen sulfide 

 intoxication in mouse brain. 

AUTHORS: 

 Savolainen H 

 Tenhunen R 

 Elovaara E 

 Tossavainen A 

SOURCE: 

 Int Arch Occup Environ Health. 1980; 46(1):87-92. [International archives 

 of occupational and environmental health] 

197 

TITLE: 

 New spectrophotometric method for the determination of hydrogen sulfide in 

 the air 

AUTHORS: 

 Stan T 

 Antonescu V 

 Stefanescu E 

 Feraru E 

SOURCE: 

 Farmacia (Bucharest); VOL 27 ISS Apr-Jun 1979, P85-89, (REF 6) 

ABSTRACT: 

 IPA COPYRIGHT: ASHP A colorimetric method for the determination of 

 hydrogen sulfide in air samples, using an acidic reaction with 

 p-phenylenediamine, is described. Minimum absorption occurred at 600 nm, 

 with the lower limit of sensitivity calculated at 0.02 mcg/ml. 

198 

TITLE: 

 Effects of subclinical hydrogen sulfide intoxication on mouse brain 

 protein metabolism. 

AUTHORS: 

 Elovaara E 

 Tossavainen A 

 Savolainen H 

SOURCE: 

 Exp Neurol. 1978, Oct; 62(1):93-8. [Experimental neurology] 

199 

TITLE: 

 Air pollution and mortality in the Rotorua geothermal area. 

AUTHORS: 

 Bates MN 

 Garrett N 

 Graham B 

 Read D 

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SOURCE: 

 Aust N Z J Public Health. 1997, Oct; 21(6):581-6. [Australian and New 

 Zealand journal of public health] 

ABSTRACT: 

 The effects on human health of geothermal emissions in the Rotorua area 

 have been little studied. We calculated standardised mortality ratios 

 (SMRs), comparing residents domiciled in the Rotorua territorial local 

 authority area with those living in the rest of New Zealand, using 

 mortality data for the decade 1981-1990. The SMRs were adjusted for age, 

 calendar year, sex, and ethnicity. Diagnostic categories examined were 

 based on known target-organ systems of hydrogen sulphide toxicity. 

 Mortality causes examined were diseases of the nervous system and sense 

 organs, diseases of the circulatory system, diseases of the respiratory 

 system, and birth defects. Of these, notably elevated SMRs were found only 

 for diseases of the respiratory system, particularly in Maori women (SMR = 

 1.61, 95 per cent confidence interval 1.19 to 2.12). A major concern was 

 the possibility of confounding by ethnicity. This is because ethnicity in 

 census data is based on self-identification, whereas ethnicity on death 

 certificates is often based on funeral directors' impressions. This leads 

 to serious underreporting of Maori mortality statistics. For the purposes 

 of this study, this situation was further complicated by indications that 

 ethnicity recording for Maori may be more accurate in the Rotorua area 

 than in the rest of New Zealand. Our analysis suggested that, in general, 

 SMRs based on ethnicity are likely to be spuriously high. Although this 

 study found no clear indications of excess mortality in the Rotorua area 

 likely to have been associated with geothermal emissions, there were 

 limitations in the data that could have prevented the recognition of 

 causal associations. 

200 

TITLE: 

 [Gaseous messengers in the nervous system] 

AUTHORS: 

 Sitdikova GF 

 Zefirov AL 

SOURCE: 

 Ross Fiziol Zh Im I M Sechenova. 2006, Jul; 92(7):872-82. [Rossiiskii 

 fiziologicheskii zhurnal imeni I.M. Sechenova / Rossiiskaia akademiia 

 nauk] 

ABSTRACT: 

 Nitric oxide is the first gaseous messenger whose functions were 

 comprehensively studied in different systems of organism. Recently, new 

 data on the physiological role of other endogenous gases: carbon monoxide 

 and hydrogen sulfide, appeared. The role of gases in gastrointestinal 

 tract and cardiovascular system have been established; however, data on 

 their function and mechanisms of action in nervous system are 

 insufficient. This article highlights the current information on the role 

 of gaseous messengers in central and peripheral nervous system. 

201 

TITLE: 

 [Influence of chronic intoxication with gas containing hydrogen sulfide on 

 fertility] 

AUTHORS: 

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 Lutsky DL 

 Nikolaev AA 

 Goncharova LA 

 Ushakova MV 

SOURCE: 

 Problemy Reproduktsii 2000;(4):36-40 

202 

TITLE: 

 ACUTE HYDROGEN SULPHIDE H-2S INTOXICATION CLINICAL PRESENTATION AND 

 SEQUELAE IN FIVE SUBJECTS 

AUTHORS: 

 BOMANS P 

 RAPPOORT G 

 MALBRAIN M 

 DEMEYERE I 

 NEMERY B 

SOURCE: 

 ANNUAL CONGRESS OF THE EUROPEAN RESPIRATORY SOCIETY, BERLIN, GERMANY, 

 SEPTEMBER 20-24, 1997. EUROPEAN RESPIRATORY JOURNAL SUPPLEMENT; 10 (25). 

 1997. 232S. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM MEETING ABSTRACT MEETING POSTER HUMAN 

 PATIENT PULMONARY MEDICINE HYDROGEN SULFIDE TOXIN ACUTE HYDROGEN SULFIDE 

 INTOXICATION NEUTROPHILS ACUTE PULMONARY INJURY REACTIVE AIRWAYS 

 DYSFUNCTION SYNDROME RADS TOXICOLOGY TOXICITY BLOOD AND LYMPHATICS IMMUNE 

 SYSTEM RESPIRATORY SYSTEM DISEASE INJURY 

203 

TITLE: 

 Assessment of subsurface fate of monoethanolamine at sour gas processing 

 plant sites-phase iii. 

AUTHORS: 

 Sorensen JA 

SOURCE: 

 Govt Reports Announcements &amp; Index (GRA&I), Issue 25, 2001 

ABSTRACT: 

 Alkanolamines are commonly used by the natural gas industry to remove 

 hydrogen sulfide, carbon dioxide, and other acid gases from the natural 

 gas in which they occur ('sour' gas if hydrogen sulfide is present). At 

 sour gas-processing plants, as at all plants that use alkanolamines for 

 acid gas removal (AGR), spills and on-site management of wastes containing 

 alkanolamines and associated reaction products have occasionally resulted 

 in subsurface contamination that is presently the focus of some 

 environmental concern. In 1994, the Energy and Environmental Research 

 Center (EERC) initiated a three-phase program to investigate the natural 

 attenuation processes that control the subsurface transport and fate of 

 the most commonly used alkanolamine in Canada, monoethanolamine (MEA). 

 Funding for the MEA research program was provided by the U.S. Department 

 of Energy (DOE), Canadian Association of Petroleum Producers (CAPP), 

 Canadian Occidental Petroleum Ltd. (CanOxy), Gas Research Institute (GRI), 

 Environment Canada 

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204 

TITLE: 

 Contributions to the spectrophotometric determination of hydrogen sulfide 

 in the air 

AUTHORS: 

 Stan T 

 Armasescu L 

 Stefanescu E 

 Balalau D 

 Van M 

SOURCE: 

 Farmacia (Bucharest); VOL 33 ISS Apr-Jun 1985, P95-102, (REF 7) 

ABSTRACT: 

 IPA COPYRIGHT: ASHP Colorimetric methods for the determination of 

 hydrogen sulfide in the air, utilizing p-aminophenol or 

 N,N-diethyl-p-phenylenediamine color complexation, are reported. 

205 

TITLE: 

 An Empirical Approach To Dose-Durationresponse Modeling And Time-Scaling. 

AUTHORS: 

 Brown KG 

 Foureman GL 

SOURCE: 

 Toxicol Sci 2005 Mar;84(1-S):78 

ABSTRACT: 

 An approach to deriving a dose-duration-response curve for dichotomous 

 data is described with objectives of: (1) taking exposure duration, as 

 well as exposure level, into account; (2) bringing to bear as much data as 

 possible, of suitable quality, in a unified analysis; (3) testing 

 co-factors that may affect response (e.g., sex, species, lab); (4) 

 determining a time-scaling relationship (effect of a unit change in 

 exposure level relative to a unit change in exposure duration). The idea 

 behind the empirical approach is to extend a dose-response model that fits 

 the data at individual exposure durations to a single model for data over 

 all exposure durations. This is accomplished by using the 

 duration-specific parameter estimates to determine a parametric function 

 to explicitly incorporate duration into the dose metric, creating a 

 dose-duration metric. The data over all exposure durations are then fit 

 simultaneously using the dose-duration metric with addition of any 

 co-factors to be tested. The approach is demonstrated using several 

 studies on mortality of rats exposed to hydrogen sulfide (H2S) for 

 durations between 10m and 6h. The resultant dose-duration metric coincides 

 with one of the choices available in EPA’s program for categorical 

 regression(CatReg). The resultant time-scaling equation differs from the 

 classical time-scaling equation of ten Berge et al. (1986) for 

 concentration (C) and time (t) of the form Cnt = k (for n a parameter, k 

 positive constant), which has been applied previously in a draft EPA 

 guideline document on H2S. The dose-duration model with the derived metric 

 fits the data significantly better than when a doseduration metric 

 consistent with the ten Berge equation is substituted. Time-scaling from 

 the derived metric produced increasingly more conservative (i.e., lower) 

 concentration levels than the ten Berge alternative, for comparable risk, 

 as exposure durations decreased from 1h. 

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206 

TITLE: 

 Spatial analysis of respiratory disease on an urbanized geothermal field. 

AUTHORS: 

 Durand M 

 Wilson JG 

SOURCE: 

 Environ Res. 2006, Jun; 101(2):238-45. [Environmental research] 

ABSTRACT: 

 Chronic exposure to hydrogen sulfide (H(2)S) in the parts per 

 billion-parts per million range occurs in the population of Rotorua, a 

 city built upon an actively degassing geothermal field in the Taupo 

 Volcanic Zone, New Zealand. H(2)S is acutely toxic at high concentrations 

 but little is understood of the health effects of chronic, low-level 

 exposure. In Rotorua, H(2)S emissions and ambient concentrations are 

 heterogeneous and approximately 30% of the greater urban area's population 

 live upon or < 4 km downwind of the geothermal field. Spatial analysis 

 of disease incidence clustering using a spatial scan statistic is a 

 powerful tool with which to investigate the spatial relationship which may 

 exist between H(2)S and respiratory disease. This paper reports findings 

 from a spatial cluster analysis of 11 years of hospital discharge data at 

 the census area unit resolution. Results indicate that the relative risk 

 (RR) of incidence of noninfectious respiratory diseases may be 

 substantially higher among residents living in the geothermal area than 

 have been reported previously. RR >5 for chronic obstructive pulmonary 

 disease and its associated conditions are found in clusters which are 

 spatially coincident with the geothermal field. Future work which 

 investigates neurological and circulatory disease groups at the same or 

 better spatial resolution may provide further insight into the chronic 

 health effects of H(2)S exposure than these preliminary findings indicate. 

207 

TITLE: 

 Hydrogen sulphide: a bacterial toxin in ulcerative colitis? 

AUTHORS: 

 Pitcher MC 

 Cummings JH 

SOURCE: 

 Gut. 1996, Jul; 39(1):1-4. [Gut] 

208 

TITLE: 

 Methionine derivatives diminish sulphide damage to 

 colonocytes--implications for ulcerative colitis. 

AUTHORS: 

 Roediger WE 

 Babidge W 

 Millard S 

SOURCE: 

 Gut. 1996, Jul; 39(1):77-81. [Gut] 

ABSTRACT: 

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 BACKGROUND: Bacterial production of anionic sulphide is increased in the 

 colon of ulcerative colitis and sulphides can cause metabolic damage to 

 colonocytes. AIMS: To assess the reversal of the damaging effect of 

 sulphide to isolated colonocytes by methionine and methionine derivatives. 

 METHODS AND SUBJECTS: Isolated colonocytes were prepared from rat colons 

 and 12 human colectomy specimens. In cell suspensions 14CO2/acetoacetate 

 generation was measured from [1-14C]-butyrate (5.0 mmol/l) in the presence 

 of 0-2.0 mmol/l sodium hydrogen sulphide. The effect of 5.0 mmol/l 

 L-methionine, S-adenosylmethionine 1,4 butane disulphonate and 

 DL-methionine-S-methylsulphonium chloride on sulphide inhibited oxidation 

 was observed. RESULTS: In rat colonocytes sodium hydrogen sulphide dose 

 dependently reduced oxidative metabolite formation from n-butyrate, an 

 action reversed in order of efficacy by S-adenosylmethionine 1,4 butane 

 disulphonate > DLmethionine-S-methyl-sulphonium chloride > L-methionine. 

 In human colonocytes S-adenosylmethionine 1,4 butane disulphonate most 

 significantly improved 14CO2 production (p = < 0.005) suppressed by 

 sodium hydrogen sulphide. CONCLUSION: Sulphide toxicity in colonocytes is 

 reversible by methyl donors. The efficiency of sulphide detoxification may 

 be an important factor in the pathogenesis and treatment of ulcerative 

 colitis for which S-adenosylmethionine 1,4 butane disulphonate may be of 

 therapeutic value. 

209 

TITLE: 

 Hydrogen sulfide 

AUTHORS: 

 ANON 

SOURCE: 

 Canadian Centre for Occupational Health and Safety, 250 Main Street East, 

 Hamilton, Ontario L8N 1H6, Canada, 1986. 18p. 44 ref. 

ABSTRACT: 

 Chemical safety information sheet. Exposure limit (ACGIH, 1985-86): 

 TLV-TWA = 14mg/m|3|. Toxicity: irritation of eyes and respiratory tract at 

 low concentrations; loss of sense of smell above 150ppm; exposure to 

 concentrations above 700ppm may be rapidly fatal; neurotoxic effects. 

210 

TITLE: 

 Hydrogen sulfide and mercaptans 

AUTHORS: 

 Câezard C 

SOURCE: 

 Encyclopâedie mâedico-chirurgicale Toxicologie-Pathologie 

 professionnelle, 2nd Quarter 1994, No.103, 8p. 148 ref. 

ABSTRACT: 

 Data sheet on the effects, the determination and the sampling of hydrogen 

 sulfide (H[2]S) and of mercaptans in the atmosphere and biological matter. 

 Even today H[2]S is one of the gases that cause the greatest number of 

 fatal occupational accidents following acute exposure. The acute effects 

 of mercaptans are on the whole less drastic. Main points covered: 

 metabolic fate; toxicity; exposure monitoring; treatment after acute 

 exposure; exposure limits: H[2]S (ceiling: 10ppm, TWA: 5ppm); 

 methylmercaptan (TWA: 0.5ppm); ethylmercaptan (TWA: 0.5ppm); 

 butylmercaptan (synonym butanethiol, TWA: 0.5ppm); phenylmercaptan 

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 (synonym thiophenol, TWA: 0.5ppm). 

211 

TITLE: 

 Influence of Short-Term Concentration Peaks on Exposure Risks in the 

 Vicinity of an Episodic Release of Hydrogen Sulphide. 

AUTHORS: 

 Anon 

SOURCE: 

 Govt Reports Announcements &amp; Index (GRA&I), Issue 07, 1983 

ABSTRACT: 

 TD3: In order to propose a methodology by which the influence of 

 short-term concentration peaks on exposure risks could be estimated in the 

 vicinity of an atmospheric release of hydrogen sulphide (H sub 2 S), an 

 extensive and up-to-date review of H sub 2 S toxicity was conducted, with 

 emphasis on acute and sub-acute poisoning. The literature on animal 

 studies and cases of human exposure were used to derive a lethal dose 

 relationship(concentration-exposure time) appropriate for the general 

 population. A statistical model was developed which calculates the 

 probability of short-term concentrations exceeding the lethal level given 

 the downwind range from the release, the short-term averaging time of 

 interest, the long-term average concentration, and metereological and 

 terrain conditions. Results were obtained for passive releases of H sub 2 

 S under a range of hypothetical conditions. Interpretation of these 

 results is given in terms of the overall probability of lethal exposure 

 during a 30-minute episode 

212 

TITLE: 

 The Maximum Permissible Concentration Of Hydrogen Sulfide In The Air Of 

 Working Locations When It Is Present Simultaneously With Lower 

 Hydrocarbons 

AUTHORS: 

 Filippova ZKh 

SOURCE: 

 Trudy Ufimskogo Nauchno-Issledovatel'skogo Instituta Gigieny i 

 Profzabolevanii, Vol. 2, pages 340-349, 14 references, 19631963 

ABSTRACT: 

 The comparative toxicity of cracking gas with and without hydrogen-sulfide 

 (7783064) (H2S), or without unsaturated hydrocarbons, and of H2S alone or 

 combined with ethylene (74851), propylene (115071), butylene (25167673), 

 and butane (106978) was studied. Lethal concentrations were determined in 

 white-mice with 2 hour exposures. The effects of the gases on flexor 

 reflex in rabbits were examined in a 40 minute experiment. Mice were 

 chronically poisoned up to 88 days; effects on the nervous system were 

 determined. Thresholds of odor and irritation were measured in humans. 

 Minimum lethal concentration of H2S during a 2 hour exposure was 0.8 

 milligram per liter (mg/l) of air. The remaining gases, without H2S, did 

 not cause death in most animals, even at 20 volume percent. Excitation of 

 the flexor reflex in rabbits was manifest after exposure to 0.01mg/l H2S. 

 Whole cracking gas produced excitation at 0.02mg/l; butylene plus H2S 

 produced excitation at more than 10mg/l. Inhibition was manifest after 

 exposure to 40mg/l butylene alone. Mice chronically exposed to 0.1mg/l 

 H2S exhibited a mean subthreshold pulse of 7.9 before poisoning and 2.7 at 

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 85 days after poisoning. Animals chronically exposed to 20mg/l butylene 

 showed a mean pulse of 7.0 before and 13.9 at 85 days after poisoning. 

 Animals exposed to a combination of butylene and H2S exhibited a mean 

 pulse of 7.7 before and 1.2 at 85 days after poisoning. At the end of 

 exposure, mean swimming time for animals exposed to H2S was 71.2 minutes; 

 for butylene, 72.9; for H2S plus butylene, 25.7; for whole cracking gas, 

 31.5; and for cracking gas without unsaturated hydrocarbons, 58.3. Human 

 smell and irritation thresholds were lower for H2S than for butylene. The 

 author concludes that higher toxicity exists from a mixture of 

 hydrocarbons with H2S than from any of the components of the mixture. In 

 production facilities where H2S is mixed with lower hydrocarbons, a 

 maximum permissible concentration of 0.003mg/l is recommended. (Russian) 

213 

TITLE: 

 The effects of microenvironment on the organism. I. Physical, chemical and 

 biological features of the microenvironment in cages made of concrete 

 containing volatile cinders and in polystyrene cages. 

AUTHORS: 

 Waniewski E 

 Roga-Franc M 

 Członkowska M 

 Wegiel J 

SOURCE: 

 Folia Biol (Krakow). 1979; 27(2):91-6. [Folia biologica] 

214 

TITLE: 

 Nephrotoxicity of mercapturic acids of three structurally related 

 2,2-difluoroethylenes in the rat. Indications for different bioactivation 

 mechanisms. 

AUTHORS: 

 Commandeur JN 

 Brakenhoff JP 

 De Kanter FJ 

 Vermeulen NP 

SOURCE: 

 Biochem Pharmacol. 1988, Dec 1; 37(23):4495-504. [Biochemical 

 pharmacology] 

ABSTRACT: 

 The biotransformation and the hepato- and nephrotoxicity of the 

 mercapturic acids (N-acetyl-1-cysteine S-conjugates) of three structurally 

 related 2,2-difluoroethylenes were investigated in vivo in the rat. All 

 mercapturic acids appeared to cause nephrotoxicity, without any 

 measureable effect on the liver. The mercapturic acid of 

 tetrafluoroethylene (TFE-NAC) appeared to be the most potent nephrotoxin, 

 causing toxicity upon an i.p. dose of 50 mumol/kg. The mercapturic acids 

 of 1,1-dichloro-2,2-difluoroethylene (DCDFE-NAC) and 

 1,1-dibromo-2,2-difluoroethylene (DBDFE-NAC) were nephrotoxic at slightly 

 higher doses, i.e. at 75 and 100 mumol/kg, respectively. In the urine of 

 TFE-NAC-treated rats significant amounts of difluoroacetic acid (DFAA) 

 could be detected. With increasing doses, the relative amount of DFAA in 

 urine increased progressively (5-18% of dose). In urine of rats treated 

 with DCDFE-NAC and DBDFE-NAC, however, the corresponding dihaloacetic 

 acids, dichloroacetic acid and dibromoacetic acid, could not be detected. 

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 Formation of DFAA and pyruvate could also be observed during in vitro 

 metabolism of the cysteine conjugate of tetrafluoroethylene (TFE-CYS) by 

 rat renal cytosol. Inhibition by aminooxyacetic acid (AOA) pointed to a 

 beta-lyase dependency for the DFAA-formation. Next to DFAA and pyruvate, 

 also formation of hydrogen sulfide and thiosulfate could be detected. 

 These results suggest that TFE-CYS is bioactivated to a significant extent 

 to difluorothionacyl fluoride, which most likely is subsequently 

 hydrolysed to difluorothio(no)acetic acid and difluoroacetic acid. 

 According to formation of pyruvate, the cysteine conjugates derived from 

 DCDFE-NAC and DBDFE-NAC also were efficiently metabolized by rat renal 

 beta-lyase. However, the formation of corresponding dihaloacetic acids, 

 dichloroacetic acid and dibromoacetic acid, could not be detected in vitro 

 at all. Only very small amounts of hydrogen sulfide and thiosulfate were 

 detected. These results suggest that bioactivation of the latter two 

 conjugates to a dichloro- or dibromothionoacyl fluoride represents only a 

 minor route. Because of better leaving group abilities of chloride and 

 bromide compared to fluoride, rearrangement of the initially formed 

 ethanethiol to a thiirane might be favoured. Based on the present in vivo 

 and in vitro data, it is concluded that the nephrotoxicity of the 

 structurally related mercapturic acids of 2,2-difluoroethylenes is 

 dependent on halogen substitution and presumably the result of at least 

 two different mechanisms of bioactivation. 

215 

TITLE: 

 [Features of the development of the body's response to increasing exposure 

 to toxic agents] 

AUTHORS: 

 Aĭtbaev TKh 

SOURCE: 

 Gig Sanit. 1987, Mar(3):26-8. [Gigiena i sanitariia] 

216 

TITLE: 

 Effects of acidic deposition and other energy emissions on wildlife: a 

 compendium. 

AUTHORS: 

 Newman JR 

 Schreiber RK 

SOURCE: 

 Vet Hum Toxicol. 1985, Oct; 27(5):394-401. [Veterinary and human 

 toxicology] 

ABSTRACT: 

 Energy emissions, including acidic depositions, pose potential problems 

 for wildlife populations. Historical and recent events show both direct, 

 acute effects and indirect, chronic effects from a variety of airborne 

 pollutants. Information on effects of selected gaseous and particulate 

 energy emissions on domestic animals and livestock and on wildlife is 

 compared. Our understanding of wildlife effects can be improved by the 

 evaluation of veterinary toxicological information and research on the 

 ecological equivalents of domestic and laboratory animals. 

217 

TITLE: 

 Health hazards from volcanic gases: a systematic literature review. 

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AUTHORS: 

 Hansell A 

 Oppenheimer C 

SOURCE: 

 Arch Environ Health. 2004, Dec; 59(12):628-39. [Archives of environmental 

 health] 

ABSTRACT: 

 Millions of people are potentially exposed to volcanic gases worldwide, 

 and exposures may differ from those in anthropogenic air pollution. A 

 systematic literature review found few primary studies relating to health 

 hazards of volcanic gases. SO2 and acid aerosols from eruptions and 

 degassing events were associated with respiratory morbidity and mortality 

 but not childhood asthma prevalence or lung function decrements. 

 Accumulations of H2S and CO2 from volcanic and geothermal sources have 

 caused fatalities from asphyxiation. Chronic exposure to H2S in geothermal 

 areas was associated with increases in nervous system and respiratory 

 diseases. Some impacts were on a large scale, affecting several countries 

 (e.g., Laki fissure eruption in Iceland in 1783-4). No studies on health 

 effects of volcanic releases of halogen gases or metal vapors were 

 located. More high quality collaborative studies involving volcanologists 

 and epidemiologists are recommended. 

218 

TITLE: 

 Sulfide tolerance of four marine species used to evaluate sediment and 

 pore-water toxicity. 

AUTHORS: 

 Knezovich JP 

 Steichen DJ 

 Jelinski JA 

 Anderson SL 

SOURCE: 

 Bull Environ Contam Toxicol. 1996, Sep; 57(3):450-7. [Bulletin of 

 environmental contamination and toxicology] 

219 

TITLE: 

 Environmental factors affecting mercury methylation in estuarine 

 sediments. 

AUTHORS: 

 Choi SC 

 Bartha R 

SOURCE: 

 Bull Environ Contam Toxicol. 1994, Dec; 53(6):805-12. [Bulletin of 

 environmental contamination and toxicology] 

220 

TITLE: 

 [Effect of various environmental factors on health status of children] 

AUTHORS: 

 Shabdarbaeva MS 

 Namazbaeva ZI 

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 Kenesariev UI 

 Nosacheva LF 

SOURCE: 

 Gig Sanit. 1990, Nov(11):12-3. [Gigiena i sanitariia] 

ABSTRACT: 

 The data of the investigation has shown that the high rates of industrial 

 development in Kazakhstan cause multicomponent ambient air contamination. 

 Regression analysis has shown the quantitative relationship between the 

 content of various ingredients in ambient air and certain nosological 

 forms of diseases in children. 

221 

TITLE: 

 [Hygienic evaluation of atmospheric air pollution in animal breeding 

 complexes] 

AUTHORS: 

 Okladnikov NI 

SOURCE: 

 Gig Sanit. 1989, Dec(12):4-6. [Gigiena i sanitariia] 

222 

TITLE: 

 Veterinary aspects of salmonid fish farming: husbandry. 

AUTHORS: 

 Shepherd CJ 

SOURCE: 

 Vet Rec. 1975, Jul 5; 97(1):4-6. [The Veterinary record] 

ABSTRACT: 

 A knowledge of environmental requirements is important in order to obtain 

 good growth and health when farming salmonid fish. Biological requirements 

 are discussed, including water quality parameters and nutritional aspects. 

 The main techniques used for farming salmonids are described together with 

 the annual cycle of operations undertaken on a commercial trout farm. 

223 

TITLE: 

 Determination of concentration-time-mortality relationships versus LC50s 

 according to OECD guideline 403. 

AUTHORS: 

 Arts JH 

 Zwart A 

 Schoen ED 

 Klokman-Houweling JM 

SOURCE: 

 Exp Pathol. 1989; 37(1-4):62-6. [Experimental pathology] 

ABSTRACT: 

 The effect of decreasing the number of animals on the accuracy of 

 estimated concentration-time-mortality relationships and the LC50 values 

 derived from these was investigated by means of simulation methods. 

 Studies of NH3, Cl2, H2S, and COCl2 were made using 5 rats per sex per 

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 group. Mortality rates were analysed in 500 new data sets obtained by 

 randomly removing 4 rats/sex/group from the original data sets. It was 

 concluded that the concentration-time-mortality relationship and the LC50 

 values can be determined over a 5-10-fold time range using one 

 rat/sex/group. The resulting 5 and 95 percentiles compare favourably with 

 the 90% confidence limits when determining a LC50 according to OECD 

 guideline 403. When using concentration-time-mortality relationships, 

 additional information can be obtained which can be used in inhalation 

 hazard risk assessment. 

224 

TITLE: 

 [Influence of ecological environment on the physiological status of 

 students from northern regions] 

AUTHORS: 

 Solonin IuG 

 Chermnykh NA 

 Iakovleva MA 

SOURCE: 

 Fiziol Cheloveka. 2002 Jul-Aug; 28(4):105-11. [Fiziologiia cheloveka] 

225 

TITLE: 

 [Methodological questions in assessing the body's reaction to the action 

 of chemical substances] 

AUTHORS: 

 Kopeĭka IG 

SOURCE: 

 Vrach Delo. 1988, Aug(8):101-4. [Vrachebnoe delo] 

226 

TITLE: 

 Studies of carbonyl sulfide toxicity: Metabolism by carbonic anhydrase. 

AUTHORS: 

 Chengelis CP 

 Neal RA 

SOURCE: 

 Toxicol Appl Pharmacol. 1980, Aug; 55(1):198-202. [Toxicology and applied 

 pharmacology] 

227 

TITLE: 

 [Investigation of air pollution caused by a desulfurizing factory and its 

 effect on the health of neighbourhood residents (author's transl)] 

SOURCE: 

 Zhonghua Yu Fang Yi Xue Za Zhi. 1979; 13(4):236-7. [Zhonghua yu fang yi 

 xue za zhi [Chinese journal of preventive medicine]] 

228 

TITLE: 

 [Immunological shifts in experimental animals exposed to a complex of 

 chemical substances] 

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AUTHORS: 

 Bukharin OV 

 Setko NP 

 Zheludeva GN 

SOURCE: 

 Gig Tr Prof Zabol. 1985, Mar(3):45-6. [Gigiena truda i professional'nye 

 zabolevaniia] 

229 

TITLE: 

 Effects of Inhalation Exposure to Carbon Disulfide and Its Combination 

 with Hydrogen Sulfide on Embryonal and Fetal Development in Rats 

AUTHORS: 

 Saillenfait AM 

 Bonnet P 

 de Ceaurriz J 

SOURCE: 

 Toxicology Letters, Vol. 48, No. 1, pages 57-66, 11 references, 1989 

ABSTRACT: 

 Embryonal and fetal developmental effects of inhalation exposure to 

 carbon-disulfide (75150) (CS2) with and without hydrogen-sulfide (7783064) 

 (H2S) were investigated in Sprague-Dawley-rats. Female rats were exposed 

 to 100 parts per million (ppm), 200ppm, 400ppm, or 800ppm CS2 for 6 

 hours/day during days six to 20 of gestation, then sacrificed. Other 

 groups were exposed to 100ppm H2S with or without 400ppm or 800ppm CS2. 

 The litter was considered the experimental unit for embryotoxicity 

 (including teratogenicity) data analysis. Numbers of implantations and 

 dead or live fetuses were comparable among groups. Results for CS2 

 exposure only indicated significant dose related reductions in maternal 

 weight gain and fetal body weights (both sexes) at 400ppm and 800ppm 

 doses. The incidence of unossified fetal sternebrae was significantly 

 increased at 800ppm. An increased (although statistically not 

 significant) club foot incidence was seen. Results for simultaneous CS2 

 and H2S exposure indicated that maternal weight gain was slightly reduced, 

 compared with CS2 alone, and the fetal sex ratio slightly favoring males. 

 A significant fetal body weight reduction was observed with CS2 alone, 

 which was enhanced by exposure to 100ppm H2S. No major skeletal anomaly 

 was detected in any treated group. No significant evidence of 

 teratogenicity was observed. The authors conclude that 400ppm or 800ppm 

 CS2 exposure alone produced significant evidence of fetal toxicity which 

 was associated with maternal toxicity. Simultaneous 100ppm H2S exposure 

 only enhanced the fetal toxicity of CS2. 

230 

TITLE: 

 Hydrogen Sulfide Exposure Causes Intracellular Acidification Of Rat Nasal 

 Respiratory Epithelial Cells. 

AUTHORS: 

 Roberts ES 

 Wong VA 

 McManus BE 

 Dorman DC 

SOURCE: 

 Toxicol Sci 2005 Mar;84(1-S):192 

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ABSTRACT: 

 Hydrogen sulfide (H2S) is a naturally occurring gas that is also generated 

 by several industries. The potential for widespread human inhalation 

 exposure to this toxic gas is recognized as a public health concern. Human 

 epidemiological investigations and experimental laboratory animal studies 

 have confirmed that the nasal epithelium is a sensitive site for 

 H2S-induced pathology. Cytochrome oxidase (Co) inhibition has been 

 postulated as one mechanism of H2S toxicity. Inhibition of Co disrupts the 

 electron transport chain and impairs oxidative metabolism, leading to 

 decreased ATP production and the build-up of lactic acid. While Co is a 

 sensitive marker of H2S exposure, there is an incomplete correlation 

 between H2S-induced nasal lesions and Co inhibition. Another mechanism by 

 which H2S (a weak organic acid) could cause nasal injury is intracellular 

 acidification and cytotoxicity. Literature reports show that changes in 

 intracellular pH due to exposure to organic acids such as vinyl acetate 

 can lead to cell death. To further understand the mechanism by which H2S 

 damages the nasal epithelium, nasal respiratory epithelial cells were 

 isolated from naive rats; loaded with the pH-sensitive dye, SNARF-1; and 

 exposed to air or 400 ppm H2S for 90 min. Vinyl acetate (1000 μM) was used 

 as a positive control. Intracellular pH was measured by flow cytometry and 

 cell lysates were used to quantify total protein and Co activity. Flow 

 cytometric analysis showed that nasal respiratory epithelial cells exposed 

 to air maintained a pH of 7.6 +/- 0.05. A significant decrease in 

 intracellular pH occurred following exposure to either vinyl acetate (15% 

 decrease from control) or H2S (5% decrease from control). Co activity in 

 air-exposed cells was 1.39 ± 0.01 delta abs/min/mg protein, while Co 

 activity in cells exposed to H2S was not detectable. The intracellular 

 acidification of nasal respiratory epithelial cells by H2S demonstrates a 

 novel mechanism of H2S-induced nasal respiratory cellular toxicity. 

231 

TITLE: 

 90-DAY VAPOR INHALATION TOXICITY STUDY OF HYDROGEN SULFIDE IN 

 SPRAGUE-DAWLEY RATS WITH EPA ACKNOWLEDGEMENT DATED 101183 

SOURCE: 

 EPA/OTS; Doc #FYI-OTS-0883-0255 

ABSTRACT: 

 In a subchronic toxicity study, male and female Sprague-Dawley rats 

 (15/sex/group) were exposed to hydrogen sulfide by inhalation at time 

 weighted average analytical concentrations of 0, 10.1, 30.5 or 80.0 ppm 

 for 6 hours/day, 5 days/week for at least 90 days. None of the animals 

 died during the study. Clinical observations included crustiness 

 associated with the ear tag on the animals ear; crusty nose, eye and 

 muzzle; lacrimation; rales; red-stained fur; irritability; swollen and red 

 ear; and swollen muzzle and/or eye. A significant decrease in body weight 

 gain was observed in the high-dose level group animals with respect to 

 cont 

 rol group animals. No significant effects were observed with respect to 

 food consumption, ophthalmology, neurological function, and clinical 

 pathology. No gross pathology or histopathology was observed which could 

 be attributed to the test material. The brain weights of high-dose level 

 group animals of both sexes were depressed relative to the brain weights 

 of control animals. No neuropathology was indicated in special 

 neuropathological studies performed on teased fibers from muscular and 

 sural branches of the tibial nerve, together with Epon embedded specimens 

 of these nerves and specimens from cervical and lumbar spinal cord from 

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control and high-dose group animals. 

232 

TITLE: 

 Phosphoric acid, phosphorus pentoxide, phosphorus oxychloride, phosphorous 

 pentachloride, phosphorus pentasulphide 

AUTHORS: 

 Payne MP 

 Shillaker RO 

 Wilson AJ 

SOURCE: 

 HSE Toxicity Review Vol:30 (1993) 22 p 

ABSTRACT: 

 Phosphoric acid. No significant toxicokinetic information is available. 

 Although the reliability of the very low inhalation LC50 value in mice is 

 open to question, the substance would appear to be toxic by this route. It 

 is also moderately toxic to rodents via the oral route. The acute dermal 

 toxicity in rabbits is low. The substance is corrosive to rabbit skin and 

 severely irritating to the eye. In a poorly reported study, "chronic" 

 inhalation of phosphoric acid aerosol was claimed to cause irritation of 

 the respiratory tract. The substance has yielded negative results in 

 bacterial mutagenicity assays, the only genotoxicity data available. There 

 are no adequate reproductive toxicity or carcinogenicity investigations in 

 animals. No clearly reliable human acute inhalation data are available. As 

 in other species the substance is corrosive, with moderate to severe 

 subjective stinging responses being recorded following dermal or ocular 

 application of very dilute solutions. Widespread corrosion of the 

 gastrointestinal tract has been reported in one case of oral ingestion. No 

 useful human data are available on the effects of repeated inhalation 

 exposure. Consumption of moderate amounts of phosphoric acid in the diet 

 failed to indicate any toxicity. No reliable human data on the 

 carcinogenic potential of phosphoric acid are available. In addition no 

 human data are available on its potential to cause genotoxicity or 

 reproductive toxicity. Phosphorus pentoxide. Data on the toxicity of 

 phosphorus pentoxide to animals are available only from studies of 

 exposure to smokes produced by burning red or white phosphorus. Phosphorus 

 pentoxide is the predominant combustion product when oxygen is not 

 limited. Variable amounts of hydrolysis products are subsequently formed. 

 No toxicokinetic studies were located. Acute inhalation of phosphorus 

 smokes is moderately toxic to several laboratory species and very toxic to 

 guinea pigs. Marked respiratory tract irritation was commonly observed and 

 in one study slight eye irritation was noted. Phosphorus pentoxide is 

 expected to be corrosive because of its rapid exothermic reaction on 

 contact with water to generate phosphoric acid. Repeated inhalation of 

 phosphorus smokes causes respiratory tract irritation. Pulmonary fibrosis 

 has been observed in one study in rats exposed to a smoke concentration of 

 300 mg/m3; a no-effect level of 50 mg/m3 was claimed but no supporting 

 data were provided to support the claim. In another study there was 

 evidence of toxicity in rats and mice following repeated exposure to 

 phosphorus smoke at a concentration approximately equivalent to 37 mg/m3 

 phosphorus pentoxide. The information available from genotoxicity and 

 animal reproductive toxicity studies of phosphorus smokes is too limited 

 to enable useful conclusions to be drawn. No animal carcinogenicity 

 studies are available. Phosphorus pentoxide concentrations of 3.6-11.3 

 mg/m3 have been claimed to cause coughing amongst inexperienced workers 

 and 100 mg/m3 to be unendurable except to hardened workers, but the 

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 reliability of this data is questionable. In contrast, phosphorus smokes 

 would appear to be tolerated at significantly higher exposure levels, 1000 

 mg/m3 being reported to be the minimum harassing level in resting men. It 

 is assumed that these reports refer to the response to a single exposure, 

 but the duration of exposure is not known. No useful human data on the 

 effects of repeated exposure to phosphorus pentoxide are available. No 

 human data are available on the genotoxic or carcinogenic potential of 

 phosphoric acid or on its potential to cause reproductive toxicity. 

 Phosphorus oxychloride. No toxicokinetic studies were located. Phosphorus 

 oxychloride is acutely very toxic when inhaled by rats and guinea pigs, 

 causing extensive irritation of the respiratory tract. It is also acutely 

 toxic to rats via the oral route. The substance is corrosive to rabbit 

 skin and causes severe eye damage. Little reliable information is 

 available on the effects of repeated inhalation in animals. Irritation of 

 the respiratory tract would be expected and has been claimed in one poorly 

 reported rat study, although no reliance can be placed on these data, 

 particularly as it is not clear if continuous or repeated exposure was 

 used. No reliable genotoxicity or animal reproductive toxicity data are 

 available. No animal carcinogenicity study was located. Single exposure of 

 humans to airborne material has been reported to cause conjunctivitis, 

 pharyngitis and respiratory tract irritation, including pulmonary oedema. 

 No reliable threshold concentration for these effects is available. 

 Similar effects were seen following repeated exposure including asthmatic 

 bronchitis and, in severe cases, emphysema. Exposure levels were 10-20 

 mg/m3, rising to 70 mg/m3, and sometimes to higher levels. Workers who 

 suffered respiratory effects were reported to show increased respiratory 

 tract sensitivity to phosphorus oxychloride and to other irritant 

 substances, particularly phosphorus bichloride and pentachloride. No human 

 data are available on the genotoxic or carcinogenic potential of 

 phosphorus oxychloride or on its potential to cause reproductive toxicity. 

 Phosphorus trichloride. No toxicokinetic studies were located. The 

 substance is very toxic to rodents following acute inhalation exposure. 

 The main effects reported in acute inhalation studies are irritation 

 and/or corrosion of the respiratory tract, eyes and skin. The substance is 

 also acutely toxic to rats via the oral route and is corrosive when 

 applied to the skin as a liquid. Phosphorus trichloride has been reported 

 to be negative in a modified Ames test. No other genotoxicity information 

 was located. No repeat dose, reproductive toxicity or carcinogenicity 

 studies in animals are available. Single exposure of humans to airborne 

 material has been reported to lead to ocular and respiratory tract 

 irritation. No reliable threshold concentration for these effects is 

 available. Repeated exposure to levels of 10-20 mg/m3, with intermittent 

 peaks of 80-150 mg/m3 has been reported to cause pharyngeal irritation, 

 coughing, catarrh and pronounced asthmatic bronchitis. These effects 

 tended to recur and, following one to two years' exposure, could develop 

 into pulmonary emphysema. No human data are available on the genotoxic or 

 carcinogenic potential of phosphorus trichloride or on its potential to 

 cause reproductive toxicity. Phosphorus pentachloride. Very little 

 information is available on phosphorus pentachloride. One poorly reported 

 study indicates that it is very toxic to rodents following acute 

 inhalation exposure. The substance is also acutely toxic via the oral 

 route. Phosphorus pentachloride would be expected to be corrosive because 

 of its hydrolysis products. A report of tissue necrosis when the substance 

 is applied to rabbit skin supports this view. Phosphorus pentachloride is 

 reported to cause irritation to the respiratory tract and eyes in humans. 

 No reliable threshold concentration for these effects is available. No 

 other useful animal or human data are available. Phosphorus pentasulphide. 

 There is virtually no information on the toxicity of phosphorus 

 pentasulphide. The substance is reported to be acutely toxic to rats 

 following oral administration and to be a moderate skin and eye irritant. 

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 Irritancy of the respiratory tract would be expected because the sustance 

 is rapidly hydrolysed to phosphoric acid and hydrogen sulphide. No good 

 human data on the effects of phosphorus pentasulphide are available. 

233 

TITLE: 

 Gases in agricultural slurry stores. 

AUTHORS: 

 GROVES JA 

 ELLWOOD PA 

SOURCE: 

 ANN OCCUP HYG; 35 (2). 1991. 139-152. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. The evolution of gases during the handling 

 of animal slurry was investigated at five sites. Particular attention was 

 paid to the mixing and emptying operations since it is when performing 

 these that personnel are most likely to be at risk of exposure. The main 

 hazard was found to be high transient concentrations of hydrogen sulphide 

 presenting in some cases a serious acute toxicity problem. Time-weighted 

 average exposures did not generally indicate any long-term exposure risk. 

 Other features noted were the evolution of ammonia and methane, although 

 not at high levels, and some increase in the carbon dioxide concentration. 

 Some reduction in oxygen concentration was measured, but generally the 

 risk of poisoning by hydrogen sulphide was more serious than the risk of 

 asphyxiation. 

234 

TITLE: 

 PAPER PRODUCTION AND PROCESSING-OCCUPATIONAL EXPOSURE AND ENVIRONMENTAL 

 RELEASE STUDY (PROJECT SUMMARY) 

AUTHORS: 

 Soklow R 

SOURCE: 

 Cincinnati, OH: Environmental Protection Agency, Industrial Environmental 

 Research Laboratory; August 1984: 4 pages (EPA-600-84120)./ETIOLOGY 

ABSTRACT: 

 HMTC Exposure to high concentrations of hydrogen sulfide, other sulfur 

 compound emissions, chlorine, and carbon monoxide is a significant 

 occupational hazard during the production and processing of paper. For 

 the vast majority of chemicals in use in the industry, emission sources, 

 worker exposure, and long-term effects data are scarce. An overview of 

 the paper industry's technology, production, economics, projected growth, 

 and operations analysis; a discussion of occupational exposure; a review 

 of previous case studies; a discussion of process control measures; a copy 

 of OSHA's regulations governing pulp and paper mills; and specific waste 

 treatment technologies are provided. 

235 

TITLE: 

 Hydrogen Sulfide Poisoning As A Hazard In The Production Of Oil 

AUTHORS: 

 Davenport SJ 

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SOURCE: 

 Bureau of Mines, U.S. Department of the Interior, Report No. IC-7329, 

 pages 1-9, 14 references, 19451945 

ABSTRACT: 

 The hazards of working with hydrogen-sulfide (7783064) (H2S) in mining and 

 mineral industries are reviewed. Physical and chemical properties of H2S, 

 its toxicity and physiologic effects, treatment of poisoning, and 

 prevention and detection of exposures are summarized. H2S has been found 

 in coal mining operations and in other types of mines during normal 

 operations, and it has been known to cause severe eye irritation, serious 

 illness, and fatalities. H2S is usually a product of the decomposition of 

 sulfur (7704349) compounds and may be produced by burning explosives 

 containing sulfur. Harmful quantities of the gas are formed by the use of 

 black blasting powder or by the use of dynamite in blasting sulfide ores. 

 It can also be released from water streams in coal or other mines. The 

 number of oil fields in the United States that produce sour crude oils 

 containing H2S and other sulfur compounds has increased in recent years. 

 H2S gas present in these fields, gas that escapes from tanks in which the 

 crude oil is stored or which evolves during some of the refining process 

 is lethal in higher concentrations. The author concludes that detection 

 and measurement of H2S and wearing protective equipment are useful in the 

 prevention of H2S poisoning. 

236 

TITLE: 

 The Effect of Tachykinin Depletion on Hydrogen Sulphide Toxicity in Rats 

AUTHORS: 

 Green FHY 

 Lopez A 

 Prior M 

 Balu A 

 Butt J 

SOURCE: 

 Proceedings of the VIIth International Pneumoconioses Conference, Part I. 

 Pittsburgh, Pennsylvania, August 23-26, 1988. NIOSH, U.S. Department of 

 Health and Human Services, DHHS (NIOSH) Publication No. 90-108 Part I, 

 pages 607-617, 29, 1990 

 references 

ABSTRACT: 

 A study was made of the effects of hydrogen-sulfide (7783064) (H2S) in 

 animals previously depleted of substance-P and focused on the 

 pathophysiology of the airway lesions. A comparison was made of the 

 histological changes induced in the lungs of the Fischer-344-rats exposed 

 to H2S with the changes observed in the lungs of humans following fatal 

 exposures to H2S. Animals exposed to H2S without capsaicin pretreatment 

 had a 20% mortality at an average concentration of 542mg/m3. Animals 

 pretreated with capsaicin and exposed to the same concentration of H2S 

 demonstrated 100% mortality. The animals also died at an earlier time 

 during exposure than animals pretreated with saline and then exposed to 

 H2S. Those pretreated with capsaicin also suffered more severe pulmonary 

 edema with a greater concentration of protein in the lavage fluid and 

 heavier lungs postmortem. The airway lesions noted in the H2S exposed 

 rats were similar to those reported for sulfur-dioxide (7446095). The 

 lesions were most severe in the proximal airways with relative sparing of 

 the bronchioles and alveolar ducts. An unexpected result was the 

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 demonstration of a potentiating effect of neuropeptide depletion on H2S 

 induced airway injury. 

237 

TITLE: 

 The Toxicity of Hydrogen Sulphide and Other Sulphides 

AUTHORS: 

 Evans CL 

SOURCE: 

 Quarterly Journal of Experimental Physiology, Vol. 52, No. 3, pages 

 231-248, 38 references, 19671967 

ABSTRACT: 

 The comparative toxicities of hydrogen-sulfide (7783064) (H2S) vapor and 

 injected sulfide solution were examined in various animals. Imprecise H2S 

 inhalation experiments were performed on cats, rabbits, and rats. Either 

 an H2S solution or a sodium-bisulfite (7631905) solution containing about 

 120 micromoles per milliliter was injected into the femoral vein, 

 brachiocephalic artery, or into the right carotid artery by catheter. 

 Both H2S and sulfite produced toxic reactions similar to cyanide: 

 paralysis; pupil constriction followed by dilation; increased respiration 

 followed by a decrease; and increased blood pressure followed by a 

 decrease. Responses varied considerably according to site and rate of 

 administration. The author concludes that H2S destruction occurs in the 

 red blood cells through the reduction of oxyhemoglobin; therefore, 

 treatment of H2S poisoning requires oxygen or artificial respiration. The 

 most conspicuous actions of sulphides are on the nerve centers (which are 

 first stimulated and are then paralyzed); however, these actions are 

 reversible. 

238 

TITLE: 

 Role of hydrosulfide ions (HS-) in methylmercury resistance in 

 Saccharomyces cerevisiae. 

AUTHORS: 

 Ono B 

 Ishii N 

 Fujino S 

 Aoyama I 

SOURCE: 

 Appl Environ Microbiol. 1991, Nov; 57(11):3183-6. [Applied and 

 environmental microbiology] 

ABSTRACT: 

 Methylmercury-resistant mutants were obtained from Saccharomyces 

 cerevisiae. They were divided into two complementation groups, met2 

 (homoserine O-acetyltransferase deficiency) and met15 (enzyme deficiency 

 unknown), as reported previously. It was found that met15 was allelic to 

 met17 (O-acetylserine and O-acetylhomoserine sulfhydrylase deficiency). 

 Methylmercury toxicity was counteracted by exogenously added HS-, and both 

 met2 and met17 (met15) mutants overproduced H2S. On the basis of these 

 results, we conclude that met2 and met17 (met15) cause accumulation of 

 hydrosulfide ions in the cell and that the increased level of hydrosulfide 

 is responsible for detoxification of methylmercury. 

239 

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TITLE: 

 Environmental exposure to natural sour gas containing sulfur compounds 

 results in elevated depression and hopelessness scores. 

AUTHORS: 

 Saadat M 

 Zendeh-Boodi Z 

 Goodarzi MA 

SOURCE: 

 Ecotoxicol Environ Saf. 2006, Oct; 65(2):288-91. [Ecotoxicology and 

 environmental safety] 

ABSTRACT: 

 Some parts of Masjid-i-Sulaiman (MIS) (Khozestan provinces, southwest of 

 Iran) are contaminated with subsurface leakage of natural sour gas 

 containing H(2)S. It is reported that the incidence of suicide by 

 self-burning in MIS is very high. High endogenous H2S levels have been 

 found in the brain and it is involved in the brain functions. Because 

 there is no report about the effect(s) of natural sour gas containing 

 sulfur compounds on the function(s) of human brain, the present study was 

 done. The study was performed on 128 individuals exposed or unexposed to 

 natural sour gas. The exposed group consisted of 64 persons (39 males, 25 

 females). Unexposed subjects were matched by sex, age, and educational 

 levels. Depression and hopelessness were determined using Beck's 

 depression inventory (BDI) and Beck's hopelessness (BHS) questionnaires. 

 Using multiple linear regression models, the averages of BDI (t=2.637, 

 P=0.009) and BHS (t=3.344, P=0.001) were significantly higher among the 

 exposed subjects than among the control group. In Lali 57.8% and 14.1% of 

 subjects had no depressed mood and moderate to severe depressed mood, 

 respectively, while in MIS 31.3% and 35.9% of subjects had no depressed 

 mood and moderate to severe depressed mood, respectively; the difference 

 was significant (chi2=12.88, df=3, P=0.005). In Lali 35.9% and 12.5% of 

 subjects had no hopelessness at all and moderate to severe hopelessness, 

 respectively, while in MIS 17.2% and 32.8% of subjects had no hopelessness 

 at all and moderate to severe hopelessness, respectively, the difference 

 was significant (chi2=11.49, df=3, P=0.009). Replication is necessary and 

 health implications are discussed. 

240 

TITLE: 

 Sulfide toxicity in anaerobic systems fed sulfate and various organics. 

AUTHORS: 

 MAILLACHERUVU KY 

 PARKIN GF 

 PENG CY 

 KUO W-C 

 OONGE ZI 

 LEBDUSCHKA V 

SOURCE: 

 WATER ENVIRON RES; 65 (2). 1993. 100-109. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Upflow anaerobic filters fed acetate and 

 propionate, and completely, mixed, suspended growth reactors fed acetate, 

 propionate, lactate, and glucose were used to investigate the effect of 

 electron donor and reactor type on the interaction between 

 sulfate-reducing bacteria (SRB) and methanogens. Organic loading rates of 

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 0.25-0.50 g chemical oxygen demand (COD)0-5.0 g COD/L to 2/1 for 

 completely mixed reactors, and 20/1 to 8/1 for anaerobic filters. Results 

 indicated that organisms involved in the conversion of lactate and glucose 

 into simpler products were not affected by sulfide toxicity. Levels of 

 60-75 mg sulfur/L of hydrogen sulfide and 150-200 mg/L of dissolved 

 sulfide (DB) caused stress in all suspended growth reactors; 100-150 mg 

 sulfur/L of hydrogen sulfide and 200-400 mg DS/L could be tolerated in 

 lactate and glucose systems, although with diminished COD and sulfate 

 removal. For similar loading conditions, lactase and glucose system had 

 higher DS levels than aceta 

241 

TITLE: 

 Hydrogen sulfide in parenteral amino-acid solutions. 

AUTHORS: 

 SOCHA P 

 HEIM P 

 KOLETZKO B 

SOURCE: 

 CLINICAL NUTRITION (EDINBURGH); 15 (1). 1996. 34-35. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. We have previously reported appreciable 

 concentrations of hydrogen sulfide (H2S) in paediatric amino-acid 

 solutions, apparently formed from cysteine during the production process. 

 Since manufacturers assured us of their aim to reduce the contents of the 

 potentially toxic H2S in these solutions, we determined whether lower 

 amounts have been achieved 2 years after our first report. Median H2S 

 content of 13 paediatric amino-acid solutions was 22.8 mug/l (range: not 

 detectable to > 280 mug/l) which is comparable to the amounts 

 previously found. Median H2S content of 8 special solutions for renal and 

 hepatic disorders was 15.8 mug/l (range not detectable to > 280 mug/l). 

 We conclude that manufacturers should make further efforts to reduce H2S 

 amounts in parenteral amino-acid solutions. 

242 

TITLE: 

 MECHANISMS OF SULFIDE TOXICITY 

AUTHORS: 

 ARP A 

SOURCE: 

 Crisp Data Base National Institutes of Health 

ABSTRACT: 

 Hydrogen sulfide poses a serious environmental health hazard to humans. 

 Virtually all documented cases of acute sulfide poisoning have resulted 

 from occupational exposure, and a least 72 occupations hazard a potential 

 exposure to sulfide. Sulfide is toxic at the micromolar level due to 

 reversible inhibition of cytochrome oxidase. The proper emergency 

 treatment for acute sulfide poisoning is currently controversial. Use of 

 sodium nitrite to induce methemoglobinemia or injection of exogenous heme 

 compounds have been proposed as therapeutic measures, but the mechanism of 

 detoxification is unknown. The beneficial action may be due to sulfide 

 binding and sequestering of sulfide from cytochromes, or to an increased 

 rate of sulfide oxidation catalyzed by ferric heme iron. The objectives of 

 this study are to elucidate the biochemical mechanisms of heme reversal of 

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 sulfide toxicity and sulfide oxidation by heme compounds in order to 

 provide a foundation for improving treatment of sulfide poisoning in 

 humans. Published reports show the presence of sulfide oxidizing heme 

 compounds in the coelomic fluid and epithelia of the marine worm Urechis 

 caupo. The research proposed is a comparison of U. caupo heme compounds to 

 the extremely sensitive human system and is divided into three sections; 

 (I) biochemical characterization of heme compounds, (II) investigations of 

 sulfide oxidase activity of enzymes and heme compounds, and (III) 

 elucidation of the cellular mechanisms of sulfide detoxification. The 

 methodology relies upon HPLC, NMR, spectrophotometry and autoradiography, 

 X-ray microanalysis and standard light and electron microscopy with 

 cytochemical staining. The research effort consistently involves 

 undergraduate and graduate students in each of the three specific aims. 

 Various subprojects will provide excellent opportunities for MBRS students 

 to formulate hypotheses and realize their research goals while training on 

 modern equipment. Publication and presentation of their results will 

 encourage and enable them to successful pursue a career in the biomedical 

 sciences. 

243 

TITLE: 

 Ditiocarb: decomposition in aqueous solution and effect of the volatile 

 product on its pharmacological use 

AUTHORS: 

 Martens T 

 Langevin-Bermond D 

 Fleury MB 

SOURCE: 

 J. Pharm. Sci.; VOL 82 ISS Apr 1993, P379-383, (REF 24) 

ABSTRACT: 

 IPA COPYRIGHT: ASHP The experimental results of the decomposition 

 reaction of sodium diethyldithiocarbamate (ditiocarb sodium; Imuthiol) in 

 either an aqueous buffered solution or in an aprotic medium as determined 

 by independent analytical methods are presented. The kinetic profile 

 indicated that the decomposition reaction was hydrogen ion-catalyzed over 

 the entire 4-10 pH range and enabled the determination of the value of the 

 acid-base equilibrium constant (Ka=4.0x10-4) at 5DGC. Decomposition of 

 sodium diethyldithiocarbamate produced volatile carbon disulfide, 

 exclusive of hydrogen sulfide, as shown with electrochemical methods. The 

 half-life of the decomposition was 45 min. It was concluded that the 

 liberation of carbon disulfide alone, exclusive of hydrogen sulfide, 

 implies a lower toxicity of sodium diethyldithiocarbamate. 

244 

TITLE: 

 Composition and toxicology of manure gas. 

AUTHORS: 

 WESTBYE O 

SOURCE: 

 NOR VET TIDSSKR; 83 (10). 1971 522-525 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. There are about 20 different gases produced in 

 manure, but most of them are in small, non-toxic concentrations. In 

 larger amounts are produced carbon dioxide, methane, ammonia and hydrogen 

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 sulfide. It is assumed that especially the latter 2 gases are responsible 

 for the toxicity of manure gas. Acute poisoning with manure gas is 

 usually caused by H2S, but it is possible that the addition of ammonia 

 increases its toxicity. Sudden death may occur without special symptoms. 

 In chronic poisoning hydrogen sulfide is the most dangerous gas, but in 

 some cases ammonium plays an important role. Symptoms of chronic 

 poisoning are irritation of mucosae, edema, bleeding tendency and poor 

 quality of horn in hoofs resulting in pressure injuries and limping. 

245 

TITLE: 

 Hazards in California dairy waste structures. 

AUTHORS: 

 Hair DM 

 Strong DR 

SOURCE: 

 Occup Health Saf. 2005, Feb; 74(2):52, 54, 56 passim. [Occupational health 

 & safety (Waco, Tex.)] 

246 

TITLE: 

 Electrocardiographic and Histochemical Studies of the Heart Muscle in 

 Acute Experimental Hydrogen Sulfide Poisoning 

AUTHORS: 

 Kosmider S 

 Rogala E 

 Pacholek A 

SOURCE: 

 Archivum Immunlogiae et Therapiae Experimentalis, Vol. 15, No. 5, pages 

 731-740, 19 references, 19671967 

ABSTRACT: 

 Effects of acute and subacute hydrogen-sulfide (7783064) (H2S) poisoning 

 on rabbit heart muscle was investigated. Thirty seven rabbits were 

 divided into three groups: 10 rabbits were exposed to acute poisoning by 

 0.1 milligram (mg) H2S per liter of air for 1.5 hours daily for 5 days; 17 

 rabbits were exposed to subacute poisoning by 0.1mg H2S per liter air for 

 0.5 hours daily for 5 days; and 10 rabbits served as controls. Baseline 

 electrocardiograms were made 10 days pretreatment and at autopsy. After 

 acute H2S poisoning, arrhythmias occurred as ventricular extrasystoles and 

 bigeminal rhythm. Subacute poisoning caused disorders of cardiac rhythm, 

 which was quickly reversed by intravenous injection of sodium-citrate in 

 doses of 0.04 to 0.3 grams depending on rabbit response time. 

 Histochemical dyes showed a decreased intensity in both 

 adenosine-triphosphate-phosphohydrolase and reduced 

 nicotinamide-adenine-dinucleotide-oxidoreductase in myocardial cells as a 

 response to H2S toxicity. The authors conclude that H2S causes decreased 

 intracellular concentration of metal ions in myocardial cells which, in 

 turn, cause electrocardiographic changes in rabbits. 

247 

TITLE: 

 Toxicity of Ammonia, Chlorine, Hydrogen Cyanide, Hydrogen Sulphide, and 

 Sulphur Dioxide Gases. I. General Methods and Correlations 

AUTHORS: 

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 McCallan SEA 

 Setterstrom C 

SOURCE: 

 Boyce Thompson Institute for Plant Research, Vol. 11, pages 325-330, 10 

 references, 19401940 

ABSTRACT: 

 The toxicity of ammonia (7664417) (NH3), chlorine (7782505) (Cl2), 

 hydrogen-cyanide (74908) (HCN), hydrogen-sulfide (7783064) (H2S), and 

 sulfur-dioxide (7446095) (SO2) gases was investigated. The following 

 organisms were tested: the plant pathogens Sclerotium-delphinii, 

 Rhizoctonia-tuliparum, Botrytis, Sclerotinia-fructicola, 

 Pestalotia-stellata, Glomerella-cingulata, Macrosporium-sarcinaeforme, and 

 Ceratostomella-ulmi; the animal pathogens Monilia-albicans and 

 Escherichia-coli (E-coli); soaked and dry rye and radish seeds; green 

 leaves and stems of tomato, tobacco, and buckwheat; houseflies, mice, and 

 rats. Organisms were exposed to the gases in concentrations of 1, 4, 16, 

 63, 250, and 1000 parts per million (ppm) of air by volume for time 

 periods of 1 to 960 minutes. The time required to kill 50 percent of the 

 organisms of a certain type (LT50) was measured, and LT50s were compared. 

 In many cases, gases were not toxic at less than 1000ppm. At 1000ppm, Cl2 

 showed LT50s from 15 to 45 minutes for the plant pathogens; SO2, from 30 

 seconds to 15 minutes; NH3 from 20 minutes to 4 hours; H2S, from 2 hours 

 to more than 16 hours; and HCN, from 3 hours to more than 16 hours. For 

 animal pathogens, the LT50s at 1000ppm ranged from 1 minute for Cl2 to 

 more than 16 hours for E-coli exposed to NH3, HCN, or H2S. Cl2, NH3, and 

 SO2 killed 50 percent of the soaked rye and radish seeds in less than 16 

 hours; however, LT50s for the dry seeds were greater than 16 hours. LT50s 

 for plant leaves were all less than 4 hours, while they ranged from 15 

 minutes (HCN) to 12 hours (H2S) for plant stems. The LT50 for mice, rats, 

 and houseflies exposed to HCN was less than 4 minutes; H2S, 4 to 15 

 minutes; Cl2, 30 to 45 minutes; SO2, 2 hours to 16 hours; and NH3, greater 

 than 16 hours. The authors conclude that SO2 and Cl2 tend to be the most 

 toxic for plant life and HCN and H2S the most toxic to animals. The 

 resting organs and seeds are the most resistant to gases in general, while 

 green leaves and animals are the most sensitive. 

248 

TITLE: 

 The Effect of Humidity on the Toxicity of Hydrogen Sulphide Gas 

AUTHORS: 

 Suzman MM 

SOURCE: 

 Journal of the Chemical Metallurgical and Mining Society of South Africa, 

 Vol. 36, pages 378-384, 19361936 

ABSTRACT: 

 The effects of humidity on the toxicity of hydrogen-sulfide (7783064) 

 (H2S) gas were examined in rats and guinea-pigs. Ten pairs of rats were 

 subjected to an atmosphere containing H2S gas, one of each pair in a dry 

 atmosphere, and the other in a humid atmosphere. Results were not 

 significant. Rats in the dry atmosphere collapsed sooner than rats in the 

 moist atmosphere. Four pairs of guinea-pigs were tested under similar 

 conditions. In all except one instance, symptoms of H2S poisoning 

 appeared, final collapse ensued, and death occurred much later in the 

 animals in the dry chamber than in those in the moist atmosphere. Autospy 

 findings showed the gross pathological picture to be the same for all 

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 animals, whether subjected to dry or humid atmosphere. The author notes 

 that no definite conclusions can be drawn from such a small number of 

 experiments. Although there is a lack of significant results, further 

 research is needed to elucidate the problem. 

249 

TITLE: 

 [Morphological characteristics of chronic colitis in workers of 

 gas-processing industry] 

AUTHORS: 

 Mkhitarian EE 

 Parkhomenko IuG 

 Solnyshkova TG 

SOURCE: 

 Arkh Patol. 2006 Mar-Apr; 68(2):39-40. [Arkhiv patologii] 

ABSTRACT: 

 Surgical and biopsy material from 76 patients who had been working for a 

 long time at Orenburg gas-processing factory was investigated. Group 1 

 consisted of 36 workers with classic lymphocytic colitis. Group 2 (40 men) 

 had diarrhea with blood, pains in the abdomen, loss of weight, ulcers at 

 colonoscopy, atypical variants of lymphocytic colitis at colonoscopy. 

 These variants may result in the ulceration leading to inevitable surgery. 

250 

TITLE: 

 The Influence of Simultaneous Exposure to Carbon Disulfide and Hydrogen 

 Sulfide on the Peripheral Nerve Toxicity and Metabolism of Carbon 

 Disulfide in Rats 

AUTHORS: 

 Gagnaire F 

 Simon P 

 Bonnet P 

 De Ceaurriz J 

SOURCE: 

 Toxicology Letters, Vol. 34, Nos. 2/3, pages 175-183, 29 references, 

 19861986 

ABSTRACT: 

 Three groups of ten male Sprague-Dawley-rats were exposed to either 500 

 parts per million (ppm) carbon-disulfide (75150) (CS2), 50ppm of 

 hydrogen-sulfide (7783064) (H2S) or to a mixture of 500ppm of CS2 and 

 50ppm of H2S, 5 days/week for 25 weeks, and neurophysiological 

 measurements were performed every week or biweekly. Except for some body 

 weight changes, none of the groups manifested signs of neurotoxicity or 

 other signs related to systemic toxicity. Rats exposed to CS2 and a 

 mixture of CS2 and H2S had significantly lower body weight than controls, 

 although there was no interactive effect. H2S exposure did not 

 significantly affect sensory tail nerve conduction velocity (SNCV) and 

 motor tail nerve conduction velocity (MNCV), but CS2 exposure 

 significantly affected both nerve conduction velocities. In rats exposed 

 to CS2 alone or in a mixture, significant decreases in MNCV occurred at 

 weeks 17, 19, and 25, and in SNCV at weeks 13, 17, 19, 21, 23, and 25, 

 although there was no interactive effect. In rats exposed to CS2 alone or 

 in a mixture, at the end of the 25 week exposure period, the extent of 

 electrophysiological deficits detected reached 4 meters/second for MNCV 

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 and 7 to 8 meters/second for SNCV. Optical and electron microscopy did 

 not reveal any structural abnormalities. In rats exposed to CS2 alone or 

 in a mixture, for each of the two exposure schedules used, there was no 

 significant difference between the 24 hour urinary 

 2-thio-thiazolidine-4-carboxylic-acid (TTCA) excretion. The authors 

 conclude that exposure to H2S would not hinder interpretation of the 

 measurement of urinary TTCA as a biological indicator of CS2 exposure. 

251 

TITLE: 

 Effects of Hydrogen Sulfide Exposure on Lung Mitochondrial Respiratory 

 Chain Enzymes in Rats 

AUTHORS: 

 Khan AA 

 Schuler MM 

 Prior MG 

 Yong S 

 Coppock RW 

 Florence LZ 

 Lillie LE 

SOURCE: 

 Toxicology and Applied Pharmacology, Vol. 103, No. 3, pages 482-490, 36 

 references, 1990 

ABSTRACT: 

 The sensitivity of mitochondrial respiratory chain enzymes was determined 

 in rat lung to hydrogen-sulfide (7783064) (H2S) inhalation and incubation 

 with sulfide solutions. Male 8 to 10 week old Fischer-344-rats were 

 exposed to concentrations of H2S gas up to 700 parts per million (ppm). 

 Rats were exposed for 4 hours, and surviving rats were killed immediately 

 after exposure, or were transferred to clean air and killed 1, 24 or 48 

 hours after exposure. Exposure to 10, 50, or 200ppm caused no marked 

 toxicity. Mitochondrial fractions were prepared from lung tissues, and 

 assayed for respiratory chain enzymes. In-vitro studies were conducted 

 with mitochondrial preparations from lungs of control rats. Mitochondrial 

 enzyme activities were determined with and without added sulfide solution. 

 The results provide strong evidence that lethal concentrations of H2S do 

 cause almost total inhibition of cytochrome-c-oxidase. This information 

 together with the pattern of cytochrome-c-oxidase inhibition at the 

 sublethal concentrations which did not produce any evidence of cellular 

 injury in nasal and bronchoalveolar regions strongly suggests that 

 inhibition of cytochrome-c-oxidase in pulmonary tissues is a primary 

 biochemical lesion of H2S toxicity. A progressive inhibition of this 

 enzyme with increased H2S concentrations results in histotoxic hypoxia and 

 impairment of ATP homeostasis, reducing the probability of survival of 

 affected tissues and may be responsible for acute injuries and death. 

252 

TITLE: 

 Dangerous and Cancer-Causing Properties of Products and Chemicals in the 

 Oil Refining and Petrochemical Industry. Part VII: Adverse Health Effects 

 and Toxic Manifestations Caused by Exposure to Hydrogen Sulfide, a 

 Component of Crude Oil 

AUTHORS: 

 Mehlman MA 

SOURCE: 

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 The Identification and Control of Environmental and Occupational Diseases: 

 Hazards and Risks of Chemicals in the Oil Refining Industry, Advances in 

 Modern Environmental Toxicology, Volume XXIII, M. A. Mehlman and A. Upton, 

 Editors; -=Princeton Scienti, 1994 

ABSTRACT: 

 The effects of exposure to hydrogen-sulfide (7783064) (H2S) in the 

 workplace were reviewed. The cellular toxicity of H2S was described and 

 resembled that of cyanide by blocking the cellular cytochrome chain of 

 oxygen. The most severely affected cells were those that required the 

 most oxygen, such as brain, cardiac, and nerve tissues. Workers handling 

 petroleum products were identified by NIOSH as those with the greatest 

 potential for H2S exposure. Toxic effects in animals have included 

 hyperpnea, cessation of breathing, and death within 20 minutes of exposure 

 to 1000 parts per million (ppm). H2S was demonstrated to manifest its 

 toxicity by acting on the nervous system. The primary pathways for H2S 

 metabolism were described, one of which involved the reaction with 

 metallic ions on disulfide containing proteins and was responsiblefor the 

 toxic effects. H2S was shown to inhibit mitochondrial heme containing 

 cytochrome enzymes. At 500ppm the respiratory rate of exposed dogs was 

 decreased slightly, but progressively, resulting in death after many hours 

 of exposure. Unusual health problems were noted in animals exposed to a 

 well blowout with up to 3ppm exposure to H2S, including infective keratod 

 conjunctivitis, pneumonia, and weight loss. Toxic effects on individual 

 tissueswere discussed including the brain and nervous tissue. In humans, 

 reports have been made of headache, nausea, tiredness, enzyme inhibition, 

 arrhythmias of the heart, respiratory paralysis and toxic convulsions, 

 vertigo, equilibrium disturbances, and permanent neurologic damage. 

 Chronic symptoms included local irritation of the eyes and respiratory 

 tract, bradycardia, cold sweats, fatigue,gastrointestinal disturbances, 

 sleep disorders, headaches, inability to concentrate, chills, mental 

 depression, and abnormal peripheral reflexes suggestive of depression of 

 nervous system function. Regulatory concentrations were listed. 

253 

TITLE: 

 Hydrogen Sulphide 

AUTHORS: 

 Guidotti TL 

SOURCE: 

 Occupational Medicine, Vol. 46, No. 5, pages 367-371, 45 references, 1996 

ABSTRACT: 

 The toxic properties of hydrogen-sulfide (7783064) (H2S) were reviewed. 

 Occupational exposure to H2S results primarily from exposure to sour gas 

 in the natural gas industry. Although sour gas is found in only a 

 relatively few natural gas fields worldwide, it is a major problem in gas 

 fields in Alberta Province, Canada which have oil and gas fields 

 containing high concentrations of sulfur. H2S is produced in pulp mills 

 where it is accompanied by varying concentrations of methyl mercaptans. 

 When inhaled, H2S enters the general circulation directly across the 

 alveolar/capillary barrier where it dissociates partially into the sulfide 

 ion (HS). HS interacts with a number of enzymes and macromolecules such 

 as hemoglobin and myoglobin. Some sulfohemoglobin is formed; however, it 

 does not appear to be the major factor in H2S acute toxicity. The major 

 target of HS appears to be cytochrome-oxidase. The result of HS 

 disrupting cytochrome-oxidase resembles that of oxygen deprivation during 

 asphyxiation, except that it occurs more quickly. The exposure response 

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 curves for H2S induced lethality are very steep and depend primarily on 

 concentration rather than duration of exposure. The strong odor of H2S 

 cannot be relied on as a means of detection as it disappears at exposure 

 concentrations as low as 100 parts per million (ppm) as a result of 

 paralysis of the olfactory system. Acute central neurotoxicity, pulmonary 

 edema, and mucosal irritation typically occur at concentrations of 20 to 

 250ppm. Loss of consciousness typically occurs at concentrations of 

 around 500ppm. This loss of consciousness, referred to as knockdown, 

 reduces the chance of escape from highly contaminated environments. 

 Repeated knockdowns may cause chronic central nervous system problems. 

 Removal from exposure is considered the most important component of 

 immediate treatment. Following removal from exposure, treatment is 

 usually done on a case by case basis using some combination of nitrite and 

 hyperbaric oxygen therapy. 

254 

TITLE: 

 40. Dihydrogensulfid 

AUTHORS: 

 Nordic Expert Group 

 Savolainen H 

SOURCE: 

 Arbete och Hälsa Vol:31 (1982) pp 1-27 

ABSTRACT: 

 Based on a survey of literature on hydrogen sulfide toxicity it is 

 concluded that the significant toxic effect on the nervous system is the 

 inhibition of the mitochondrial terminal oxidase of the respiratory chain. 

 Hydrogen sulfide gas is also irritating: pulmonary edema and conjunctival 

 damage are seen already at vapour levels without symptoms indicative of 

 acute nervous system toxicity. As the mucous membrane irritation is a 

 forewarning effect it should be taken into consideration in the 

 establishment of the standard for an occupational limit. 

255 

TITLE: 

 Methyl Mercaptan 

AUTHORS: 

 Anonymous 

SOURCE: 

 ACGIH. Documentation of the threshold limit values and biological exposure 

 indices Vol:7th Ed (2001) 3 p 

ABSTRACT: 

 A TLV-TWA of 0.5 ppm (0.98 mg/m3) is recommended for methyl mercaptan to 

 minimize the potential for exposure to the highly objectionable odor and 

 at higher but still low-level exposure concentrations, headache, nausea, 

 eye and mucous membrane irritation, and possible central nervous system 

 (CNS) effects. The toxic effects from exposure to methyl mercaptan or 

 hydrogen sulfide are similar but methyl mercaptan is acutely less toxic 

 (see the current TLV Documentation for Hydrogen Sulfide). Sufficient data 

 were not available to recommend Skin, SEN, or carcinogenicity notations or 

 a TLV-STEL. 

256 

TITLE: 

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 Hydrogen sulfide 

AUTHORS: 

 ANON 

SOURCE: 

 Institut national de recherche et de sâecuritâe, 30 rue 

 Olivier-Noyer, 75680 Paris Cedex 14, France, 1994. 4p. 20 ref. 

ABSTRACT: 

 Chemical safety information sheet. Acute toxicity: irritation of the eyes 

 and respiratory tract; asphyxia; respiratory insufficiency; pulmonary 

 oedema; cardiovascular disorders; arrythmia; metabolic disturbances. 

 Chronic toxicity: neurotoxic effects (central nervous system); irritation 

 of the eyes, skin (dermatitis) and respiratory tract (bronchitis); 

 digestive disorders; may increase the risk of abortion. French exposure 

 limit: 10ppm (14mg/m|3|) (VLE). 

257 

TITLE: 

 Hydrogen sulfide 

SOURCE: 

 Institut national de recherche et de sécurité, 30 rue 

 Olivier-Noyer, 75680 Paris Cedex 14, France, CD-ROM CD 613, May 2000. 

 Rev.ed. 5p. Illus. 20 ref. 

ABSTRACT: 

 Chemical safety information sheet. Update of data sheet already summarized 

 in CIS 95-856. Acute toxicity: irritation of the eyes and respiratory 

 tract; asphyxia; respiratory insufficiency; pulmonary oedema; 

 cardiovascular disorders; arrythmia; metabolic disturbances. Chronic 

 toxicity: neurotoxic effects (central nervous system); irritation of the 

 eyes, skin (dermatitis) and respiratory tract (bronchitis); digestive 

 disorders; may increase the risk of abortion. Exposure limits (France): 

 TWA = 7mg/m³ (5ppm); ceiling limit = 14mg/m³ (10ppm). EC number 

 and mandatory labelling codes: No.016-001-00-4; T+, N, F+, R12, R26, R50, 

 S9, S16, S28, S36/37, S45, S61, 231-977-3. Complete datasheet collection 

 on CD-ROM analysed under CIS 01-201. 

258 

TITLE: 

 Toxicity of hydrogen sulfide to various life history stages of bluegill 

 (Lepomis macrochirus). 

AUTHORS: 

 SMITH L L JR 

 OSEID DM 

 KIMBALL GL 

 EL-KANDELGY SM 

SOURCE: 

 TRANS AM FISH SOC; 105 (3). 1976 442-449 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. Bluegill (L. macrochirus) eggs, fry, juveniles 

 and adults were exposed to H2S concentrations to determine acute toxicity. 

 Seventy-two-hour LC50 for eggs was 0.0190 mg/l; 96-h LC50 for 35 day old 

 fry was 0.0131 mg/l for juveniles 0.0478 mg/l and for adults 0.0448 mg/l. 

 Exposure to lower levels of H2S resulted in some acclimation. Chronic 

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 exposure to sublethal levels of H2S for up to 826 days resulted in no egg 

 deposition at 0.0022 mg/l and reduced deposition after 97 days at 0.0010 

 mg/l. Growth was adversely affected at levels from 0.0031-0.0107 mg/l H2S 

 depending on the life history stage at which chronic exposure was started. 

 When exposure was started with eggs, the lower level retarded growth. Food 

 consumption was reduced at 0.0085 mg/l H2S. Time to anesthesia with MS 222 

 was reduced at levels from 0.0014-0.0031 mg/l H2S. The most sensitive 

 stage to acute toxicity was the feeding fry and to chronic toxicity was 

 the spawning adult. 

259 

TITLE: 

 Dithiocarbamate pesticides, ethylenethiourea, and propylenethiourea: A 

 general introduction 

SOURCE: 

 Environmental Health Criteria , 78 (1988) 140 p 

ABSTRACT: 

 Sources, Environmental Transport and Distribution Most dithiocarbamates 

 were developed during and after World War II. However, a few compounds 

 (ziram and thiram) were introduced around 1931. Dithiocarbamates, with 

 their insecticidal, herbicidal, and fungicidal properties, have a wide 

 range of applications and are produced in great quantities. Because of 

 their high biological activity, dithio- carbamates are also used in 

 medicine, the rubber industry, and in the treatment of chronic alcoholism. 

 Alkyl dithiocarbamates are stable in an alkaline medium. By splitting off 

 carbon disulfide and hydrogen sulfide, as well as by oxidative 

 degradation, a number of break-down products, such as ETU, are formed in 

 soil and water. The rate of degradation depends on a number of factors, 

 including pH and type of cation. Ethylene bisdithio- carbamates (EBDCs) 

 are generally unstable in the presence of moisture, oxygen, or biological 

 systems, and decompose rapidly in water. The mobility of EBDCs in soil 

 varies considerably, depending on their individual water solubilities and 

 the type of soil. ETU is water-soluble and mobile. It is taken up by plant 

 roots, is translocated, and meta- bolized, forming ethyleneurea (EU), 

 other 2-imidazole derivatives, and various unidentified metabolites. In 

 addition, ETU is readily photo- oxidized to EU in the presence of 

 photosensitizers. Residues of EBDCs and ETU are found in and/or on crops 

 treated with EBDCs. The residue levels change during storage, processing, 

 and cooking due to environmental factors. During these processes, the 

 parent compound may be converted to ETU. Effects on Organisms in the 

 Environment: Soil microorganisms are capable of metabolizing 

 dithiocarbamates. From the limited information available, it seems that 

 the breakdown products can affect enzyme activities, respiration, and 

 nitrification at dose levels of the order of 10 mg/kg dry soil or more. 

 Dithiocarbamates have an LC50 of less than 1 mg/litre for invertebrates 

 (Daphnia) and between 1 and 4 mg/litre for algae(Chlorella). The acute 

 toxicity of dithio- carbamates for fish is rather high. In general, the 

 acute LC50 of dialkyldithiocarbamates for fish is less than 1 mg/litre, 

 and that of EBDCs is in the range 1 - 8 mg/litre water. The sac fry and 

 early fry stages of the rainbow trout have a higher sensitivity than other 

 early life stages, and embryotoxic and teratogenic effects are induced by 

 certain dithiocarbamates. However, bioaccumulation is low 

 (bioconcentration factor (100). The toxicity of ETU and EU for fish, 

 Daphnia, Chlorella, and two bacteria species is very low, of the order of 

 g/litre. Several dithiocarbamates were shown to intervene with testicular 

 development and function and to cause nerve fibre degeneration in domestic 

 fowl. Information on the influence of dithiocarbamates on honey bees is 

 lacking. Effects on Experimental Animals and In Vitro Test Systems: The 

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 acute oral and dermal toxicities of the different dithiocarbamates are 

 generally low. Most compounds have a low volatility, and only limited 

 information concerning inhalation toxicity is available. Local irritation 

 of the respiratory tract occurs when dithiocarbamates are inhaled as dust, 

 which can also induce eye and dermal irritation. Some dithiocarbamates are 

 sensitizing agents. ETU also has a low acute oral toxicity. Many short- 

 and long-term toxicity studies have been carried out on different dithio- 

 carbamates. In rats, some dithiocarbamates tested at high dose levels 

 induced dose- dependent adverse effects on the reproduction and endocrine 

 structures and functions, thus reducing reproductive capacity. Some 

 dithiocarbamates also showed effects on reproduction in birds. In 

 teratogenicity studies on mice and rats, dithiocarbamates induced an 

 increase in resorption sites and somatic and skeletal malformations (cleft 

 palate, hydrocephaly, and other abnormalities). The dose levels needed to 

 produce these effects were usually higher than 200 mg/kg body weight in 

 rats, and above 100 mg/kg body weight in mice. In general, the results of 

 mutagenicity studies with dithiocarbamates have been negative. From the 

 available long-term carcinogenicity studies on mice and rats, there is no 

 clear indication of a carcinogenic effect. Some of the dithiocarbamates 

 have shown a goitrogenic effect at high dose levels. There is evidence 

 that certain dithiocarbamates may be converted in vivo to N-nitroso 

 derivatives, which are considered to be both mutagenic and carcinogenic. 

 However, the levels of nitroso compounds that can be ex- pected to result 

 from the dietary intake of dithiocarbamate pesticide residues are 

 negligible compared with those of the nitroso precursors, which occur 

 naturally in food and drinking-water. In rats, high levels of 

 dithiocarbamates produce an increase in thyroid weight, a reduction in 

 colloid in follicles, hyperplasia, and nodular goitre. These distinct 

 morphological changes are in agreement with an increase in 

 thyroid-stimulating hormone (TSH). Hypophyseal stimulation of the thyroid 

 is the consequence of decreased blood level of thyroxin, the synthesis of 

 which is inhibited by dithiocarbamates. The thyroid hyper- plasia induced 

 by dithiocarbamates is largely reversible on cessation of exposure. 

 Another intriguing phenomenon is the induction of alcohol intolerance by 

 most of the alkyldithiocarbamates. This phenomenon has been studied in 

 rats and produced in man. It has even led to the use of disulfiram in the 

 treatment of chronic alcoholism. At dose levels above 50 mg/kg body 

 weight, dithiocarbamates produce neurotoxic effects in rats and rabbits, 

 charac- terized by ataxia and paralysis of the hind legs, and 

 demyelination and degeneration of peripheral nerves. In birds, paralysis 

 and muscular and peripheral nerve atrophy have also been observed. 

 Dithiocarbamates have been reported to cause a redistribution of heavy 

 metals, e.g., lead and cadmium, in organs such as the brain. Furthermore, 

 because of their chelating properties, these dithiocarbamates may have an 

 effect on the function of enzymes containing metals, such as zinc and 

 copper. Effects on Man: Regular contact with dithiocarbamates can cause 

 functional changes in the nervous and hepatobiliary systems. Skin contact 

 with dithiocarbamates may induce contact dermatitis, and some of these 

 compounds will induce sensi- tization. Alcohol intolerance can be induced 

 by certain dithiocarbamates, as indicated in section 1.7. There are 

 indications that the mean incidence of chromosomal aberrations in 

 lymphocytes is increased in workers exposed to certain dithiocarbamates. 

 Epidemiological studies on workers exposed to dithiocarbamates or ETU did 

 not show any increase in the incidence of thyroid tumours. However, only 

 a relatively small number of workers was involved. Ethylenethiourea and 

 propylenethiourea: Effects on Organisms in the Environment: The available 

 LC50 levels of ETU and EU for fish are in the range of 7500 - 13 000 

 mg/litre. Effects on Experimental Animals and In Vitro Test Systems: 

 Ethylenethiourea: The acute oral toxicity in experimental animals is low, 

 and the long-term effects are mainly characterized by an antithyroid 

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 action. At dose levels > 25 mg/kg body weight, decreases in serum T3, 

 T4, and protein-bound iodine (PBI) and increases in thyroid-stimulating 

 hormone (TSH) have been found in studies on - experimental animals. At 

 higher dose levels ( > 100 mg/kg body weight), increases in thyroid 

 weight and hyperplasia occurred, which finally resulted in the 

 development of adenocarcinomas. The effects of short-term exposure to low 

 levels of ETU seem to be reversible, but those of long-term exposure to 

 higher levels become, at a certain stage, irreversible. A level of 

 approximately 5 mg/kg body weight seems to be without effects. Most 

 mutagenicity studies on ETU, especially those with mammalian test 

 systems, have given negative results. A number of carcinogenicity studies 

 have been carried out on mice, rats, and hamsters. In addition to an 

 antithyroid action, ETU has been found to induce, subsequently, thyroid 

 tumours (hyperplastic goitre, solid-cell adenomas, and follicular and 

 papillary carcinomas) in mice and rats. In an earlier study on mice, liver 

 tumours, lung tumours, and lymphomas were also detected, but these 

 findings have not been confirmed. No tumours except thyroid tumours have 

 been found in rats, and in hamsters, no tumours of the thyroid gland or 

 other organs were observed, even at 200 mg/kg diet. At dose levels above 

 approximately 10 mg/kg body weight, ETU, has clear teratogenic effects in 

 rats and hamsters, different types of central nervous system and skeletal 

 anomalies being induced. However, in mice, no teratogenic effects were 

 found at much higher dose levels (up to 800 mg/kg body weight). 

 Propylenethiourea: In a long-term study on mice using propylenethiourea 

 (PTU) an increased incidence of hepatocellular adenomas was observe at 

 dose levels of 10 mg/kg diet or more. No thyroid tumour were found, but 

 increased thyroid hypercellularity occurred at dose level of 1000 mg/kg 

 diet. In rats, goitrogenic effect were seen with PTU at dose levels as 

 low as 1 mg/kg diet. (shortened) 

260 

TITLE: 

 Evaluation and use of sediment toxicity reference sites for statistical 

 comparisons in regional assessments. 

AUTHORS: 

 Hunt JW 

 Anderson BS 

 Phillips BM 

 Newman J 

 Tjeerdema RS 

 Fairey R 

 Puckett HM 

 Stephenson M 

 Smith RW 

 Wilson CJ 

 Taberski KM 

SOURCE: 

 Environ Toxicol Chem. 2001, Jun; 20(6):1266-75. [Environmental toxicology 

 and chemistry / SETAC] 

ABSTRACT: 

 Sediment reference sites were used to establish toxicity standards against 

 which to compare results from sites investigated in San Francisco Bay 

 (California, USA) monitoring programs. The reference sites were selected 

 on the basis of low concentrations of anthropogenic chemicals, distance 

 from active contaminant sources, location in representative hydrographic 

 areas of the Bay, and physical features characteristic of depositional 

 areas (e.g., fine grain size and medium total organic carbon [TOC]). Five 

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 field-replicated sites in San Francisco Bay were evaluated over three 

 seasons. Samples from each site were tested with nine toxicity test 

 protocols and were analyzed for sediment grain size and concentrations of 

 trace metals, trace organics, ammonia, hydrogen sulfide, and TOC. The 

 candidate sites were found to have relatively low concentrations of 

 measured chemicals and generally exhibited low toxicity. Toxicity data 

 from the reference sites were then used to calculate numerical tolerance 

 limits to be used as threshold values to determine which test sites had 

 significantly higher toxicity than reference sites. Tolerance limits are 

 presented for four standard test protocols, including solid-phase sediment 

 tests with the amphipods Ampelisca abdita and Eohaustorius estuarius and 

 sea urchin Strongylocentrotus purpuratus embryo/larval development tests 

 in pore water and at the sediment-water interface (SWI). Tolerance limits 

 delineating the lowest 10th percentile (0.10 quantile) of the reference 

 site data distribution were 71% of the control response for Ampelisca, 70% 

 for Eohaustorius, 94% for sea urchin embryos in pore water, and 87% for 

 sea urchins embryos exposed at the SWI. The tolerance limits are discussed 

 in terms of the critical values governing their calculation and the 

 management implications arising from their use in determining elevated 

 toxicity relative to reference conditions. 

261 

TITLE: 

 METABOLISM OF S-2 CHLORO-1 1 2-TRIFLUOROETHYL-L-CYSTEINE TO HYDROGEN 

 SULFIDE AND THE ROLE OF HYDROGEN SULFIDE IN S-2 CHLORO-1 1 

 2-TRIFLUOROETHYL-L-CYSTEINE-INDUCED MITOCHONDRIAL TOXICITY 

AUTHORS: 

 BANKI K 

 ELFARRA AA 

 LASH LH 

 ANDERS MW 

SOURCE: 

 BIOCHEM BIOPHYS RES COMMUN; 138 (2). 1986. 707-713. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM RAT THIOSULFATE NEPHROTOXICITY 

262 

TITLE: 

 Evidence for the intrinsic toxicity of hydrogen sulfide to 

 sulphate-reducing bacteria. 

AUTHORS: 

 REIS M AM 

 LEMOS PC 

 ALMEIDA JS 

 CARRONDO M JT 

SOURCE: 

 APPL MICROBIOL BIOTECHNOL; 36 (1). 1991. 145-147. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. A sulphate-reducing culture of the genus 

 Desulfovibrio was directly inhibited by the hydrogen sulphide (H2S) 

 produced. Batch experiments carried out at pH 6.2 and 6.6 show that 

 complete inhibition is achieved for almost the same H2S concentration of 

 approximately 550 mg/l. 

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263 

TITLE: 

 Use of sulfate reducing cell suspension bioreactors for the treatment of 

 SO2 rich flue gases. 

AUTHORS: 

 Lens PN 

 Gastesi R 

 Lettinga G 

SOURCE: 

 Biodegradation. 2003, Jun; 14(3):229-40. [Biodegradation] 

ABSTRACT: 

 This paper describes a novel bioscrubber concept for biological flue gas 

 desulfurization, based on the recycling of a cell suspension of 

 sulfite/sulfate reducing bacteria between a scrubber and a sulfite/sulfate 

 reducing hydrogen fed bioreactor. Hydrogen metabolism in sulfite/sulfate 

 reducing cell suspensions was investigated using batch activity tests and 

 by operating a completely stirred tank reactor (CSTR). The maximum 

 specific hydrogenotrophic sulfite/sulfate reduction rate increased with 

 10% and 300%, respectively, by crushing granular inoculum sludge and by 

 cultivation of this sludge as cell suspension in a CSTR. Operation of a 

 sulfite fed CSTR (hydraulic retention time 4 days; pH 7.0; sulfite loading 

 rate 0.5-1.5 g SO3(2-) l(-1) d(-1)) with hydrogen as electron donor showed 

 that high (up to 1.6 g l(-1)) H2S concentrations can be obtained within 10 

 days of operation. H2S inhibition, however, limited the sulfite reducing 

 capacity of the CSTR. Methane production by the cell suspension 

 disappeared within 20 days reactor operation. The outcompetition of 

 methanogens in excess of H2 can be attributed to CO2 limitation and/or to 

 sulfite or sulfide toxicity. The use of cell suspensions opens 

 perspectives for monolith or packed bed reactor configurations, which have 

 a much lower pressure drop compared to air lift reactors, to supply H2 to 

 sulfite/sulfate reducing bioreactors. 

264 

TITLE: 

 THE FORECASTING OF HYDROGEN SULPHIDE GAS BUILD-UP IN SEWERAGE COLLECTION 

 SYSTEMS 

AUTHORS: 

 MATOS JS 

 SOUSA E RD 

SOURCE: 

 PROCEEDINGS OF THE SIXTEENTH BIENNIAL CONFERENCE OF THE INTERNATIONAL 

 ASSOCIATION ON WATER POLLUTION RESEARCH AND CONTROL, WASHINGTON, D.C., 

 USA, MAY 24-30, 1992. WATER SCI TECHNOL; 26 (1-11). 1992. 915-922. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM SEWERS METHODS TOXICITY HYDROGEN SULFIDE 

 WASTE DISPOSAL CORROSION MODELS WORKER DEATHS 

265 

TITLE: 

 Low concentrations of hydrogen sulphide alter monoamine levels in the 

 developing rat central nervous system. 

AUTHORS: 

 SKRAJNY B 

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 HANNAH RS 

 ROTH SH 

SOURCE: 

 CAN J PHYSIOL PHARMACOL; 70 (11). 1992. 1515-1518. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. The central nervous system is one of the 

 primary target organs for hydrogen sulphide (H2S) toxicity; however, there 

 are limited data on the neurotoxic effects of low-dose chronic exposure on 

 the developing nervous system. Levels of serotonin and norepinephrine in 

 the developing rat cerebellum and frontal cortex were determined following 

 chronic exposure to 20 and 75 ppm H2S during perinatal development. Both 

 monoamines were altered in rats exposed to 75 ppm H2S compared with 

 controls; serotonin levels were significantly increased at days 14 and 21 

 postnatal in both brain regions, and norepinephrine levels were 

 significantly increased at days 7, 14, and 21 postnatal in cerebellum and 

 at day 21 in the frontal cortex. Exposure to 20 ppm H2S significantly 

 increased the levels of serotonin in the frontal cortex at day 21, whereas 

 levels of norepinephrine were significantly reduced in the frontal cortex 

 at days 14 and 21, and at day 14 in the cerebellum. 

266 

TITLE: 

 Sulphur management strategies in anaerobic treatment of a BCTMP effluent. 

AUTHORS: 

 STEPHENSON RJ 

 BRANION R MR 

 PINDER KL 

SOURCE: 

 WATER POLLUTION RESEARCH JOURNAL OF CANADA; 28 (3). 1993. 635-664. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Anaerobic treatment of a bleached 

 chemithermomechanical/thermomechanical BCTMP (2:1 by volume) effluent 

 obtained from Quesnel River Pulp Co. was studied on a laboratory scale at 

 35êC. The experimental apparatus consisted of upflow anaerobic sludge bed 

 (UASB) acidogenic reactors followed by hybrid upflow anaerobic sludge 

 bed/fixed-film methanogenic reactors. Under anaerobic conditions, sulphite 

 and sulphate are reduced to sulphide, presenting problems of toxicity, 

 odour, corrosion and reduced methane yields, and treatment efficiencies. 

 The fate of these compounds was examined under various hydraulic retention 

 times and sulphur management strategies, including: (i) pH control; (ii) 

 inhibition of the sulphur reducing bacteria via molybdenum addition, and 

 (iii) stripping hydrogen sulphide dissolved in the reactor liquor by 

 recycling hydrogen sulphide-free off gas. Controlling the pH of the 

 acidogenic reactor from 5.5 (uncontrolled) to 8.0, in order to shift the 

 formed sulphi 

267 

TITLE: 

 Effects of repeated exposures of hydrogen sulphide on rat hippocampal EEG. 

 

AUTHORS: 

 SKRAJNY B 

 REIFFENSTEIN RJ 

 SAINSBURY RS 

 ROTH SH 

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SOURCE: 

 TOXICOLOGY LETTERS (SHANNON); 84 (1). 1996. 43-53. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Exposure to high levels of hydrogen sulphide 

 (H2s) in humans has been associated with a number of respiratory and 

 neurological symptoms. Acute toxicity following exposure to high 

 concentrations is well-documented, however, there is little scientific 

 information concerning the effects of exposure to low concentrations. The 

 effects of low levels of H2S on electroencephalographic (EEG) activity in 

 the hippocampus and neocortex were investigated on the freely moving rat 

 (Sprague-Dawley). Hippocampal electrodes were implanted in the dentate 

 gyrus (DG) and CA1 region. Activity was recorded for 10 min just prior to 

 H2S exposure in the presence of air (pre-exposure). Rats were exposed to 

 H2S (25, 50, 75 or 100 ppm) for 3 h/day; data was collected during the 

 final 10 min of each exposure. The total power of hippocampal theta 

 activity increased in a concentration-dependent manner in both DG and CA1; 

 repeated exposures for 5 consecutive days resulted in a cumulative effect 

 that r 

268 

TITLE: 

 EFFECT OF HYDROGEN SULPHIDE ON TWO SPECIES OF PENAEID PRAWNS PENAEUS 

 INDICUS H. MILNE EDWARDS AND METAPENAEUS DOBSONI MIERS 

AUTHORS: 

 GOPAKUMAR G 

 KUTTYAMMA VJ 

SOURCE: 

 BULLETIN OF ENVIRONMENTAL CONTAMINATION AND TOXICOLOGY; 57 (5). 1996. 

 824-828. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM RESEARCH ARTICLE PENAEUS-INDICUS 

 METAPENAEUS-DOBSONI PRAWN HYDROGEN SULFIDE TOXICITY TOXICOLOGY 

269 

TITLE: 

 Hydrogen sulphide. 

AUTHORS: 

 GUIDOTTI TL 

SOURCE: 

 OCCUPATIONAL MEDICINE (LONDON); 46 (5). 1996. 367-371. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Hydrogen sulphide (H2S) is the primary 

 chemical hazard in natural gas production in 'sour' gas fields. It is also 

 a hazard in sewage treatment and manure-containment operations, 

 construction in wetlands, pelt processing, certain types of pulp and paper 

 production, and any situation in which organic material decays or 

 inorganic sulphides exist under reducing conditions. H2S dissociates into 

 free sulphide in the circulation. Sulphide binds to many macromolecules, 

 among them cytochrome oxidase. Although this is undoubtedly an important 

 mechanism of toxicity due to H2S, there may be others. H2S provides little 

 opportunity for escape at high concentrations because of the olfactory 

 paralysis it causes, the steep exposure-response relationships, and the 

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 characteristically sudden loss of consciousness it can cause which is 

 colloquially termed 'knockdown.' Other effects may include mucosal 

 irritation, which is associated at lower concentrations with a 

 keratoconjunctivitis called 

270 

TITLE: 

 CYTOCHROME-INDEPENDENT HYDROGEN SULFIDE TOXICITY IN MUSCLE 

AUTHORS: 

 JULIAN D 

 LANG OA 

 ARPAND AJ 

SOURCE: 

 ANNUAL MEETING OF THE SOCIETY FOR INTEGRATIVE AND COMPARATIVE BIOLOGY, 

 BOSTON, MASSACHUSETTS, USA, JANUARY 3-7, 1998. AMERICAN ZOOLOGIST; 37 (5). 

 1997. 123A. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM MEETING POSTER MYTILUS-EDULIS 

 URECHINUS-CAUPO CARASSIUS-AURATUS LAMELLIBRACHIA RIFTIA-PACHYPTILA 

 BATHYMODIOLUS-THERMOPHILUS HYDROGEN SULFIDE TOXIN MUSCLE NEUROMUSCULAR 

 ACTIVITY TOXICOLOGY INTESTINE MUSCULAR SYSTEM DIGESTIVE SYSTEM 

271 

TITLE: 

 Fatal inhalation of liquid manure gas 

AUTHORS: 

 Hagley SR 

 South DL 

SOURCE: 

 Med. J. Aust.; VOL 2 ISS Oct 29 1983, P459-460, (REF 3) 

ABSTRACT: 

 IPA COPYRIGHT: ASHP A case of fatal inhalation of hydrogen sulfide 

 produced by manure gases was reported. 

272 

TITLE: 

 Antidote dimethylaminophenol 

AUTHORS: 

 Daunderer M 

SOURCE: 

 Krankenhauspharmazie; VOL 7 ISS Aug 1986, P369-374, (REF 37) 

ABSTRACT: 

 IPA COPYRIGHT: ASHP A review of practical experiences gained in a 

 detoxification center over 15 yr in the application of 

 4-dimethylaminophenol (4-DMAP; I) for the treatment of cyanide, hydrogen, 

 sulfide, and hydrogen azide (hydrazoic acid) poisonings in man, was 

 presented. The characteristics, mechanisms of action, side effects, dosage 

 regimens, compatibility with other antidotes and effects of overdose of I 

 were included in the review. 

273 

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TITLE: 

 Acute toxic inhalation injury 

AUTHORS: 

 Witorsch P 

SOURCE: 

 Hosp. Ther.; VOL 12 ISS Dec 1987, P77-78, 83-84, (REF 7) 

ABSTRACT: 

 IPA COPYRIGHT: ASHP The respiratory tract injuries produced by various 

 toxic gases namely, ammonia, chlorine, nitrogen dioxide, hydrogen sulfide, 

 acetaldehyde, cadmium oxide, and carbon monoxide from chemicals in the 

 environment are described as well as appropriate measures for the initial 

 evaluation of patients with known or suspected acute toxic inhalation 

 injury which include use of sympathomimetics, aminophylline, or 

 corticosteroids. 

274 

TITLE: 

 Problems and pitfalls in the use of hyperbaric oxygen for the treatment of 

 poisoned patients 

AUTHORS: 

 Gorman DF 

SOURCE: 

 Med. Toxicol.; VOL 4 ISS Nov-Dec 1989, P393-399, (REF 48) 

ABSTRACT: 

 IPA COPYRIGHT: ASHP The use of hyperbaric oxygen as an antidote to 

 carbon monoxide, cyanide, and hydrogen sulfide, and its use in the 

 treatment of liver toxins such as carbon tetrachloride, are reviewed. 

275 

TITLE: 

 Preliminary analysis of the impact of cold mix asphalt concretes on air 

 and water quality. 

AUTHORS: 

 Kuhn EA 

 Papagiannakis AT 

 Loge FJ 

SOURCE: 

 Bull Environ Contam Toxicol. 2005, Mar; 74(3):501-8. [Bulletin of 

 environmental contamination and toxicology] 

276 

TITLE: 

 Factors influencing acute toxicity estimates of hydrogen sulfide to 

 freshwater invertebrates. 

AUTHORS: 

 OSEID DM 

 SMITH L L JR 

SOURCE: 

 WATER RES; 8 (10). 1974 739-746 

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ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. Acute bioassay tests of H2S were run on 

 Asellus militaris Hay, Crangonyx richmondensis laurentianus Bousfield, 

 Baetis vagans MdDonough, Ephemera simulans Walker and Hexagenia limbata 

 (Serville). Size and type of test chamber, type of substrate for 

 burrowing forms or those seeking shelter in gravel, O2 concentration, pH, 

 and season of collection influenced the sensitivity of organisms. H2S 

 exposure at sublethal levels reduced feeding activity of Gammarus. Data 

 indicate that test conditions should approximate natural habitat 

 conditions as closely as practical. The most acceptable 96-h LC50 

 hydrogen sulfide concentrations for the various species are: Asellus 1.07 

 mg 1--1. Crangonyx 0.84 mg 1--1, Gammarus 0.059 mg 1--1, Baetis 0.020 mg 

 1--1, Ephemera 0.316 mg 1--1, and Hexagenia 0.0111 mg 1--1. Chronic 

 exposure tests now in progress suggest that the no-effect levels are 8-12% 

 of the 96-h LC50. 

277 

TITLE: 

 The toxicity of hydrogen sulfide in animal feeding: A survey of the 

 literature. 

AUTHORS: 

 WESTERMANN HD 

 THALMANN A 

 KUMMER H 

SOURCE: 

 LANDWIRTSCH FORSCH; 28 (1). 1975 70-80 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. Hydrogen sulfide (H2S) can, with inhaled air, 

 be rapidly introduced into blood circulation of domestic animals via the 

 lungs or, as sulfide with contaminated fodder, via the digestive tract. 

 Its toxic action may depend on blockage of enzymes containing Cu and Fe, 

 resulting in damage to the oxygen transport system and a reduction of the 

 liver Cu reserves. Action on the CNS is also a possibility. The severity 

 of H2S poisoning depends on the blood concentration of H2S. This is 

 influenced less by the total intake of H2S than by the concentration in 

 which the H2S of the ventilating air or in the digestive tract reacts on 

 the organism. With sublethal intoxications, H2S from air ventilation is 

 removed from the body by eructation and intestinal gases; it is also 

 oxidized to sulfate and excreted with the urine. Apart from protracted 

 incidence through continually increasing introduction of H2S or its 

 formation in the digestive tract, sequelae do not occur. Lethal doses 

 lead to stoppage of respiration and of the heart. The literature contains 

 apparently reliable data concerning the tolerance for warm-blooded animals 

 of H2S taken in with the ventilation air, but there is no information on 

 the tolerance limits of H2S entering the organism with fodder. On the 

 basis of values which were calculated from the available data, maximum 

 levels recommended are the following: in the total ration for horned 

 cattle, 0.5% S or S compounds; sheep, 1%; pigs, 0.03% sulfide and young 

 poultry, 0.1%. 

278 

TITLE: 

 Acute and chronic toxicity of hydrogen sulfide to the fathead minnow, 

 Pimephales promelas. 

AUTHORS: 

 SMITH L L JR 

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 OSEID DM 

 OLSON LE 

SOURCE: 

 ENVIRON SCI TECHNOL; 10 (6). 1976 565-572 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. Toxic effects of molecular hydrogen sulfide to 

 eggs, fry and juveniles of P. promelas Rafinesque were determined in 

 flow-through bioassays. The 96-h LC50 of laboratory-cultured juveniles at 

 20ê C was 0.0243 mg/l H2S. Fry were approximately twice as sensitive. 

 Response with temperature in wild stock juveniles varied from a 96-h LC50 

 of 0.7754 mg/l at 6.5ê C to 0.0423 mg/l H2S at 25ê C. In chronic exposure 

 to H2S from egg through 2 generations of laboratory-cultured stock in 

 flow-through bioassays, adverse effects on growth, survival and fecundity 

 occurred above 0.004 mg/l H2S. Chronic exposure of wild stock up to 346 

 days caused adverse effects on growth and survival above 0.008 mg/l H2S. 

 At comparable temperatures apparent safe levels with long exposure were 5- 

 to 7-fold lower than the 96-h LC50 for both stocks. 

279 

TITLE: 

 ENVIRONMENTAL HEALTH CRITERIA VOL. 19. HYDROGEN SULFIDE 

AUTHORS: 

 WHO 

SOURCE: 

 WHO. ENVIRONMENTAL HEALTH CRITERIA, VOL. 19. HYDROGEN SULFIDE. 48P. WHO: 

 GENEVA, SWITZERLAND. ILLUS. PAPER. ISBN 92-4-154079-6.; 0 (0). 1981 (RECD. 

 1982). 48P. 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. BOOK HUMAN WORKER ANIMAL NEURO TOXICITY 

 PULMONARY EDEMA SEWAGE AIR POLLUTION 

280 

TITLE: 

 Sulfide-detoxifying enzymes in the human colon are decreased in cancer and 

 upregulated in differentiation. 

AUTHORS: 

 Ramasamy S 

 Singh S 

 Taniere P 

 Langman MJ 

 Eggo MC 

SOURCE: 

 Am J Physiol Gastrointest Liver Physiol. 2006, Aug; 291(2):G288-96. 

 [American journal of physiology. Gastrointestinal and liver physiology] 

ABSTRACT: 

 H2S is highly toxic and selectively inhibits butyrate oxidation in 

 colonocytes. Ineffective detoxification may result in mucosal insult, 

 inflammation, and ultimately in colorectal cancer (CRC). Rhodanese can 

 detoxify H2S and is comprised of two isoenzymes: thiosulfate 

 sulfurtransferase (TST) and mercaptopyruvate sulfurtransferase (MST). 

 Using specific antisera to discriminate TST from MST, we found that only 

 TST could detoxify H2S. In sections of normal colon, both enzymes were 

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 located on the luminal mucosal surface, and they were expressed in the 

 colonocytes but not in the mucin-secreting goblet cells. Expression of 

 both enzymes was focally lost in ulcerative colitis and markedly reduced 

 in advanced colon cancer, the disease progression correlating with the 

 decreased expression of MST and TST. In HT-29 cells, a human colon cancer 

 cell line, TST activity and expression were significantly increased by 

 butyrate and by histone deacetylase inhibition, agents that promote HT-29 

 cell differentiation. Sulfide (0.1 mM) also increased TST activity, but 

 higher sulfide concentrations (0.3-3 mM) were toxic. Preincubation in 

 butyrate to increase TST expression, decreased sensitivity of the cells to 

 sulfide toxicity. We conclude that decreased expression of TST (or MST) is 

 a tumor marker for CRC. TST expression is increased in colonocyte 

 differentiation. Dysregulation of TST expression and activity resulting in 

 inability to effectively detoxify could be a factor in the cell loss and 

 inflammation that accompany ulcerative colitis and ultimately then in CRC. 

281 

TITLE: 

 [Comprehensive review. Ammonia, losses and performances in large animal 

 housing] 

AUTHORS: 

 Marschang F 

SOURCE: 

 Dtsch Tierarztl Wochenschr. 1973, Feb 15; 80(4):88-91 contd. [DTW. 

 Deutsche tierarztliche Wochenschrift] 

282 

TITLE: 

 Carbon Disulfide and Hydrogen Sulfide. II. A Follow-Up Clinical Study of 

 Low Grade Exposures 

AUTHORS: 

 Rubin HH 

 Arieff AJ 

 Tauber FW 

SOURCE: 

 Archives of Industrial Hygiene and Occupational Medicine, Vol. 2, No. 5, 

 pages 529-533, 5 references, 19501950 

ABSTRACT: 

 A followup clinical study was made of 100 shift operators exposed to 

 carbon-disulfide (75150) (CS2) and hydrogen-sulfide (7783064) (H2S) in the 

 viscose rayon industry (SIC-2823). Employees were aged 21 to 47 and had 1 

 to 17 years occupational exposure. Questionnaires were used to determine 

 possible symptoms, and physical examinations stressed neurological and 

 psychiatric changes. Serum cholesterol and urinary concentrations of CS2 

 were measured in some subjects. Air sampling records were reviewed. 

 Psychiatric symptoms were comparable to a previous study. Fatigue was 

 reported in the present group. One subject had occasional leg pains. 

 Stomach distress affected four subjects and impaired appetite was reported 

 by three subjects. One subject had blurred vision. Objective 

 neurological signs were found in 39 subjects: hyperactive deep tendon 

 reflexes, questionable Babinski signs, decreased superficial reflexes, 

 tremors in fingers, and sluggish pupillary reflexes. Mean serum 

 cholesterol was 218.07 milligrams per 100 cubic centimeters. Urinary 

 tests for CS2 and H2S were below 10 parts per million except for 

 occasional short exposures. The authors conclude that no correlation 

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 between psychic and neurological symptoms and correlation toxicity could 

 be found. 

283 

TITLE: 

 Hydrogen Sulfide 

AUTHORS: 

 Markwith RH 

SOURCE: 

 Adult Hygiene Division, Ohio Department of Health, Columbus, Ohio, Project 

 No. 665-42-3-413, 12 pages, 26 references, 19401940 

ABSTRACT: 

 Information on hydrogen-sulfide (HS) is reviewed. HS has always been 

 associated with its offensive odor of decaying eggs. Only in the last 25 

 years has HS become a major industrial health hazard. Primary uses of HS 

 include purification of hydrochloric-acid and sulfuric-acid, precipitating 

 sulfides of metals, and reagents for analytical chemistry. The major mode 

 of entrance is inhalation. As one of the most poisonous gases, its 

 toxicity and rapidity of action parallels hydrogen-cyanide (74908). In 

 large doses, respiratory failure occurs in a few seconds. HS acts as an 

 irritant gas exerting local action on the mucous membranes of the eyes, 

 mouth, throat, and air passages. Conjunctivitis may be mild or severe 

 with secretions, itching, vascular changes, erosion, roughness of lids, 

 and blurred vision. Low concentrations may produce subacute symptoms such 

 as irritation of ocular and respiratory mucous membranes, bronchitis, 

 confusion, excitement, headache, vertigo, ataxia, colic, nausea, vomiting, 

 bradycardia, and pulmonary edema with bronchial pneumonia. Acute 

 poisoning may cause hyperpnea and unconsciousness in a few seconds without 

 pain or significant warning. A choking sensation may be experienced, but 

 unconsciousness, tonic convulsions, followed by cessation of respiration 

 may occur before the individual can escape. Recovery from acute poisoning 

 usually occurs, but some cases result in permanent psychosis. A 

 concentration of 0.05 percent in 30 minutes causes cough, dyspnea, 

 palpitation, lassitude, pallor, sweating, headache, and giddiness. A HS 

 concentration of 0.07 to 0.08 percent becomes life threatening in a few 

 minutes. 

284 

TITLE: 

 Cyclic selenium sulfides. 

AUTHORS: 

 Steudel R 

 Laitinen R 

SOURCE: 

 Top Curr Chem. 1982; 102:177-97. [Topics in current chemistry] 

285 

TITLE: 

 Strategies adopted by the mudskipper Boleophthalmus boddaerti to survive 

 sulfide exposure in normoxia or hypoxia. 

AUTHORS: 

 Ip YK 

 Kuah SS 

 Chew SF 

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SOURCE: 

 Physiol Biochem Zool. 2004 Sep-Oct; 77(5):824-37. [Physiological and 

 biochemical zoology : PBZ] 

ABSTRACT: 

 The effects of sulfide on the energy metabolism of Boleophthalmus 

 boddaerti in normoxia and hypoxia were examined. The 24-, 48-, and 96-h 

 LC50 values of sulfide for B. boddaerti with body weight ranging from 11.6 

 to 14.2 g were 0.786, 0.567, and 0.467 mM, respectively. The tolerance of 

 B. boddaerti to sulfide was not due to the presence of a 

 sulfide-insensitive cytochrome c oxidase. There was no accumulation of 

 lactate in the muscle and liver of specimens exposed to sulfide in 

 normoxia. In addition, the levels of ATP, AMP, and energy charge in both 

 the muscle and the liver were unaffected. These results indicate that B. 

 boddaerti was able to sustain the energy supply required for its metabolic 

 needs via mainly aerobic respiration when exposed to sulfide (up to 0.4 

 mM) in normoxia. Exposure of B. boddaerti simultaneously to hypoxia and 

 0.2 mM sulfide for 48 h resulted in decreases in the ATP levels in the 

 muscle and liver. However, the energy charge in both tissues remained 

 unchanged, and the level of lactate accumulated in the muscle was too low 

 to have any major contribution to the energy budget of the fish. Our 

 results reveal that B. boddaerti possesses inducible mechanisms to 

 detoxify sulfide in an ample supply or a lack of O2. In normoxia, it 

 detoxified sulfide to sulfate, sulfite, and thiosulfate. There were 

 significant increases in the activities of sulfide oxidase in the muscle 

 and liver of specimens exposed to sulfide, with that in the liver being 

 >13-fold higher than that in the muscle. However, in hypoxia, sulfide 

 oxidase activity in the liver was suppressed in response to environmental 

 sulfide. In such conditions, there were significant increases in the 

 activities of sulfane sulfur-forming enzyme(s) in the muscle and liver 

 that were not observed in specimens exposed to sulfide in normoxia. 

 Correspondingly, there were no changes in the levels of sulfate or sulfite 

 in the muscle or liver. Instead, B. boddaerti detoxified sulfide mainly to 

 sulfane sulfur in hypoxia. In conclusion, B. boddaerti was able to 

 activate different mechanisms to detoxify sulfide, producing different 

 types of detoxification products in normoxia and hypoxia. 

286 

TITLE: 

 International Symposium on Toxicology of Carbon Disulphide 

AUTHORS: 

 Lieben J 

SOURCE: 

 Journal of Occupational Medicine, Vol. 16, No. 7, pages 483-484, 19741974 

ABSTRACT: 

 Papers presented at an international symposium on toxicology of 

 carbon-disulfide (75150) (CS2) are reviewed. Major topics of discussion 

 and areas of prime interest, such as cardiovascular effects of CS2, 

 metabolism of CS2, the effects of CS2 on the blood, urine, liver, and 

 gonads, and threshold limit values and maximum allowable concentrations of 

 CS2, are presented. Lack of agreement on the question of permitting women 

 to work in CS2 exposures is noted. Thirteen recommendations of the 

 Committee on Occupational Health are presented, including development of 

 uniform personal sampling methods; use of the iodine-azide test to sample 

 atmospheres with CS2 concentrations of 50 milligrams or more; continued 

 research on quantitative exposure test methods; further study of the 

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 effects of CS2 in combination with hydrogen-sulfide, alcohol, and drugs; 

 investigations of CS2 metabolism and the effects of CS2 on the adrenals, 

 thyroid, and testes to enable development of early biological tests of 

 overexposure; evaluation of electromyography, nerve conduction velocity, 

 alterations in lipid metabolism, urinary concentrations of 

 xanthurenic-acid, urinary and blood hormonal balances as early diagnostic 

 procedures; investigation of shift rotation to reduce exposure; further 

 study of the effects of CS2 on women; development of psychological 

 indicators of CS2 overexposure; studies of the effects of CS2 on the 

 cardiovascular system; development of preventive tests; periodic 

 reevaluation of allowable exposure limits; and investigation of the 

 toxicity of chemicals used in the production of polyacrylic, polyamid, 

 polyester, and fire retardant fibers. 

287 

TITLE: 

 Sulfur isotope fractionation by Salmonella heidelberg: inverse isotope 

 effects during growth on high concentrations of Na2SO3. 

AUTHORS: 

 McCready RG 

 Krouse HR 

SOURCE: 

 Can J Microbiol. 1979, Dec; 25(12):1387-93. [Canadian journal of 

 microbiology] 

ABSTRACT: 

 During growth on minimal salts - glucose media supplemented with high 

 concentrations of Na2SO3 (10-3 and 10-2 M), Salmonella heidelberg 

 exhibited cytological and growth responses which indicated increased 

 cellular toxicity with increasing sulfite concentrations. The large 

 quantities of sulfide evolved during growth at both SO32- concentrations 

 were accompanied by large normal and inverse isotope effects. Consistent 

 with earlier findings, this organism was found capable of rapidly 

 metabolizing both the sulfane and sulfonate sulfur of thiosulfate. 

 Therefore, the isotope effects do not appear to be caused by extracellular 

 chemical thiosulfate formation. 

288 

TITLE: 

 Low S-adenosylmethionine concentrations found in patients with severe 

 inflammatory bowel disease. 

AUTHORS: 

 Schmedes A 

 Nielsen JN 

 Hey H 

 Brandslund I 

SOURCE: 

 Clin Chem Lab Med. 2004; 42(6):648-53. [Clinical chemistry and laboratory 

 medicine : CCLM / FESCC] 

ABSTRACT: 

 BACKGROUND: S-adenosylmethionine is a methyl donor in many cellular 

 reactions including detoxification of constantly produced hydrogen 

 sulphide in the colon. A reduced capacity to detoxify hydrogen sulphide 

 may be implicated in the pathogenesis of inflammatory bowel disease. 

 S-adenosylmethionine could be low if this assumption is correct. We 

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 compared S-adenosylmethionine concentrations in whole blood in patients 

 with severe and moderate inflammatory bowel disease with healthy reference 

 persons. METHODS: S-adenosylmethionine concentrations in whole blood were 

 measured using high-pressure liquid chromatography. Patients with Crohn's 

 disease (n=21), ulcerative colitis (n=7) and healthy age-matched reference 

 persons (or controls) (n=17) were studied. RESULTS: S-adenosylmethionine 

 concentrations were significantly decreased in patients with severe 

 inflammatory bowel disease (mean 1.10 mg/l) as compared to patients with 

 moderate Crohn's disease and ulcerative colitis (mean 1.83 mg/l) and 

 reference persons (mean 1.84 mg/l). Statistically significant inverse 

 correlations were found between S-adenosylmethionine concentration and 

 activity index (p < 0.01 and R2=0.86) as well as Crohn's disease activity 

 index (p < 0.01 and R2=0.50) scores. CONCLUSIONS: Low concentrations of 

 S-adenosylmethionine were found in patients with severe inflammatory bowel 

 disease. Future studies will show whether S-adenosylmethionine is a marker 

 for disease activity and a possible tool for investigation of sulphur 

 toxicity as a causative mechanism in inflammatory bowel disease. 

289 

TITLE: 

 Workersescuers Continue to Die in Confined Spaces 

AUTHORS: 

 Pettit TA 

 Sanderson LM 

 Linn HI 

SOURCE: 

 Professional Safety, Vol. 32, No. 2, pages 15-20/22, 4 references, 

 19871987 

ABSTRACT: 

 Five separate fatal accidents involving wastewater treatment systems were 

 reviewed with regard to the number of serious accidents occurring in 

 confined spaces. The first case involved two laborers who were 

 asphyxiated when a propane fire ignited in the floating cover of a 

 digestion tank that they were preparing for painting at a secondary sewage 

 treatment facility. The second case involved two workers who died from 

 carbon-monoxide (630080) poisoning at a sewer construction site. A third 

 case involved two plumbing employees who were overcome by sulfuric-acid 

 (7664939) fumes while attempting to unclog a sewage drain and repair a 

 septic tank. The fourth case involved two sanitation workers who drowned 

 when raw sewage flooded a 50 foot deep underground pumping station. A 

 police officer and the sewage system field manager also died when they 

 were overcome by gas during rescue operations. The fifth case involved 

 two workers who were overcome by hydrogen-sulfide (7783064) while 

 attempting to retrieve a Plexiglas cover from a sludge chamber. The five 

 cases were discussed with regard to NIOSH criteria for safety and health 

 in confined workspaces. Confined spaces were defined and categorized as 

 open topped but deep enclosures or enclosures with extremely limited 

 openings for entry and exit. The spaces were classified according to the 

 oxygen level, the flammability of the atmosphere, and the toxicity of the 

 contents. Health hazards, hazardous atmospheres, and NIOSH 

 recommendations for confined workspaces were discussed. 

290 

TITLE: 

 Cadmium-specific formation of metal sulfide 'Q-particles' by Klebsiella 

 pneumoniae. 

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AUTHORS: 

 Holmes JD 

 Richardson DJ 

 Saed S 

 Evans-Gowing R 

 Russell DA 

 Sodeau JR 

SOURCE: 

 Microbiology. 1997, Aug; 143 ( Pt 8):2521-30. [Microbiology (Reading, 

 England)] 

ABSTRACT: 

 Klebsiella pneumoniae overcomes cadmium toxicity through the 

 'biotrans-formation' of cadmium ions into photoactive, nanometre-sized CdS 

 particles deposited on the cell surface. The kinetics of particle 

 formation during batch culture growth was monitored by electron microscopy 

 (EM), energy-dispersive X-ray analysis and electronic absorption 

 spectroscopy (EAS). During the deceleration phase of bacterial growth, the 

 presence of CdS particles on the outer cell wall of K. pneumoniae (> or = 

 5 nm in diameter) was detected by EM. The size of these electron-dense 

 particles continued to increase throughout the stationary phase of growth, 

 with some of the particles reaching a diameter > 200 nm. The formation of 

 the extracellular CdS particles contributed to around 3-4% of the total 

 cell biomass. EAS undertaken on these extracellular 'bio-CdS' particles 

 suggested that the large 'superparticles' observed by EM, e.g. 200 nm, 

 were aggregates of smaller particles termed 'Q-particles', approximately 4 

 nm in diameter. Metal sulfide particles were not formed in batch cultures 

 of K. pneumoniae grown in the presence of lead, zinc, mercury, copper or 

 silver ions. Growth in the presence of lead ions resulted in the formation 

 of extracellular electron-dense particles containing lead but not sulfide 

 or phosphate. Intracellular phosphorus-containing electron-opaque 

 particles were formed during growth in the presence of copper and mercury. 

 Intracellular electron-dense particles were formed in the presence of zinc 

 ions but these did not contain phosphorus. From these results it was 

 thought that metal sulfide formation in K. pneumoniae showed some 

 cadmium-specificity. When cadmium and zinc ions were both added to the 

 growth medium, metal sulfide particles were formed that were predominantly 

 composed of cadmium, e.g. 48.6% cadmium and 0.04% zinc. Similarly, when 

 cadmium and lead ions were both present during growth only CdS particles 

 formed. In both cases analysis of the cells by EAS confirmed the presence 

 of CdS only. These observations suggest that the mechanism of CdS 

 formation is unlikely to occur simply through a cadmium-induced release of 

 hydrogen sulfide by the cells into the external environment. If hydrogen 

 sulfide production was the mechanism of sulfide formation then metal 

 sulfide particles containing lead and zinc ions in addition to cadmium 

 ions should have been produced. 

291 

TITLE: 

 Immune Response To Zymosan-Induced Pulmonary Inflammation In Rats. 

AUTHORS: 

 Young S 

 Robert JR 

 Antonini JM 

SOURCE: 

 Toxicol Sci 2005 Mar;84(1-S):192 

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ABSTRACT: 

 1- > 3-beta-Glucans have been associated with increased pulmonary 

 inflammation in mold-related indoor air problems. The objective of the 

 present investigation was to determine the immune response to 

 zymosan-induced pulmonary inflammation in SD rats. Rats received a single 

 dose of zymosan A (2.5 mg/kg body weight) via intratracheal instillation 

 (IT) and were euthanized on days 1, 4, 6, and 8 post IT. Inflammation and 

 lung injury were assessed by measuring (1) neutrophil (PMN) infiltration 

 into bronchoalveolar lavage fluid (BALF) and (2) albumin, total protein 

 and lactate dehydrogenase levels in BALF. Alveolar macrophage activation 

 was determined by chemiluminescence (CL). Immune response was investigated 

 via immunophenotyping of lymphocytes and lymphokine production. 

 Immunophenotyping was performed on BAL cells and lung-associated lymph 

 node cells. Lymphokine production was measured from lymph node cells with 

 or without concanavalin A stimulation by an enzyme-linked immunosorbent 

 assay. Upon challenge with zymosan, rats exhibited increased inflammation 

 and injury at the early time points post-IT exposure. Although elevations 

 in PMN infiltration and CL had returned to control levels on day 4, 

 lung-associated lymphocytes continued to proliferate and reached a maximum 

 on day 6. The ratio of CD4 to CD8 T cells in the lymph node and BAL was 

 lower in zymosan-treated rats than in control rats, indicating a greater 

 increase in CD8 T cells as compare to CD4 T cells. Zymosan also increased 

 the number of infiltrating NK cells, B cells, and T cells in BAL at all 

 time points. B cells in BALF were found to be highest in number on day 1 

 for zymosan- treated rats. The ratio of T/B cells in BALF increased 

 significantly on day 6 and 8. Zymosan treatment increased IL-2, IL-10 and 

 IFNgamma but not IL-4 production in lymphocytes. These data along with 

 immunophenotyping of lymphocytes suggests that helper CD4 T and cytotoxic 

 CD8 T cells are involved in the immune activation caused by zymosan 

 treatment. In summary, rats exposed to zymosan had increased inflammation 

 and altered lymphocyte profile, indicating an activation of innate and/or 

 adaptive immune response in rats. 

292 

TITLE: 

 TOXICITY OF HYDROGEN SULFIDE TO VARIOUS LIFE HISTORY STAGES OF BLUEGILL 

 (LEPOMIS MACROCHIRUS) 

AUTHORS: 

 SMITH LL JR 

 OSEID DM 

 KIMBALL GL 

 EL-KANDELGY SM 

SOURCE: 

 TRANS AM FISH SOC 105:442-449,1976 

293 

TITLE: 

 A CRITICAL REVIEW OF THE LITERATURE ON HYDROGEN SULFIDE TOXICITY 

AUTHORS: 

 BEAUCHAMP RO JR 

 BUS JS 

 POPP JA 

 BOREIKO CJ 

 ANDJELKOVICH DA 

SOURCE: 

 CRC CRIT REV TOXICOL 13:25-97,1984 

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294 

TITLE: 

 A CRITICAL REVIEW OF THE LITERATURE ON HYDROGEN SULFIDE TOXICITY 

AUTHORS: 

 BEAUCHAMP RO JR 

 BUS JS 

 POPP JA 

 BOREIKO CJ 

 ANDJELKOVICH DA 

SOURCE: 

 CRC CRIT REV TOXICOL 13:25-97,1984 

295 

TITLE: 

 Probabilistic Consequence Assessment of Hydrogen Sulphide Releases from a 

 Heavy Water Plant. Scope Determination. 

AUTHORS: 

 Anon 

SOURCE: 

 Govt Reports Announcements &amp; Index (GRA&I), Issue 26, 1985 

ABSTRACT: 

 TD3: This report is concerned with the evaluation of the consequences to 

 the public of an accidental release of hydrogen sulphide (H sub 2 S) to 

 the atmosphere following a pipe or pressure envelope failure, or some 

 other process upset, at a heavy water plant. It covers the first stage of 

 a programme in which the nature of the problem was analyzed and 

 recommendations made for the implementation of a computer model. The 

 concepts of risk assessment and consequence assessment are discussed and a 

 methodology proposed for combining the various elements of the problem 

 into an overall consequence model. These elements are identified as the 

 'Initiating Events', 'Route to Receptor' and 'Receptor Response' and each 

 is studied in detail in the report. Such phenomena as the blowdown of H 

 sub 2 S from a rupture, the initial gas cloud behaviour, atmospheric 

 dispersion and the toxicity of H sub 2 S and sulphur dioxide (SO sub 2 ) 

 are addressed. Critical factors are identified and modelling requirements 

 specified, wi 

296 

TITLE: 

 A new look at physiologic respiratory response to H[2]S poisoning 

AUTHORS: 

 Ammann HM 

SOURCE: 

 Journal of Hazardous Materials Aug. 1986, Vol.13, No.3, p.369-374. Illus. 

 17 ref. 

ABSTRACT: 

 Ever since the role of the carotid bodies in controlling ventilation was 

 elucidated by Heymans in 1932, researchers have puzzled over the seeming 

 paradox presented by the action of hydrogen sulfide gas on the nervous 

 system. The dominant effect is depression of function, but the neural 

 receptors of the carotids appear to be stimulated, resulting in hyperpnoea 

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 at sublethal exposures. This effect is examined in the light of the known 

 cellular mechanisms of poisoning by H[2]S, which inhibits the enzyme 

 cytochrome oxidase, stopping oxidative metabolism. The argument is made 

 that H[2]S affects the carotid sensors in the same manner as reduced 

 oxygen tension, thus resulting in increased rate and depth of ventilation. 

 

297 

TITLE: 

 Hydrogen sulfide 

AUTHORS: 

 ANON 

SOURCE: 

 Arbetarskyddsnèamnden, Box 3208, 103 64 Stockholm, Sweden, 1987. 

 3p. 

ABSTRACT: 

 Chemical safety information sheet taken from the Kemiska èAmnen 

 Register (CIS 89-214). Exposure limits: TLV = 14mg/m|3|; ceiling value = 

 20mg/m|3|. Toxicity: irritates the eyes, skin and mucous membranes; higher 

 concentrations will block the sense of smell; at very high concentrations 

 it will affect the central nervous system. 

298 

TITLE: 

 VIIIth International Symposium on occupational health in the production of 

 organic artificial fibres, France - 2nd day: H[2]S, CS[2], viscose 

AUTHORS: 

 ANON 

SOURCE: 

 Cahiers de notes documentaires - Sâecuritâe et hygiáene 

 du travail 2nd Quarter 1990, No.139, p.451-483. Bibl.ref. 

ABSTRACT: 

 Proceedings of meetings held on Day II of the VIIIth Symposium on 

 occupational health in the production of man-made organic fibres and 

 pertaining to hydrogen sulfide (H[2]S), carbon disulfide (CS[2]) and 

 viscose. Topics: toxicity mechanisms of H[2]S; analysis of 

 ophthalmological data on workers exposed to CS[2] and H[2]S in a Belgian 

 cellulose fibre factory - preliminary results; assessment with the help of 

 a questionnaire of neuropsychiatric symptoms among workers exposed to 

 CS[2]; glutathione level in blood of workers exposed to CS[2]; 

 occupational exposure to CS[2] and vestibular disorders - clinical 

 findings; evaluation of passive dosimeters used for CS[2] sampling; 

 occupational exposure to CS[2] and H[2]S in a vegetable sponge factory - 

 assessment after technological change. 

299 

TITLE: 

 Nitrate promotes biological oxidation of sulfide in wastewaters: 

 experiment at plant-scale. 

AUTHORS: 

 García de Lomas J 

 Corzo A 

 Gonzalez JM 

 Andrades JA 

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 Iglesias E 

 Montero MJ 

SOURCE: 

 Biotechnol Bioeng. 2006, Mar 5; 93(4):801-11. [Biotechnology and 

 bioengineering] 

ABSTRACT: 

 Biogenic production of sulfide in wastewater treatment plants involves 

 odors, toxicity and corrosion problems. The production of sulfide is a 

 consequence of bacterial activity, mainly sulfate-reducing bacteria (SRB). 

 To prevent this production, the efficiency of nitrate addition to 

 wastewater was tested at plant-scale by dosing concentrated calcium 

 nitrate (Nutriox) in the works inlet. Nutriox dosing resulted in a sharp 

 decrease of sulfide, both in the air and in the bulk water, reaching 

 maximum decreases of 98.7% and 94.7%, respectively. Quantitative molecular 

 microbiology techniques indicated that the involved mechanism is the 

 development of the nitrate-reducing, sulfide-oxidizing bacterium 

 Thiomicrospira denitrificans instead of the direct inhibition of the SRB 

 community. Denitrification rate in primary sedimentation tanks was 

 enhanced by nitrate, being this almost completely consumed. No significant 

 increase of inorganic nitrogen was found in the discharged effluent, thus 

 reducing potential environmental hazards to receiving waters. This study 

 demonstrates the effectiveness of nitrate addition in controlling sulfide 

 generation at plant-scale, provides the mechanism and supports the 

 environmental adequacy of this strategy. 

300 

TITLE: 

 [Liquid manure systems] 

AUTHORS: 

 Mannebeck H 

SOURCE: 

 Dtsch Tierarztl Wochenschr. 1984, Jan 9; 91(1):27-31. [DTW. Deutsche 

 tierarztliche Wochenschrift] 

301 

TITLE: 

 INITIAL SUBMISSION: DRFT FINAL REPORT, A VAPOR INHAL REPRODUCTIVE, 

 DEVELOPMENTAL, AND NEURO-TOXICITY STUDY IN CRL:CD(SD)BR RATS EXPOSED TO 

 HYDROGEN SULFIDE, W/CVR LTR DATED 9/15/98 

SOURCE: 

 EPA/OTS; Doc #FYI-OTS-0998-1339 

302 

TITLE: 

 INITIAL SUBMISSION: FINAL REPORT, A VAPOR INHALATION REPRODUCTIVE, 

 DEVELOPMENTAL, AND NEURO-TOXICITY STUDY IN CRL:CD(SD)CR RATS EXPOSED TO 

 HYDROGEN SULFIDE, W/CVR LTR DATED 1/6/99 

SOURCE: 

 EPA/OTS; Doc #FYI-OTS-0199-1347 

303 

TITLE: 

 Hydrogen sulfide poisoning: Clarification of some controversial issues. 

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AUTHORS: 

 MILBY TH 

 BASELT RC 

SOURCE: 

 AMERICAN JOURNAL OF INDUSTRIAL MEDICINE; 35 (2). 1999. 192-195. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Background. Hydrogen sulfide is a toxic gas 

 about which much has been written. We discuss here several issues we 

 believe would benefit from further clarification. Conclusions. We conclude 

 that: 1) Certain neurotoxic effects of exposure are probably due to a 

 direct toxic effect on the brain, while others are almost certainly a 

 result of hypoxia secondary to H2S-induced respiratory insufficiency; 2) 

 pulmonary edema is a common consequence of poisoning and there is 

 suggestive evidence of hyperactive airway responses in some individuals 

 following brief H2S-induced unconsciousness (knockdown); 3) criteria for 

 acceptable community levels are very different than those governing 

 occupational standards; 4) urinary thiosulfate determinations can be 

 useful for monitoring occupational exposure; and 5) determination of 

 sulfide ion concentrations in blood or major organs can be useful in 

 corroborating a diagnosis of fatal H2S toxicity, but there are many 

 pitfalls in collecting, stori 

304 

TITLE: 

 Volatile sulfides and their toxicity in freshwater sediments. 

AUTHORS: 

 BROUWER H 

 MURPHY T 

SOURCE: 

 ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY; 14 (2). 1995. 203-208. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Three forms of volatile sulfides (free 

 hydrogen sulfide, acid-volatile sulfides (AVS) and a new form, 

 heat-volatile sulfides (HVS)), were measured and their relationships 

 discussed. Purging of some contaminated sediments with nitrogen at 22êC 

 failed to remove all of the free H2S, even after 6 h. With freshly 

 H2S-Spiked uncontaminated sediment, purging of H2S was complete after 2 h; 

 however, if the spiked sediment was allowed to stand for 53 d, H2S 

 continued to be purged, even after 43 h. The H2S likely originates from 

 equilibrium reactions involving reduced sulfur species in the sediment. 

 Uncontaminated sediment spiked with H2S was found to be highly toxic using 

 a sediment-contact bioassay employing Photobacterium phosphoreum. Addition 

 of Fe3+, which sequesters the S2-, reduced the toxicity. Two other 

 bioassays (ATP-TOX and Toxi-Chromotest), both involving a DMSO/methanol 

 extract of the spiked sediment, showed greatest toxicity with spiked 

 sediment that had been standi 

305 

TITLE: 

 ENVIRONMENT CANADA'S NEW REFERENCE METHOD FOR MEASURING SEDIMENT TOXICITY 

 USING MARINE OR ESTUARINE AMPHIPODS 

AUTHORS: 

 MCLEAY DJ 

 SCROGGINS R 

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 OSBORNE J 

SOURCE: 

 24TH ANNUAL AQUATIC TOXICITY WORKSHOP, NIAGARA FALLS, ONTARIO, CANADA, 

 OCTOBER 20-22, 1997. CANADIAN TECHNICAL REPORT OF FISHERIES AND AQUATIC 

 SCIENCES; 0 (2192). 1997. 32. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM MEETING ABSTRACT RHEPOXYNIUS-ABRONIUS 

 EOHAUSTORIUS-WASHINGTONIANUS EOHAUSTORIUS-ESTUARIUS AMPHIPOREIA-VIRGINIANA 

 AMPHIPOD MARINE ESTUARINE BIOINDICATOR SEDIMENT TOXICITY REFERENCE METHOD 

 FEDERAL OCEAN DUMPING REGULATIONS CANADIAN ENVIRONMENTAL PROTECTION ACT 

 AMMONIA TOXIN HYDROGEN SULFIDE METHODOLOGY TOXICOLOGY ASSESSMENT METHOD 

306 

TITLE: 

 Toxicity of ozonated animal manure to the house fly, Musca domestica. 

AUTHORS: 

 Masten SJ 

 Kim-Yang H 

 Walker ED 

 Roman H 

 Yokoyama MT 

SOURCE: 

 J Environ Qual. 2001 Sep-Oct; 30(5):1624-30. [Journal of environmental 

 quality] 

ABSTRACT: 

 Swine manure slurries were ozonated at a dosage of 1 g/L and tested for 

 their toxicity to the house fly (Musca domestica). The observed toxicity 

 of ozonated swine manure was consistent and independent of origin of the 

 swine manure. A dose (dilution) response curve was performed. A 50% 

 dilution in the ozonated swine manure slurry resulted in 90% reduction in 

 toxicity. Neither the synthetic nor ozonated synthetic swine manure, both 

 of which contained higher concentrations of formaldehyde and three other 

 unidentified carbonyl compounds than the ozonated swine manure, were toxic 

 to the flies. Ozonated swine manure slurry was centrifuged and passed 

 through a 0.45-microm filter. The liquid phase was as toxic as the 

 unfiltered slurry; as such, the toxicant appears to be present in liquid 

 phase. Neither ammonia, hydrogen sulfide, formaldehyde, nor other simple 

 aldehydes appeared to be the toxic agent. The toxic agent appears to be a 

 polar chemical compound and is concentrated in the urine. Several possible 

 compounds have been identified. The toxicity of untreated and ozonated 

 manure slurries from different livestock was compared. Six animal manure 

 slurries (beef and dairy cattle, horse, poultry, sheep, and swine) were 

 ozonated (dosage of 1 g/L) and tested for toxicity to the house fly. 

 Ozonated dairy cattle manure slurry showed 78% mortality after 72 h, 

 whereas ozonated swine manure slurry achieved a 100% mortality rate in 48 

 h. Neither the unozonated dairy nor swine manure slurries, nor any of the 

 other raw or ozonated manure slurries, were toxic to the flies. 

307 

TITLE: 

 Carbon Disulfide 

AUTHORS: 

 Anonymous 

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SOURCE: 

 Concise International Chemical Assessment Document (CICAD) Vol:46 (2002) 

 38 p 

ABSTRACT: 

 This CICAD on carbon disulfide was prepared by the Environmental Health 

 Directorate of Health Canada and the Commercial Chemicals Evaluation 

 Branch of Environment Canada based on documentation prepared concurrently 

 as part of the Priority Substances Program under the Canadian 

 Environmental Protection Act (CEPA). The objective of assessments on 

 priority substances under CEPA is to assess potential effects of indirect 

 exposure in the general environment on human health as well as 

 environmental effects. Data identified as of the end of May 1999 were 

 considered in these reviews. 1 Information on the nature of the peer 

 review and availability of the source document is presented in Appendix 1. 

 Other source documents for the health and environmental effects include 

 reports prepared by IPCS (1979), the Nofer Institute (Rolecki & Tarkowski, 

 2000), and the United Kingdom Department of Environment (Crookes et al., 

 1993). Other reviews that were also consulted include BUA (1993) and ATSDR 

 (1996). Information on the peer review of this CICAD is presented in 

 Appendix 2. This CICAD was approved as an international assessment at a 

 meeting of the Final Review Board, held in Ottawa, Canada, on 29 October - 

 1 November 2001. Participants at the Final Review Board meeting are listed 

 in Appendix 3. The International Chemical Safety Card (ICSC 0022) for 

 carbon disulfide, produced by the International Programme on Chemical 

 Safety (IPCS, 2000), has also been reproduced in this document. The 

 worldwide production capacity of carbon disulfide (CAS No. 75-15-0) is 

 approximately 1 million tonnes; most of it is used in the production of 

 viscose fibre and cellophane film. It is also released as a byproduct in 

 oil and gas processing. Additional industrial releases result from its use 

 in the chemical industry and tire manufacturing. Virtually all 

 anthropogenic and natural releases are to air. Carbon disulfide is also 

 produced naturally by soil and sediment microorganisms, vegetation, forest 

 and grass fires, and volcanoes. Worldwide, at least 40% and possibly as 

 much as 80% of releases are a result of natural or biogenic activity. 

 Carbon disulfide is ubiquitous throughout the environment. It has been 

 detected in air, water, sediment, and soil; however, it is present 

 primarily in air. The highest concentrations of carbon disulfide in air in 

 the source country for this CICAD (i.e., Canada) have been measured near 

 industrial sources, in particular near natural gas processing plants and 

 sites with sulfur-containing natural gas flares. Carbon disulfide is 

 removed from the air primarily by reaction with hydroxyl radicals, 

 resulting in a half-life of 1-2 weeks. This half-life in air makes it a 

 candidate for long-range transport; however, it is rapidly diluted to 

 natural background levels. Carbon disulfide is rapidly metabolized by 

 organisms and does not bioconcentrate or biomagnify. Available data upon 

 which to base estimates of human exposure to carbon disulfide are 

 extremely limited; however, air appears to be the major route of exposure 

 for members of the general population. Airborne exposures are estimated to 

 be elevated for populations in the vicinity of industrial point sources. 

 Carbon disulfide is extensively absorbed by inhalation, but also via the 

 skin. It is metabolized to several metabolites, one of which 

 (2-thiothiazolidine-4-carboxylic acid) is the basis for biomonitoring of 

 exposure at the workplace. Available data to serve as a basis for 

 assessment of the potential of carbon disulfide to induce irritancy or 

 sensitization are limited. While it has been reported in secondary 

 accounts of seemingly limited early studies that carbon disulfide is 

 severely irritating to the eyes and skin, it has not been possible to 

 verify these data. While inhalation in viscose rayon plants is irritating 

 to the mucous membranes, including the respiratory system, the role of 

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 concomitant exposure to hydrogen sulfide and sulfuric acid in induction of 

 these effects is unknown. Based on the results of studies of workers 

 exposed to carbon disulfide and supporting data from experiments conducted 

 on animals, the nervous system appears to be the critical target for 

 carbon disulfide-induced toxicity, manifested most often as reduced 

 conduction velocity in the peripheral nerves and impaired performance in 

 psychomotor testing. Other effects for which there is considerable weight 

 of evidence in humans exposed to carbon disulfide include alterations in 

 serum lipids and blood pressure that are associated with increased risk of 

 cardiovascular disease, systemic ophthalmological effects, including those 

 on colour vision and damage to the blood vessels of the retina, and (with 

 higher exposures) increased mortality from heart disease. No evidence of 

 carcinogenicity has been observed in limited epidemiological studies; 

 long-term studies on carcinogenicity in experimental animals have not been 

 reported. There is no clear evidence of genotoxicity, although there is 

 some evidence of weak and/or equivocal clastogenicity in vitro or in vivo. 

 There are several reports of decreased libido and/or impotence among males 

 occupationally exposed to high concentrations of carbon disulfide, but 

 there is no consistent evidence based on limited study of other adverse 

 reproductive effects in humans. In experimental animals, carbon disulfide 

 is embryotoxic and fetotoxic at high concentrations and causes terata at 

 exposure levels toxic to the dam. In the sample risk characterization, the 

 estimated mean airborne exposure to carbon disulfide for the general 

 population and for populations in the vicinity of point sources is 

 considerably less than a tolerable concentration of 100 ug/m3. This 

 tolerable concentration was derived based on the benchmark concentration 

 estimated for a 5% excess risk of an abnormal response (defined based on 

 the 5th percentile of the unexposed workers in the critical study) for the 

 most sensitive response variable  i.e., peroneal motor nerve conduction 

 velocity (MCV)1 in viscose rayon workers - adjusting to continuous 

 exposure (24 h/day, 7 days/ week) and applying an overall uncertainty 

 factor of 50. Since most carbon disulfide is released to air, for 

 environmental effects, it is terrestrial organisms in the vicinity of 

 industrial sources that are at greatest potential risk. Aquatic organisms 

 close to discharge points might also be potentially affected. However, 

 based on the sample risk characterization, conservative comparisons of 

 estimated exposure with no-effect values indicate that it is unlikely that 

 carbon disulfide causes adverse effects on populations of terrestrial or 

 aquatic organisms. 

308 

TITLE: 

 Measurements of toxicity and critical stages of development. 

AUTHORS: 

 Hoffman DJ 

SOURCE: 

 Wildlife Toxicology and Population Modeling: Integrated Studies of 

 Agroecosystems (SETAC Special Publications series) 1994;:47-67 

ABSTRACT: 

 First reports of anthropogenic environmental contaminants causing adverse 

 effects in wildlife began to accumulate during the Industrial Revolution 

 of the 1850s, when arsenic emissions, hydrogen sulfide fumes, and lead 

 ingestion were implicated in wildlife mortality. Studies on the effects of 

 modern pesticides on wildlife began soon after the introduction of DDT in 

 1943. Measured endpoints of toxicity in laboratory and field studies have 

 included lethality, reproductive impairment, behavioral aberrations, 

 alterations in growth and development, and changes in physiological 

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 indicators that may foreshadow effects crucial to reproduction and 

 survival. In toxicity evaluation of agricultural and other environmental 

 contaminants, critical stages of development in which vertebrate species 

 are most vulnerable include embryogenesis and the neonatal or early 

 posthatching period. This chapter focuses on effects during these critical 

 periods of development. Measurements discussed include embryotoxicity, 

 teratogenicity, and physiological perturbations in avian embryos and 

 hatchlings. Examples are drawn upon from both laboratory and field studies 

 including effects of petroleum, insecticides, herbicides, and agricultural 

 drainwater contaminants. Interactive effects among toxicants and other 

 environmental factors are discussed. 

309 

TITLE: 

 Effect of polycyclic aromatic hydrocarbons on somatic chromosomes of coal 

 tar workers. 

AUTHORS: 

 Yadav JS 

 Seth N 

SOURCE: 

 Cytobios 1998;93(374):165-73 

ABSTRACT: 

 The genotoxic effect of polycyclic aromatic hydrocarbons (PAHs) on somatic 

 human chromosomes obtained from lymphocytes of 49 coal tar workers exposed 

 to 26 micrograms/m3 benzo(a)pyrene, 16 mg/m3 benzene and 0.04 mg/m3 H2S in 

 the ambient air, compared to equal numbers of matched controls breathing 

 air containing 1 microgram/m3 benzo(a)pyrene, 1.5 mg/m3 benzene and 0.02 

 mg/m3 H2S, was investigated. The mitotic index (MI), chromosome 

 aberrations (CAs), sister chromatid exchanges (SCEs) and satellite 

 associations (SAs) were analysed. All the parameters showed a significant 

 increase (p < 0.01 and 0.05) in the exposed individuals compared with 

 the controls: viz MI, 4.59-7.92; CAs, 0.77-3.0; SCEs, 5.89-6.80; and SAs, 

 8.18-14.26. The occurrence of the DG type of satellite associations were 

 highest and the 3D type lowest. The frequency of SCEs was highest in coal 

 tar workers with an exposure period of 6-10 years. It is suggested that 

 these results show PAH is genotoxic for humans. 

310 

TITLE: 

 The Assessment of Major Hazards: The Factors Affecting Lethal Toxicity 

 Estimates and the Associated Uncertainties 

AUTHORS: 

 Withers RMJ 

 Lees FP 

SOURCE: 

 Hazards in the Process Industries: Hazards IX, The Institution of Chemical 

 Engineers Symposium Series No. 97, The Institution of Chemical Engineers, 

 pages 185-199, 55 references, 19861986 

ABSTRACT: 

 Methods for deriving toxicity data for toxic gases from experimental work 

 were reviewed and the use of toxicity data in hazard assessment was 

 outlined. Equations for calculating lethal concentration and load were 

 described. The actions of some irritant gases, ammonia (7664417), 

 chlorine (7782505), hydrogen-sulfide (7783064) and hydrogen-cyanide 

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 (74908), were described briefly. The problems involved with determination 

 of toxicity using animal experiments were discussed, as well as 

 considerations concerning the statistical interpretation of such 

 experiments. Methods for estimating lethal toxicity, which was described 

 as being generally a function of concentration and time, were considered. 

 The need to take into account the effect of breathing rate when applying 

 the results of animal experiments to man was discussed. The development 

 and application of toxicokinetic models, particularly the one compartment 

 model, were summarized. The question of whether or not interspecies 

 extrapolation is valid was examined, and the need to consider regular and 

 vulnerable populations separately was considered. The use of hazard 

 impact models in estimating the lethality of gases at low concentrations 

 was discussed. The authors conclude that there is a need to put the 

 estimation of the lethal toxicity of gases on a more fundamental basis. 

311 

TITLE: 

 AERIAL CONCENTRATIONS OF AMMONIA AND PUBERTY IN REPLACEMENT GILTS 

AUTHORS: 

 MALAYER JR 

 GREEN ML 

 BRANDT KE 

 KELLY DT 

 DIEKMAN MA 

 SUTTON AL 

SOURCE: 

 79TH ANNUAL MEETING OF THE AMERICAN SOCIETY OF ANIMAL SCIENCE (MIDWESTERN 

 SECTION), DES MOINES, IOWA, USA, MARCH 23-25, 1987. J ANIM SCI; 65 (SUPPL. 

 1). 1987. 153. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM ABSTRACT HYDROGEN SULFIDE 

312 

TITLE: 

 THE VICIA LEAF TIP CELL-MICRONUCLEUS BIOASSAY AND AIR POLLUTION MONITORING 

 

AUTHORS: 

 CHEN G 

 JIN B 

 LI M 

 WENG X 

SOURCE: 

 WANG, W., J. W. GORSUCH AND W. R. LOWER (ED.). ASTM (AMERICAN SOCIETY FOR 

 TESTING AND MATERIALS) SPECIAL TECHNICAL PUBLICATION, 1091. PLANTS FOR 

 TOXICITY ASSESSMENT; SYMPOSIUM ON USE OF PLANTS FOR TOXICITY ASSESSMENT, 

 ATLANTA, GEORGIA, USA, APRIL 19-20, 1989. VII+363P. AMERICAN SOCIETY FOR 

 TESTING AND MATERIALS: PHILADELPHIA, PENNSYLVANIA, USA. ILLUS. ISBN 

 0-8031-1397-8.; 0 (0). 1990. 170-174. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM XYLENE HYDROGEN SULFIDE 

313 

TITLE: 

 Sardines in edible oil: I. Evaluation of official physical-chemical 

 parameters related with the microbiological examination and study of 

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 product-packaging compatibility in relation to migrated compounds. 

AUTHORS: 

 BACETTI LB 

 TAVARES M 

 PASCUET NS 

 TIGLEA P 

 GELLI DS 

 LOBANCO CM 

 MORAIS CD 

SOURCE: 

 REVISTA DO INSTITUTO ADOLFO LUTZ; 54 (1). 1994. 44-50. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Results of physical-chemical and 

 microbiological analysis (according to the Brazilian legislation) of 

 canned sardines (Sardina pilchardus) in soybean oil were reported in this 

 study. The compatibility between the packaging (chromated plate coated 

 with epoxi-phenolic varnish) and product in relation to migrated compounds 

 was evaluated. Iron and chromium levels that were found indicated that 

 these elements present in the fish didn't proceed from metalic packaging. 

 Total volatile bases (TVB) were higher than the limit permitted (0,030 

 g/100 g) and Eber reaction for hydrogen sulfide (H2S) was inconclusive. 

 These results didn't demonstrate any relation with microbiological 

 analysis whose results were in agreement with the legislation. The Eber 

 reaction and TVB values were not conclusive about the quality of this kind 

 of product. Given the results we will suggest a review of TVB values 

 established by legislation and the necessity of new studies in different 

 fish species about 

314 

TITLE: 

 [Therapy of experimental thallium poisoning with stabilized hydrogen 

 sulphide of BAL.] 

AUTHORS: 

 MOESCHLIN S 

 DEMIRAL B 

SOURCE: 

 Schweiz Med Wochenschr. 1952, Jan 19; 82(3):57-8. [Schweizerische 

 medizinische Wochenschrift] 

315 

TITLE: 

 [Occupational disease due to hydrogen sulfide.] 

AUTHORS: 

 SROKA KH 

SOURCE: 

 Munch Med Wochenschr. 1952, Jan 25; 94(4):171-3. [Munchener medizinische 

 Wochenschrift (1950)] 

316 

TITLE: 

 Ecological and toxicological effects of inorganic nitrogen pollution in 

 aquatic ecosystems: A global assessment. 

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AUTHORS: 

 Camargo JA 

 Alonso A 

SOURCE: 

 Environ Int. 2006, Aug; 32(6):831-49. [Environment international] 

ABSTRACT: 

 We provide a global assessment, with detailed multi-scale data, of the 

 ecological and toxicological effects generated by inorganic nitrogen 

 pollution in aquatic ecosystems. Our synthesis of the published scientific 

 literature shows three major environmental problems: (1) it can increase 

 the concentration of hydrogen ions in freshwater ecosystems without much 

 acid-neutralizing capacity, resulting in acidification of those systems; 

 (2) it can stimulate or enhance the development, maintenance and 

 proliferation of primary producers, resulting in eutrophication of aquatic 

 ecosystems; (3) it can reach toxic levels that impair the ability of 

 aquatic animals to survive, grow and reproduce. Inorganic nitrogen 

 pollution of ground and surface waters can also induce adverse effects on 

 human health and economy. Because reductions in SO2 emissions have reduced 

 the atmospheric deposition of H2SO4 across large portions of North America 

 and Europe, while emissions of NOx have gone unchecked, HNO3 is now 

 playing an increasing role in the acidification of freshwater ecosystems. 

 This acidification process has caused several adverse effects on primary 

 and secondary producers, with significant biotic impoverishments, 

 particularly concerning invertebrates and fishes, in many atmospherically 

 acidified lakes and streams. The cultural eutrophication of freshwater, 

 estuarine, and coastal marine ecosystems can cause ecological and 

 toxicological effects that are either directly or indirectly related to 

 the proliferation of primary producers. Extensive kills of both 

 invertebrates and fishes are probably the most dramatic manifestation of 

 hypoxia (or anoxia) in eutrophic and hypereutrophic aquatic ecosystems 

 with low water turnover rates. The decline in dissolved oxygen 

 concentrations can also promote the formation of reduced compounds, such 

 as hydrogen sulphide, resulting in higher adverse (toxic) effects on 

 aquatic animals. Additionally, the occurrence of toxic algae can 

 significantly contribute to the extensive kills of aquatic animals. 

 Cyanobacteria, dinoflagellates and diatoms appear to be major responsible 

 that may be stimulated by inorganic nitrogen pollution. Among the 

 different inorganic nitrogenous compounds (NH4+, NH3, NO2-, HNO2NO3-) that 

 aquatic animals can take up directly from the ambient water, unionized 

 ammonia is the most toxic, while ammonium and nitrate ions are the least 

 toxic. In general, seawater animals seem to be more tolerant to the 

 toxicity of inorganic nitrogenous compounds than freshwater animals, 

 probably because of the ameliorating effect of water salinity (sodium, 

 chloride, calcium and other ions) on the tolerance of aquatic animals. 

 Ingested nitrites and nitrates from polluted drinking waters can induce 

 methemoglobinemia in humans, particularly in young infants, by blocking 

 the oxygen-carrying capacity of hemoglobin. Ingested nitrites and nitrates 

 also have a potential role in developing cancers of the digestive tract 

 through their contribution to the formation of nitrosamines. In addition, 

 some scientific evidences suggest that ingested nitrites and nitrates 

 might result in mutagenicity, teratogenicity and birth defects, contribute 

 to the risks of non-Hodgkin's lymphoma and bladder and ovarian cancers, 

 play a role in the etiology of insulin-dependent diabetes mellitus and in 

 the development of thyroid hypertrophy, or cause spontaneous abortions and 

 respiratory tract infections. Indirect health hazards can occur as a 

 consequence of algal toxins, causing nausea, vomiting, diarrhoea, 

 pneumonia, gastroenteritis, hepatoenteritis, muscular cramps, and several 

 poisoning syndromes (paralytic shellfish poisoning, neurotoxic shellfish 

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 poisoning, amnesic shellfish poisoning). Other indirect health hazards can 

 also come from the potential relationship between inorganic nitrogen 

 pollution and human infectious diseases (malaria, cholera). Human sickness 

 and death, extensive kills of aquatic animals, and other negative effects, 

 can have elevated costs on human economy, with the recreation and tourism 

 industry suffering the most important economic impacts, at least locally. 

 It is concluded that levels of total nitrogen lower than 0.5-1.0 mg TN/L 

 could prevent aquatic ecosystems (excluding those ecosystems with 

 naturally high N levels) from developing acidification and eutrophication, 

 at least by inorganic nitrogen pollution. Those relatively low TN levels 

 could also protect aquatic animals against the toxicity of inorganic 

 nitrogenous compounds since, in the absence of eutrophication, surface 

 waters usually present relatively high concentrations of dissolved oxygen, 

 most inorganic reactive nitrogen being in the form of nitrate. 

 Additionally, human health and economy would be safer from the adverse 

 effects of inorganic nitrogen pollution. 

317 

TITLE: 

 THE GLUTATHIONE PATHWAY TO THE FORMATION OF PHENOLS 

AUTHORS: 

 LERTRATANANGKOON K 

SOURCE: 

 Crisp Data Base National Institutes Of Health 

ABSTRACT: 

 RPROJ N-acetylated cysteine conjugates (premercapturic acids) of 

 bromobenzene 3,4-oxide were found to act as precursors of 3- and 

 4-bromophenol in the rat and guinea pig. The formation of phenols through 

 this pathway is species dependent. The guinea pig shows a higher 

 conversion than the rat and this difference could be due to the degree of 

 acetylate/deacetylate process of cysteine conjugates. This route to 

 phenols may be the major mode of phenol formation for many aromatic 

 compounds whose metabolism involve the reaction of oxides with 

 glutathione. This pathway may be responsible for bromobenzene toxicity in 

 high dosage. The toxicity could be due to the formation of hydrogen 

 sulfide, or to the formation of thiocatechols and/or thioquinones. 

 The specific aims of this proposed studies are: 1. To 

 study the generality of this sulfur-conjugate pathway to the formation of 

 phenols. Several types of aromatic compounds will be tested. The 

 premercapturic acids will be biosynthesized and purified. Each will be 

 administered to the guinia pig and rat, and the formation of phenols by 

 this pathway will be examined. 

 2. To define the sequence of reactions and emphasis will be placed on the 

 identification of the direct intermediate for the formation of 3- and 

 4-bromophenol. The 4-S- and 3-S-cysteine and mercaptopyruvate conjugates 

 and the methylthiohydroxydihydro metabolites of bromobenzene will be 

 synthesized. Each will be tested both in vivo an in vitro for the 

 formation of 3- and 4-bromophenol and the mechanism of sulfur elimination 

 will be studied. 

 3. To determine the role of acetylation in phenol formation. Synthetic 

 4-S- and 3-S-cysteine conjugates of bromobenzene will be administered to 

 three differences strain of mice (A/J, C57BL/6J, Swiss Webster). The 

 affect of fast and slow acetylation to the formation of 3- and 

 4-bromophenol will be examined. 4. The toxicity of the reactive 

 intermediates which could be formed in this sulfur-conjugate pathway to 

 phenols will be studied. Synthetic 4-S- and 3-S-cysteine and 

 mercaptopyruvate conjugate of bromobenzene will be administered to guinea 

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 pig, rat and mice, and the liver and kidney toxicity will be examined. 

318 

TITLE: 

 Toxicity and character of the effect of some zinc compounds. 

AUTHORS: 

 Shabalina LP 

 Spiridonova VS 

SOURCE: 

 J Hyg Epidemiol Microbiol Immunol. 1988; 32(4):397-405. [Journal of 

 hygiene, epidemiology, microbiology, and immunology] 

ABSTRACT: 

 Investigation of the parameters of toxicity of 8 zinc compounds revealed 

 some differences in the degree of their risk for persons working with 

 them. The following TSELs (tentative safe exposure levels of harmful 

 substances) have been determined: 0.5 mg/m3 for zinc nitrate and hydrogen 

 and dihydrogen zinc phosphates, 2 mg/m3 for zinc carbonate and zinc 

 selenide, as well as MAC (maximum allowable concentration) for zinc 

 sulphide equal to 5 mg/m3. No TSEL have been set for zinc caprylate and 

 zinc stearate, but intratracheal administration of 50 mg caprylate caused 

 100%, of stearate 50% death of experimental animals due to pulmonary 

 edema. Maximum tolerable doses were 10 and 1 mg, respectively. Zinc 

 nitrate shows an expressed irritative effect on the skin and a highly 

 expressed effect on the conjunctiva. Zinc phosphates, zinc caprylate and 

 zinc stearate are resorbed by the skin. In all cases, working persons must 

 be protected from the effect of the compounds under study because even 

 though the toxicity of a compound may be rather low, highly noxious 

 compounds may develop in the course of the technological process, e.g., in 

 mechanical treatment of zinc selenide and zinc sulphide monocrystals, 

 hydrogen selenide and hydrogen sulphide, respectively, can be isolated. 

319 

TITLE: 

 Acute Toxic Inhalations 

AUTHORS: 

 Rorison DG 

 McPherson SJ 

SOURCE: 

 Emergency Medicine Clinics of North America, Vol. 10, No. 2, pages 

 409-435, 159 references, 1992 

ABSTRACT: 

 Acute toxic inhalation exposures were reviewed and discussed. Sources of 

 inhaled toxicants were considered. The general problems of diagnosing and 

 managing victims of toxic inhalation exposures were summarized. The major 

 problem is identifying the agent so that the proper treatment can be 

 started. This is very important in acute exposures that produce systemic 

 toxicity since death can occur very rapidly. The general characteristics 

 of inhalationaltoxicant pathogenesis were discussed. Many inhaled 

 toxicants act by causing direct pulmonary damage or systemic toxicity. 

 Pulmonary damage, which includes pulmonary injury and sensitization, 

 generally results from inhalation of respiratory irritants and substances 

 that cause immunological reactions. Systemic toxicity is usually caused 

 by inhaling asphyxiants, organophosphates, hydrocarbons, and metal fumes. 

 Most accidental inhalational injuries result from occupational exposures 

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 and fires. Factors that determine the inherent toxicity of inhaled 

 substances consisted of the pulmonary site affected, particle size, and 

 solubility in water. The pathological effects and treatments for 

 pulmonary irritants including ammonia (7664417), chlorine (7782505), 

 phosgene (75445), nitrogen-dioxide (10102440), formaldehyde (50000), 

 acrolein (107028), and sulfur-dioxide (7446095) were discussed. 

 Occupational asthma and toluene-diisocyanate (26471625) were considered. 

 Hypersensitivity pneumonitis was reviewed. The clinical effects and 

 treatments for systemic inhalation toxicants including carbon-monoxide 

 (630080), hydrogen-cyanide (74908), hydrogen-sulfide (7783064), 

 organophosphates(nerve gases), and metal fumes were discussed. 

320 

TITLE: 

 Issues of human exposure to agents causing developmental toxicity. 

AUTHORS: 

 Tabacova S 

 Vukov M 

SOURCE: 

 Teratology 1991 May;43(5):410 

ABSTRACT: 

 The evaluation of human developmental toxicity resulting from 

 environmental exposures is a complex process. Important considerations in 

 assessing data collected following exposures to multiple environmental 

 agents will be presented. Specific examples are based on a study which 

 assessed the relationship of exposure to pollutants and reproductive 

 outcomes in areas contaminated by metallurgy, chemical and petrochemical 

 industrial sources. Rates of spontaneous abortion, malformation, 

 stillbirths, prematurity, and early neonatal morbidity and mortality were 

 determined for a 5-yr retrospective period which included 238,221 births 

 and 30,579 spontaneous abortions. Exposures via air (SO2, NO2, H2S, 

 particulates, Pb aerosols), soil and water (e.g., Pb, Cd, Cr, Mn, Zn) were 

 studied in parallel. Correlation analysis was used to assess the 

 relationships among environmental and reproductive parameters. Other known 

 developmental hazards also were considered, e.g., background radiation, 

 rubella and varicella morbidity, and pertinent disease states. Significant 

 correlations were found between the rate of malformations at birth and Cd, 

 Cr and particulate pollution as well as Zn deficiency. Also, Zn was 

 negatively correlated with the rate of spontaneous abortion. Strong 

 positive correlations were found between Cd and stillbirths, and Cr and 

 premature births. Pb exposure was not correlated with the above outcomes, 

 but was related to maternal toxemia and neonatal morbidity. Ambient H2S 

 also was related to maternal toxemia, and Mn exposure contributed to 

 increased prematurity and neonatal morbidity. Ambient NO2 pollution was 

 related to prematurity and neonatal mortality. The natural radiation 

 background did not influence any of the reproductive parameters studied. 

321 

TITLE: 

 HYDROGEN SULFIDE IN LOUISIANA USA RICE FIELDS 

AUTHORS: 

 HOLLIS J P JR 

SOURCE: 

 ACTA PHYTOPATHOL ACAD SCI HUNG; 20 (3-4). 1985 (RECD. 1986). 321-326. 

Page 165 of 245

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ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM NITROGEN GAS FERROUS IRON CLAY IRON 

 SULFIDE ORGANIC MATTER TOXICITY 

322 

TITLE: 

 ZEOLITE FILTER TEST TO PREPARE DRINKING WATER FOR THE CENTRAL PART OF THE 

 BAIKAL-AMUR RAILWAY RUSSIAN-SFSR USSR 

AUTHORS: 

 BEREZA AI 

 RUDIK TG 

 GRIBANOV OI 

SOURCE: 

 GIG SANIT; 0 (5). 1986. 65-66. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM HUMAN STRONTIUM LEAD MAGNESIUM IRON 

 HYDROGEN SULFIDE FLUORINE ZEOLITE TOXICITY 

323 

TITLE: 

 THE INFLUENCE OF SIMULTANEOUS EXPOSURE TO CARBON DISULFIDE AND HYDROGEN 

 SULFIDE ON THE PERIPHERAL NERVE TOXICITY AND METABOLISM OF CARBON 

 DISULFIDE IN RATS 

AUTHORS: 

 GAGNAIRE F 

 SIMON P 

 BONNET P 

 DE CEAURRIZ J 

SOURCE: 

 TOXICOL LETT (AMST); 34 (2-3). 1986 (RECD. 1987). 175-184. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM INDUSTRIAL CHEMICAL OCCUPATIONAL HEALTH 

324 

TITLE: 

 BIOLOGICAL ASPECTS OF OPTIMALIZATION OF THE ENVIRONMENT 

AUTHORS: 

 SIDOROVICH EA 

 KULAGIN YU Z 

 SERGEICHIK SA 

SOURCE: 

 ROCZ SEKC DENDROL POL TOW BOT; 34 (0). 1986 (RECD. 1987). 25-36. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM CARBON DISULFIDE HYDROGEN SULFIDE SULFUR 

 DIOXIDE TOXICITY NECROSIS MORPHOLOGY ECOLOGY 

325 

TITLE: 

 ANAEROBIC TREATMENT USING NEW TECHNOLOGY FOR CONTROLLING HYDROGEN SULFIDE 

 TOXICITY 

Page 166 of 245

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AUTHORS: 

 SARNER E 

 HULTMAN BG 

 BERGLUND AE 

SOURCE: 

 TAPPI (TECH ASSOC PULP PAP IND) J; 71 (2). 1988. 41-45. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM WATER POLLUTION WASTEWATER TREATMENT 

 WASTE MANAGEMENT PAPER INDUSTRY METHANE BIOLOGICAL OXYGEN DEMAND CHEMICAL 

 OXYGEN DEMAND 

326 

TITLE: 

 USE OF SULFUR HEXAFLUORIDE AND A THREE-DIMENSIONAL SAMPLING GRID FOR 

 EVALUATION OF INHALATION CHAMBER PERFORMANCE 

AUTHORS: 

 PRIOR MG 

 HENRY P 

 KELLY WE 

 DACHS J 

 LOPEZ A 

SOURCE: 

 AM IND HYG ASSOC J; 49 (11). 1988. 591-592. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM RAT TOXICITY TESTING AIR POLLUTION 

 MONITORING HYDROGEN SULFIDE 

327 

TITLE: 

 ATTEMPT TO DEVELOP A TOXICITY GRADIENT OF THE LEEWARD SIDE OF FUMAROLES OF 

 SOUFRIERE IN GUADELOUPE FRENCH WEST INDIES 

AUTHORS: 

 GARNIER J 

 GARNIER M 

 SASTRE C 

SOURCE: 

 C R SEANCES SOC BIOGEOGR; 64 (4). 1988. 129-135. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM PLANT AIR COMPOSITION SOIL PH ALUMINUM 

 SULFUR DIOXIDE HYDROGEN SULFIDE 

328 

TITLE: 

 PROBLEMS OF OCCUPATIONAL HYGIENE IN THE PRESENT-DAY PROCESSING OF HYDROGEN 

 SULFIDE-CONTAINING GAS AND HYDROCARBON CONDENSATE 

AUTHORS: 

 ZEBZEEV VV 

 SETKO NP 

 ZHELUDEVA GN 

SOURCE: 

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 GIG TR PROF ZABOL; 0 (5). 1989. 32-34. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM HUMAN DIETHANOLAMINE SULFUR DIOXIDE 

 TOXICITY 

329 

TITLE: 

 OCCUPATIONAL HAZARDS AND OCULAR TOXICITY 

AUTHORS: 

 WAY JL 

 BAXTER L 

 MCGUINN D 

 ZITZER AH 

 PETRIKOVICS I 

SOURCE: 

 CHIOU, G. C. Y. (ED.). TARGET ORGAN TOXICOLOGY SERIES: OPHTHALMIC 

 TOXICOLOGY. XV+328P. RAVEN PRESS: NEW YORK, NEW YORK, USA. ILLUS. ISBN 

 0-88167-939-9.; 0 (0). 1992. 291-305. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM HUMAN AMMONIA CARBON DISULFIDE ETHYLENE 

 OXIDE FORMALDEHYDE N HEXANE CYANIDE HYDROGEN FLUORIDE HYDROGEN SULFIDE 

 TOLUENE DIISOCYANATE 

330 

TITLE: 

 KUWAITI OIL FIRES SOURCE ESTIMATES AND PLUME CHARACTERIZATION 

AUTHORS: 

 HUSAIN T 

SOURCE: 

 ATMOSPHERIC ENVIRONMENT; 28 (13). 1994. 2149-2158. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM RESEARCH ARTICLE HUMAN SULFUR DIOXIDE 

 CARBON MONOXIDE CARBON DIOXIDE HYDROGEN SULFIDE NITROGEN OXIDES GASEOUS 

 POLLUTANTS PARTICULATES AIR POLLUTION HEALTH HAZARD VEGETATION TOXICITY 

 REMOTE SENSING EMISSIONS MONITORING KUWAIT 

331 

TITLE: 

 Sediment quality assessment: Status and outlook. (First International 

 Symposium on Sediment Quality Assessment Rationale, Challenges and 

 Strategies, Goteborg, Sweden, August 22-25, 1994). 

AUTHORS: 

 CHAPMAN PM 

SOURCE: 

 JOURNAL OF AQUATIC ECOSYSTEM HEALTH; 4 (3). 1995. 183-194. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. This paper is a synthesis of the 44 

 presentations at the First International Symposium on Sediment Quality 

 Assessment (Sweden, August 1994). The paper includes Initial Premises, 

 Sediments, Tools (with particular emphasis on bioassays), Strategies and 

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 Challenges. Major testable hypotheses are proposed as follows (ranging in 

 complexity, recognizing differences apparent at the Symposium in level of 

 expertise and knowledge): (1) there is no single 'perfect' method of 

 sediment assessment, there are only 'tools in the toolbox'; (2) 

 significant sediment pollution (contamination resulting in adverse 

 biological effects) comes from non-anthropogenic sources; (3) artificial 

 sediments will provide future reference comparisons; (4) knowledge of 

 suspended sediments is required to understand bedded sediments; (5) 

 ammonia and/or hydrogen sulfide cannot explain all sediment toxicity, in 

 particular non-acute responses; (6) subcellular (e.g., genetic) responses 

 are a research tool, not ye 

332 

TITLE: 

 40TH ANNIVERSARY OF UFA RESEARCH INSTITUTE FOR OCCUPATIONAL MEDICINE AND 

 HUMAN ECOLOGY SCIENTIFIC RESULTS 

AUTHORS: 

 KARAMOVA LM 

 GAZIZOV MF 

 BURENKO GN 

SOURCE: 

 MEDITSINA TRUDA I PROMYSHLENNAYA EKOLOGIYA; 0 (12). 1995. 1-6. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM HISTORICAL ARTICLE HYDROGEN SULFIDE 

 BENZENE TOLUENE ALPHA-METHYLSTYRENE ISOPROPYLBENZENE BENZO-A-PYRENE DIOXIN 

 HEAVY METALS PESTICIDES NITRATES SKIN PATHOLOGY IMMUNOLOGY SEX DIFFERENCES 

 OIL INDUSTRY TOXICITY AIR POLLUTION WATER POLLUTION ENVIRONMENTAL CONTROL 

 PREVENTIVE TREATMENT LEGISLATION BASHKORTOSTAN RUSSIA 

333 

TITLE: 

 Cancer incidence, morbidity and geothermal air pollution in Rotorua, New 

 Zealand. 

AUTHORS: 

 BATES MN 

 GARRETT N 

 GRAHAM B 

 READ D 

SOURCE: 

 INTERNATIONAL JOURNAL OF EPIDEMIOLOGY; 27 (1). 1998. 10-14. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Background: The New Zealand city of Rotorua 

 sits on a geothermal field. However, little is known about the possible 

 health impacts of the geothermal emissions. This was an ecological study 

 that examined cancer incidence and morbidity data for Rotorua. Methods: 

 Cancer registry and hospital discharge (morbidity) data were obtained for 

 the decade 1981-1990. Standardized incidence ratios (SIR) were calculated 

 comparing Rotorua residents with those living in the rest of New Zealand. 

 Diagnostic categories examined were based on known target organ systems 

 of hydrogen sulphide toxicity. Results: Of the cancer sites, there was an 

 elevated rate for nasal cancers. However, this was based on only four 

 cases. The SIR for cancers of the trachea, bronchus and lung in Maori 

 women was 1.48 (95% CI: 1.03-2.06). This was not explained by higher 

 smoking rates. In the hospital discharge data, a number of diseases showed 

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 elevated SIR, notably diseases of the nervous system and the eye. To so 

334 

TITLE: 

 IDENTIFICATION OF HYDROGEN SULFIDE AND METHANETHIOL IN A TRANSAMINATIVE 

 PATHWAY OF METHIONINE CATABOLISM 

AUTHORS: 

 STEELE RD 

 BENEVENGA NJ 

SOURCE: 

 FED PROC; 37 (3). 1978 263 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. ABSTRACT RAT LIVER MITOCHONDRIA TOXICITY GAS 

 CHROMATOGRAPHY 

335 

TITLE: 

 The combined toxicity of ethanol and hydrogen sulfide. 

AUTHORS: 

 BECK JF 

 CORMIER F 

 DONINI JC 

SOURCE: 

 TOXICOL LETT (AMST); 3 (5). 1979. 311-314. 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. An 8% solution of ethanol in saline was 

 administered i.p. to male rats at dose levels of 0.33 and 0.66 g/kg body 

 wt. When exposed to an 800 ppm concentration of H2S, 30 min after 

 injection, the alcohol-treated animals displayed a heightened sensitivity 

 to the gas compared to saline-treated rats. 

336 

TITLE: 

 The flux of sulfur-containing gases to vegetation. 

AUTHORS: 

 TAYLOR G E JR 

 MCLAUGHLIN S B JR 

 SHRINER DS 

 SELVIDGE WJ 

SOURCE: 

 ATMOS ENVIRON; 17 (4). 1983. 789-796. 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. The flux of 5 S gases to vegetation exposed to 

 each gas individually at an ambient concentration of 0.12 mul-1 (5 mumol 

 m-3) was assessed using a whole-plant, gaseous exchange system. Total leaf 

 flux of each gas was partitioned into leaf surface (adsorption ) and 

 internal (absorption) fractions. Internal flux varied 4- to 7-fold among 

 gases, and the magnitude of flux was in the following order: SO2 > 

 hydrogen sulfide > carbonyl sulfide > methyl mercaptan > carban 

 disulfide. The regression of internal flux on water solubility and 

 molecular size accounted for 73 and 87% of the variation in Glycine max 

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 and Phaseolus vulgaris, respectively. Leaf conductance, which was adjusted 

 for each gas based on their respective diffusivities in air, did not 

 improve the regression significantly. Estimates of internal flux based on 

 the product of leaf conductance and ambient concentration may not be an 

 accurate technique to assess the rate of absorption for all pollutant 

 gases into the leaf interior under daylight conditions. For highly soluble 

 and chemically reactive gases such as SO2, the latter technique tends to 

 underestimate flux by 50%, which may result from a mean SO2 diffusive path 

 length that is less than that for water vapor. The relationship between 

 flux and the physicochemical properties of a gas may provide a technique 

 for screening atmospheric emissions for their potential toxicity to 

 vegetation. 

337 

TITLE: 

 Safety in the Chemical Industry. Safety in Plant Operation and 

 Maintenance (Petroleum) 

AUTHORS: 

 Yonge DA 

SOURCE: 

 Chemistry and Industry, pages 272-275, 19581958 

ABSTRACT: 

 Safe operation of petroleum processing operations is reviewed. Essential 

 factors for safe operation are outlined: safety in the design of the 

 process; the design of the facility to withstand the required conditions, 

 with the requisite safety devices; adequate training of personnel; and 

 regular and thorough safety inspections. The toxicity of petroleum 

 hydrocarbons and products of distillation, such as hydrogen-sulfide 

 (7783064) sulfuric-acid (7664939), or other decomposition products is 

 discussed. Fire risk is considered, particularly as a result of static 

 electricity or the introduction of chemical reagents. Special attention 

 to ventilation is stressed in view of the threshold limits of some process 

 chemicals, including ammonia (7664417), liquid sulfur-dioxide (7446095), 

 phenol (108952), cresol (1319773), furfural (98011), and benzol (71432). 

 Safety procedures for maintenance operations are emphasized; ventilation 

 of the area, disconnection of pipes, closing of valves, and disconnection 

 of power prior to entering the area. The use of breathing apparatus and 

 protective clothing for work in areas where gas freedom cannot be achieved 

 is discussed. Inspection, safety certificates and permits to work are 

 noted as necessary to ensure safety in maintenance and repair operations. 

 Concentrations, standards, and explosive limits for atmospheric 

 concentrations of petroleum gases are listed. 

338 

TITLE: 

 Health Hazard Evaluation Report No. HETA-83-143-1419, United States Assay 

 Office, San Francisco, California 

AUTHORS: 

 Belanger PL 

 Coye MJ 

SOURCE: 

 Hazard Evaluations and Technical Assistance Branch, NIOSH, U.S. Department 

 of Health and Human Services, Cincinnati, Ohio, Report No. 

 HETA-83-143-1419, 16 pages, 9 references, 19841984 

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ABSTRACT: 

 Environmental and breathing zone samples were analyzed for metal fume 

 particulates, polynuclear aromatic hydrocarbons (PNA), hydrogen-sulfide 

 (7783064) (H2S), and carbon-monoxide (630080) (CO) at the United States 

 Assay Office (SIC-9999), San Francisco, California in March and April 

 1983. Evaluation was requested out of concern for exposure to metal fumes 

 from the melting of coins and possible work related headaches, nausea, and 

 kidney disease. Twelve workers were interviewed and the medical records 

 of six employees working in the melting room were reviewed. Metal fumes, 

 CO, and H2S concentrations were below all relevant standards. Two PNA 

 compounds, fluoranthene (206440) and pyrene (129000), were detected at 

 concentrations of 0.91 to 1.34 and 0.97 to 1.58 micrograms per cubic 

 meter, respectively. There is no current standard for fluoranthene or 

 pyrene. No pattern of medical symptoms or physical findings that were 

 work related were found. The authors conclude that no overexposure to 

 environmental contaminants has occurred. Recommendations include 

 substituting the quenching oil used as a mold release with a 

 sodium-silicate wash to eliminate PNA exposure and using an appropriate 

 respirator in the melting room. 

339 

TITLE: 

 [Studies on the toxic action mechanism of hydrogen sulfide] 

AUTHORS: 

 Kośmider S 

 Rogala E 

 Pacholek A 

SOURCE: 

 Int Arch Arbeitsmed. 1966, Apr 13; 22(1):60-76. [Internationales Archiv 

 fur Arbeitsmedizin] 

340 

TITLE: 

 Toxic Effects of Manure Pit Gases 

AUTHORS: 

 Hurst TS 

SOURCE: 

 Agricultural Health and Safety. Workplace, Environment, Sustainability, 

 H. H. McDuffie, J. A. Dosman, K. M. Semchuk, S. A. Olenchock, and A. 

 Senthilselvan, Editors; CRC Press Inc., Boca Raton, pages 547-550, 6 

 references, 1995 

ABSTRACT: 

 The toxic effects of manure pit gases were discussed in this chapter. Of 

 the components of manure gas, hydrogen-sulfide (7783064) (H2S) was 

 considered to be the most toxic. The agitation/pumping of manure 

 slurries, which occurred during pit emptying, often led to the release of 

 H2S. At low concentrations, H2S irritated mucous membranes, eyes, and 

 airways. As concentrations increased, H2S caused pneumonia, bronchitis, 

 pulmonary edema, central nervous system depression, unconsciousness, and 

 death. The effects of H2S were acute; no cumulative poisoning effects 

 were noted. With methane (74828) and carbon-dioxide (124389) (CO2), 

 increases in concentration result in decreases in the oxygen 

 concentration. Thus, exposure to high concentrations may result in 

 hypoxia. With increasing concentrations of ammonia (7664417), the adverse 

 health effects ranged from mucous membrane inflammation to death. 

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 Carbon-monoxide (630080) (CO) combines with the hemoglobin of the red 

 blood cells, usurping oxygen's active sites. In addition, hemoglobin had 

 a significantly higher affinity for CO than for oxygen. Thus, exposure to 

 CO ultimately led to hypoxia. The author concludes that the competent 

 designing of animal buildings and manure handling systems, sufficient 

 ventilation, strict entrance control, posted warnings, worker education, 

 personal protective equipment usage, and building evacuation will help 

 prevent injuries and deaths resulting from exposure to manure gases. 

341 

TITLE: 

 TOXICOLOGY OF HYDROGEN SULFIDE 

AUTHORS: 

 REIFFENSTEIN RJ 

 HULBERT WC 

 ROTH SH 

SOURCE: 

 CHO, A. K. (ED.). ANNUAL REVIEW OF PHARMACOLOGY AND TOXICOLOGY, VOL. 32. 

 X+698P. ANNUAL REVIEWS INC.: PALO ALTO, CALIFORNIA, USA. ILLUS. ISBN 

 0-8243-0432-2.; 0 (0). 1992. 109-134. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM HUMAN MOUSE HISTORICAL BACKGROUND 

 NEUROTOXICITY RESPIRATORY TOXICITY REPRODUCTIVE TOXICITY DEVELOPMENTAL 

 TOXICITY 

342 

TITLE: 

 Review of the toxicology of carbonyl sulfide, a new grain fumigant. 

AUTHORS: 

 Bartholomaeus AR 

 Haritos VS 

SOURCE: 

 Food Chem Toxicol. 2005, Dec; 43(12):1687-701. [Food and chemical 

 toxicology : an international journal published for the British Industrial 

 Biological Research Association] 

ABSTRACT: 

 Carbonyl sulfide (COS) is a new grain fumigant which has been developed to 

 replace methyl bromide, being phased out due to its ozone depletion 

 properties, and to supplement phosphine gas which is experiencing 

 increased insect resistance. Treatment of commodities with COS, a highly 

 effective fumigant, results in residues that are near or indistinguishable 

 to natural background levels of this compound. COS is a naturally 

 occurring gas, being the predominant sulfur moiety in the atmosphere, 

 occurs naturally in food and is a normal by-product of mammalian aerobic 

 metabolism. COS has low acute inhalational toxicity but with a steep dose 

 response curve; COS is neither genotoxic nor a developmental toxicant but 

 does reversibly impair male fertility. Prolonged, repeated exposure to COS 

 is likely to present similar neurotoxicity hazards to that of the 

 structurally and toxicologically related compound carbon disulfide. 

 Although the occupational risks presented by COS as a fumigant of bulk 

 grain are significant, these are, as they have been for a considerable 

 time for phosphine and methyl bromide, manageable by good occupational 

 safety practices. Consideration may need to be given to scrubbing of 

 ventilated COS and its breakdown product hydrogen sulfide, at the 

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 completion of fumigation to minimise worker and bystander exposure. In 

 terms of classical regulatory toxicology studies, the available database 

 for COS is deficient in many aspects and registration in most 

 jurisdictions will depend on sound scientific argument built upon the 

 totality of the existing scientific data as there are strong arguments 

 supporting the registration of this compound. 

343 

TITLE: 

 HYDROGEN SULFIDE IN PEDIATRIC PARENTERAL AMINO ACID SOLUTIONS 

AUTHORS: 

 DECSI T 

 KOLETZKO B 

SOURCE: 

 JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION; 17 (4). 1993. 

 421-423. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM RESEARCH ARTICLE HUMAN INFANT CYSTEINE 

 HUMAN MILK PROTEIN NUTRITIONAL REQUIREMENT COMMERCIAL SUPPLEMENT HEAT 

 STERILIZATION POTENTIAL TOXICITY INFUSION 

344 

TITLE: 

 Kinetics of growth, substrate utilization and sulfide toxicity for 

 propionate, acetate, and hydrogen utilizers in anaerobic systems. 

AUTHORS: 

 MAILLACHERUVU KY 

 PARKIN GF 

SOURCE: 

 WATER ENVIRONMENT RESEARCH; 68 (7). 1996. 1099-1106. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Batch reactors and serum bottles were used 

 to determine kinetics of growth, substrate utilization, and sulfide 

 inhibition (dissolved sulfide (DS) and hydrogen sulfide (H2S)) in 

 anaerobic systems fed propionate and sulfate. Thermodynamic analyses 

 indicated six major groups of organisms were active in such systems: 

 incomplete propionate oxidation by sulfate-reducing bacteria (SRB), 

 propionate fermentation to acetate and hydrogen, acetate-oxidizing SRB, 

 aceticlastic methanogenesis, hydrogenotrophic SRB, and hydrogenotrophic 

 methanogens. Kinetic parameters determined for each of these groups were 

 bacterial yield, decay coefficient, maximum specific substrate utilization 

 coefficient, half-velocity constant, and inhibition coefficient 

 (uncompetitive). Results indicated that the kinetic and thermodynamic 

 advantages of acetate-utilizing SRB were erased by their sensitivity to 

 sulfide toxicity. In addition, propionate fermenters were also very 

 sensitive to sulfide toxicity. The 

345 

TITLE: 

 SULFATE REDUCTION AND METAL MOBILITY AND TOXICITY 

AUTHORS: 

 ARIAS YD 

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SOURCE: 

 Crisp Data Base National Institutes Of Health 

ABSTRACT: 

 RPROJ Heavy metal pollution is an important environmental problem, yet the 

 biogeochemical processes that affect heavy metal toxicity are poorly 

 understood. The wetlands of Mare Island Naval Shipyard (MINSY), closed 

 April 1996, have been strongly impacted by toxic levels of lead, copper, 

 chromium, cadmium, and nickel released to the environment during decades 

 of shipbuilding and repairs. The reuse plans for MINSY include 

 recreational fishing areas and public parks. These metals are toxic in 

 high doses, with infants and children being the most susceptible. 

 The chemical speciation (redox chemistry) of heavy metals controls the 

 mobility, bioavailability, and toxicity of the metals in t he environment. 

 Some oxidized metals, are soluble, bioavailable, and can become 

 bioconcentrated in the food chain. The reduced form of the aforementioned 

 metals are less soluble and less toxic. 

 Sulfate reducing bacteria (SRB) use sulfate (SO4=) as the terminal 

 electron acceptor and produce hydrogen sulfide (HS0) which chemically 

 reacts forming insoluble metal sulfides. HS- is especially reactive with 

 iron, forming iron sulfides, which may entrap other metals in the iron 

 sulfide matrix. Cultures of marine SRB enriched for tolerance to heavy 

 metal concentrations will be used to determine th precipitation of single 

 or complex mixtures of heavy metals by SRB. The metals of focus will be 

 chromium, copper, cadmium, lead, and nickel. Iron will also be 

 investigated for formation of metal sulfides. SRB may thus shift soluble 

 toxic metals into insoluble, non-toxic forms. 

346 

TITLE: 

 Report of an Investigation of the Pathological Consequences of Chronic 

 Exposure to Sulfur Dioxide, Hydrogen Sulfide, Chlorine and Chlorine 

 Dioxide 

AUTHORS: 

 Leduc G 

SOURCE: 

 Archives des Maladies Professionnelles de Medecine du Travail et de 

 Securite Sociale, Vol. 28, pages 307-311, 19671967 

ABSTRACT: 

 The results of questionnaires sent to 70 physicians and specialists in 

 various French industries concerning acute and chronic intoxication are 

 reported. Only the parts dealing with chlorine (7782505) and 

 chlorine-dioxide (10049044) are translated. Of the seven physicians who 

 responded, three reported 5 cases of acute poisoning with chlorine and one 

 with chlorine-dioxide. Concerning chronic poisoning, possible symptoms 

 include gastric upsets, gastric burns indicating gastritis, and breathing 

 difficulties. Two lethal poisonings and 2 serious poisonings were 

 reported by 27 industrial physicians. Subacute poisonings, or chlorine 

 intakes, produce immediate profuse sweating, dyspnea, and coughing 

 sometimes accompanied by vomiting. No symptoms of chronic chlorine 

 intoxication were reported among the industrial physicians. Questionable 

 symptoms were reported for chronic chlorine-dioxide exposure: skin 

 irritation, pulmonary oppression during physical exertion, and digestive 

 disorders. (French; English translation available) 

347 

TITLE: 

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 Differential sensitivity of lung and brain to sulfide exposure: a 

 peripheral mechanism for apnea. 

AUTHORS: 

 Almeida AF 

 Guidotti TL 

SOURCE: 

 Toxicol Sci. 1999, Aug; 50(2):287-93. [Toxicological sciences : an 

 official journal of the Society of Toxicology] 

ABSTRACT: 

 Acute exposure to hydrogen sulfide (H2S) causes 4 dose-dependent 

 responses: hyperpnea, unconsciousness or knockdown, apnea, and death. At 

 present, scientific mechanisms for these effects are unknown, but 

 inhibition of cytochrome oxidase in the central nervous system (CNS) by 

 sulfide has been suggested. In this study, the premise of brain as target 

 is examined by comparing peripheral with direct delivery of sulfide to 

 brain. NaHS was administered to anesthetized Sprague-Dawley male rats, by 

 femoral intravenous, or carotid intra-arterial injection. With apnea as 

 the test, ED100 values of 0.6 and 3.0 mg kg(-1) were found for peripheral 

 and direct delivery to brain, respectively. Peripheral delivery is 5 times 

 as effective as direct delivery to the brain, and greater if the relative 

 dilution factors are considered. Lidocaine, applied to the vagus, 

 prevented apnea, so lung-brain transmission was essential. It was 

 therefore concluded that the lung is the peripheral site of action. 

 Hyperpnea increased in duration with dose. The carotid body, located 

 distal to the arterial catheter, sensed the high doses of NaHS but did not 

 trigger apnea. Intravenous infusion or intraperitoneal injection with 

 NaHCO3 prevented hyperpnea, apnea, and death. The following conclusions 

 are drawn: the carotid body is not implicated in NaHS-induced apnea, the 

 lung and not brain harbors the primary site of action of H2S, and an 

 afferent neural signal from the lung via the vagus induces the apnea. 

 Finally, NaHCO3 appears to prevent toxicity from sulfide, and therefore 

 H2S, by some unexplained mechanism. Practical emergency treatment for 

 acute toxicity in the field may be possible. 

348 

TITLE: 

 A Critical Review Of The Literature On Carbon Disulfide Toxicity 

AUTHORS: 

 Beauchamp RO Jr 

 Bus JS 

 Popp JA 

 Boreiko CJ 

 Goldberg L 

SOURCE: 

 CRC Critical Reviews in Toxicology, Vol. 11, No. 3, pages 169-278, 1299 

 references, 19831983 

ABSTRACT: 

 Carbon-disulfide (75150) toxicity is reviewed. Human studies are 

 summarized. Inhalation is the major route of occupational exposure. 

 Equilibrium between inhaled and exhaled carbon-disulfide is generally 

 attained during the first 2 hours of exposure. Elimination by the lung 

 and kidney accounts for approximately 10 to 30 percent of absorbed 

 carbon-disulfide. Studies of the uptake, distribution, metabolism, and 

 elimination of carbon-disulfide in experimental animals are considered. A 

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 proposed metabolic pathway for carbon-disulfide is presented. 

 Pathophysiological effects of carbon-disulfide in experimental animals are 

 discussed. Effects of carbon-disulfide on the central nervous system, 

 peripheral nervous system, cardiovascular system, liver, endocrine system, 

 gastrointestinal system, testis, kidney, lung, and skin are reviewed. 

 Simultaneous exposure to carbon-disulfide and hydrogen-sulfide (7783064) 

 is discussed. Genotoxicity of carbon-disulfide is considered. 

 Carbon-dioxide has been found to lack genotoxic activity in a variety of 

 test systems; however, technical problems in the studies make 

 interpretation of the results difficult. Carcinogenicity, teratogenicity, 

 and reproductive effects of carbon-disulfide are summarized. Although no 

 long term bioassays have been conducted, chronic exposure of animals to 

 carbon-disulfide for periods less than 1 year has not revealed any 

 evidence of tumor formation. Human toxicity is discussed. Central 

 peripheral distal axonopathy has been produced by occupational exposure. 

 Increased mortality from coronary heart disease, with aging and 

 hypertension as contributing factors, has been reported in male workers 

 exposed to carbon-disulfide. Vascular changes have been observed in the 

 eyes of the workers having carbon-disulfide exposure. Environmental 

 effects of carbon-disulfide are noted. The principal environmental 

 concerns center on the presence of carbon-disulfide in the atmosphere and 

 drinking water. 

349 

TITLE: 

 Preparation and characteristics of antibacterial sepiolite containing 

 povidone-iodine as a useful pharmaceutical product for patient care. 

AUTHORS: 

 Ohta S 

 Nagai K 

 Maruyama M 

 Inoue H 

 Katsuyama Y 

 Atobe O 

 Ogata H 

 Yamato S 

 Tachikawa E 

 Zenda H 

SOURCE: 

 Biol Pharm Bull. 1999, Jan; 22(1):42-7. [Biological & pharmaceutical 

 bulletin] 

ABSTRACT: 

 Povidone-iodine (PVP-I), an antibacterial medicine, was infiltrated in 

 sepiolite (SPL). The available iodine content in this new pharmaceutical 

 product, a sepiolite preparation containing povidone-iodine (PVP-I-SPL), 

 was retained at 98.9 and 98.3% during storage at 40 degrees C for 3 and 6 

 months, respectively. The effective removal of various gasses, including 

 ammonia, hydrogen sulfide, ethylmercaptan and acetaldehyde, was achieved 

 by use of PVP-I-SPL. Especially, the concentration of ammonia gas was 

 reduced more than half after 30 min of exposure, suggesting that PVP-I-SPL 

 has excellent ability to adsorb ammonia gas. The satisfactory 

 antibacterial effect of PVP-I-SPL was also obtained by testing its minimum 

 bactericidal concentration (MBC). No irritation reactions to the rabbit 

 auricle or ophthalmic mucosa or to human skin were observed by the skin 

 irritation test. The PVP-I-SPL preparation has bactericidal activity and 

 gas-adsorbing ability; therefore, this pharmaceutical product should be 

 useful for the prevention of infections and deodorization in hospital 

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 rooms and houses, as well as in nursing homes for elderly people. 

350 

TITLE: 

 Experimental toxicology of the isothioureas. 

AUTHORS: 

 Petit L 

 Leperchey F 

 Fournier E 

SOURCE: 

 Poumon Coeur26(8): 893-894; 1970 

ABSTRACT: 

 PESTAB The acute toxicity of alpha-naphthylthiourea (ANTU), commonly used 

 as a rat killer, was studied. Rats administered a single dose of 50 mg 

 of naphthylthiourea either survived without displaying any symptoms of 

 poisoning or died from highly acute pulmonary edema within a few minutes. 

 The acute oral toxicity of naphthylthiourea ranged from 5 mg/kg to 400 

 mg/kg in various animal species. The great discrepancy in the toxicity of 

 naphthylthiourea seems to be conditioned by the metabolic fate of this 

 substance in the animal and most probably by the eventual liberation of 

 hydrogen sulfide in the course of enzymatic desulfurization. 

351 

TITLE: 

 Phosphorus Pentasulfide 

AUTHORS: 

 Anonymous 

SOURCE: 

 ACGIH. Documentation of the threshold limit values and biological exposure 

 indices Vol:7th Ed (2001) 2 p 

ABSTRACT: 

 A TLV-TWA of 1 mg/m3 and a TLV-STEL of 3 mg/m3 are recommended for 

 occupational exposure to phosphorus pentasulfide to minimize the potential 

 for eye, skin, and respiratory tract irritation. In the almost void of 

 toxicity data for phosphorus pentasulfide and the fact that the substance 

 readily hydrolyses in moist air to phosphoric acid (and hydrogen sulfide), 

 the toxicity data and TLV for phosphoric acid are considered applicable 

 for phosphorus pentasulfide (see the current TLV Documentation for 

 Phosphoric acid). Sufficient data were not available to recommend Skin, 

 SEN, or carcinogenicity notations. 

352 

TITLE: 

 A Bioassay Experiment to Determine Water Quality Impacts Related to Trout 

 Mortality at a Hatchery Downstream of Lake Sidney Lanier, Georgia 

AUTHORS: 

 Lehman ME 

 Crezee MR 

 Jones RH 

 Schulze RL 

 Leslie MK 

SOURCE: 

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 Govt Reports Announcements &amp; Index (GRA&I), Issue 23, 1982 

ABSTRACT: 

 TD3: A major trout kill occurred at Buford Trout Hatchery in northern 

 Georgia during its first year of operation in autumn 1976. Several studies 

 linked toxicity to anoxic conditions in the hypolimnion of Lake Sidney 

 Lanier (the reservoir formed by Buford Dam, 1 1/2 miles up the 

 Chattahoochee River from the hatchery). No consensus as to the toxic 

 agent(s) was reached as a result of the initial studies. Waters from 

 different depths in the reservoir were tested for toxicity to rainbow 

 trout swim-up fry, and each water was extensively analyzed chemically. 

 Bottom water was most toxic and had the highest levels of manganese (Mn) 

 and iron (Fe). No other metals were detectable, no humics or pesticides 

 could be measured, and no hydrogen sulfide was found. The study concluded 

 that Mn and Fe explained all toxicity observed at the hatchery and 

 demonstrated in the river, with no evidence for involvement of any other 

 metal nor of any organic compound. Recommendations were made with respect 

 to possible solutions to 

353 

TITLE: 

 Modulation of cysteine biosynthesis in chloroplasts of transgenic tobacco 

 overexpressing cysteine synthase [O-acetylserine(thiol)-lyase]. 

AUTHORS: 

 Saito K 

 Kurosawa M 

 Tatsuguchi K 

 Takagi Y 

 Murakoshi I 

SOURCE: 

 Plant Physiol. 1994, Nov; 106(3):887-95. [Plant physiology] 

ABSTRACT: 

 Cysteine synthase [O-acetyl-L-serine(thiol)-lyase, EC 4.2.99.8] (CSase), 

 which is responsible for the terminal step of cysteine biosynthesis, 

 catalyzes the formation of L-cysteine from O-acetyl-L-serine (OAS) and 

 hydrogen sulfide. Three T-DNA vectors carrying a spinach (Spinacia 

 oleracea) cytoplasmic CSase A cDNA (K. Saito, N. Miura, M. Yamazaki, H. 

 Horano, I. Murakoshi [1992] Proc Natl Acad Sci USA 89: 8078-8082) were 

 constructed as follows: pCSK3F, cDNA driven by the cauliflower mosaic 

 virus (CaMV) 35S RNA promoter with a sense orientation; pCSK3R, cDNA 

 driven by the CaMV 355 promoter with an antisense orientation; pCSK4F, 

 cDNA fused with the sequence for chloroplast-targeting transit peptide of 

 pea ribulose-1,5-biphosphate carboxylase small subunit driven by the CaMV 

 35S promoter with a sense orientation. These chimeric genes were 

 transferred into tobacco (Nicotiana tabacum) with Agrobacterium-mediated 

 transformation, and self-fertilized progeny were obtained. CSase 

 activities in cell-free extracts of pCSK3F and pCSK4F transformants were 

 2- to 3-fold higher than those of control and pCSK3R plants. CSase 

 activities in chloroplasts of pCSK4F transformants were severalfold higher 

 than those of control and pCSK3F plants, indicating that the foreign CSase 

 protein is transported and accumulated in a functionally active form in 

 chloroplasts of pCSK4F plants. Isolated chloroplasts of a pCSK4F 

 transformant had a more pronounced ability to form cysteine in response to 

 addition of OAS and sulfur compounds than those of a control plant. In 

 particular, feeding of OAS and sulfite resulted in enhanced cysteine 

 formation, which required photoreduction of sulfite in chloroplasts. The 

 enhanced cysteine formation in a pCSK4F plant responding to sulfite was 

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 also observed in leaf discs. In addition, these leaf discs were partially 

 resistant to sulfite toxicity, possibly due to metabolic detoxification of 

 sulfite by fixing into cysteine. These results suggested that 

 overaccumulated foreign CSase in chloroplasts could modulate biosynthetic 

 flow of cysteine in response to sulfur stress. 

354 

TITLE: 

 HYGIENIC STUDIES IN LIVESTOCK BREEDING 

AUTHORS: 

 TSAPKO VG 

 PROKOPOV VA 

SOURCE: 

 GIG SANIT; 0 (2). 1986. 30-33. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM ESCHERICHIA-COLI STAPHYLOCOCCI HELMINTH 

 EGG VIRUS BACTERIA FUNGUS COW AMMONIA HYDROGEN SULFIDE ANIMAL WASTE MILK 

 ENDOTOXIN SOIL POLLUTION WATER POLLUTION NOISE MASTITIS RESPIRATORY 

 INFECTION NEUROTOXICITY 

355 

TITLE: 

 Sulfide toxicity: mechanical ventilation and hypotension determine 

 survival rate and brain necrosis. 

AUTHORS: 

 Baldelli RJ 

 Green FH 

 Auer RN 

SOURCE: 

 J Appl Physiol. 1993, Sep; 75(3):1348-53. [Journal of applied physiology 

 (Bethesda, Md. : 1985)] 

ABSTRACT: 

 Occupational exposure to hydrogen sulfide is one of the leading causes of 

 sudden death in the workplace, especially in the oil and gas industry. 

 High-dose exposure causes immediate neurogenic apnea and death; lower 

 doses cause "knockdown" (transient loss of consciousness, with 

 apnea). Because permanent neurological sequelae have been reported, we 

 sought to determine whether sulfide can directly kill central nervous 

 system neurons. Ventilated and unventilated rats were studied to allow 

 administration of higher doses of sulfide and to facilitate physiological 

 monitoring. It was extremely difficult to produce cerebral necrosis with 

 sulfide. Only one of eight surviving unventilated rats given high-dose 

 sulfide (a dose that was lethal in > or = 50% of animals) showed cerebral 

 necrosis. Mechanical ventilation shifted the dose that was lethal in 50% 

 of the animals to 190 mg/kg from 94 mg/kg in the unventilated rats. 

 Sulfide was found to potently depress blood pressure. Cerebral necrosis 

 was absent in the ventilated rats (n = 11), except in one rat that showed 

 profound and sustained hypotension to < or = 35 Torr. 

 Electroencephalogram activity ceased during exposure but recovered when 

 the animals regained consciousness. We conclude that very-high-dose 

 sulfide is incapable of producing cerebral necrosis by a direct histotoxic 

 effect. 

356 

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TITLE: 

 SULFUR HYDROGEN SULFIDE TOXICOSIS IN CATTLE 

AUTHORS: 

 SHORT SB 

 EDWARDS WC 

SOURCE: 

 VET HUM TOXICOL; 31 (5). 1989. 451-453. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM DIETARY ELEMENT FEED SUPPLEMENT TICK 

 CONTROL ANAPLASMOSIS CONTROL 

357 

TITLE: 

 Sulfide tolerance and detoxification in shallow-water marine fishes. 

AUTHORS: 

 BAGARINAO T 

 VETTER RD 

SOURCE: 

 MAR BIOL (BERL); 103 (3). 1989. 291-302. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Hydrogen sulfide is a potent inhibitor of 

 aerobic respiration. Sulfide is produced in sediments, and many species of 

 fish live in association with the bottom. Tolerance tests, enzyme assays, 

 and chromatography of sulfur compounds in thirteen species of 

 shallow-water marine fishes (collected in San Diego, California, USA in 

 1987-1988) indicate adaptations to sulfide that vary with habitat and 

 lifestyle. Tidal-marsh inhabitants, like Gillichthys mirabilis and 

 Fundulus parvipinnis, have higher tolerance to sulfide (96 h LC50 at 525 

 to 700 muM) relative to outer-bay and open-coast inhabitants (surviving 

 < 12 h at much lower concentrations). The cytochrome c oxidase of all 

 species shows high activity and susceptibility to sulfide poisoning, with 

 50% inhibition at 30 to 500 nM in various tissues. The two marsh species 

 are able to survive at sulfide concentrations already inhibitory to their 

 cytochrome c oxidase and fatal to other species. All species detoxify 

 sulfide by oxi 

358 

TITLE: 

 THE EFFECT OF DISSOLVED HYDROGEN SULFIDE AND CARBON DIOXIDE ON SHORT-TERM 

 PHOTOSYNTHESIS OF SKELETONEMA-COSTATUM A MARINE DIATOM 

AUTHORS: 

 BRETELER RJ 

 BUHL RL 

 MAKI AW 

SOURCE: 

 GORSUCH, J. W., ET AL. (ED.). ASTM (AMERICAN SOCIETY FOR TESTING 

 MATERIALS) SPECIAL TECHNICAL PUBLICATIONS, 1115. PLANTS FOR TOXICITY 

 ASSESSMENT: SECOND VOLUME; SYMPOSIUM, SAN FRANCISCO, CALIFORNIA, USA, 

 APRIL 23-24, 1990. VII+401P. AMERICAN SOCIETY FOR TESTING AND MATERIALS: 

 PHILADELPHIA, PENNSYLVANIA, USA. ILLUS. MAPS. ISBN 0-8031-1422-2.; 0 (0). 

 1991. 118-125. 

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ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM TOXICITY PH OFF-SHORE NATURAL GAS 

 PRODUCTION PLATFORMS 

359 

TITLE: 

 Mutagenicity of the reaction products of dibenzo-p-dioxin with nitrogen 

 oxides. 

AUTHORS: 

 Watanabe T 

 Kusumoto M 

 Ikeda M 

 Hirayama T 

SOURCE: 

 Mutat Res. 1992, Apr; 281(4):247-54. [Mutation research] 

ABSTRACT: 

 Dibenzo-p-dioxin (DD) was made to react with various concentrations of 

 nitrogen oxides in the dark. The mutagenicities of the reaction products 

 were tested using Salmonella typhimurium strains TA98, TA100, TA98NR and 

 TA98/1,8-DNP6 in the presence or absence of a mammalian metabolic 

 activation system (S9 mix). DD-NOx (molar ratios 1:3, 1:6 and 1:18) 

 reaction products exhibited mutagenic potency in strains TA98 and 

 TA98/1,8-DNP6 without S9 mix. In a gas chromatography/mass spectrometry 

 study, 2-nitrodibenzo-p-dioxin (NDD) was identified with authentic sample 

 in the mutagenic reaction products. DD-NOx (1:18) reaction products were 

 reduced by sodium hydrogen sulfide and the reduction mixture was analyzed 

 by HPLC. 2,7-Dinitrodibenzo-p-dioxin (DNDD) and 2,8-DNDD were identified 

 as corresponding diamino-DDs in the reduction mixture. 2-NDD, 2,7-DNDD and 

 2,8-DNDD were also mutagenic in strains TA98 and TA98/1,8-DNP6 without S9 

 mix and the mutagenicity of DD-NOx reaction products was largely accounted 

 for by the nitro-DDs. 

360 

TITLE: 

 COMPENDIUM OF RICE DISEASES 

AUTHORS: 

 WEBSTER RK 

 GUNNELL PS 

SOURCE: 

 WEBSTER, R. K. AND P. S. GUNNELL (ED.). COMPENDIUM OF RICE DISEASES. 

 VIII+62P. AMERICAN PHYTOPATHOLOGICAL SOCIETY: ST. PAUL, MINNESOTA, USA. 

 ILLUS. PAPER. ISBN 0-89054-126-4.; 0 (0). 1992. VIII+62P. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM BOOK BACTERIA FUNGI VIRUSES 

 MYCOPLASMA-LIKE ORGANISMS NEMATODES BIOTIC DISEASES ABIOTIC DISEASES 

 SYMPTOMOLOGY EPIDEMIOLOGY DISEASE CONTROL HYDROGEN SULFIDE TOXICITY 

 ORGANIC ACID EFFECTS TOXIC GASES HERBICIDE INJURY NUTRIENT DEFICIENCY 

 TOXICITY 

361 

TITLE: 

 Spectrophotometric determination of Zineb (a dithiocarbamate fungicide) by 

 the methylene blue method. 

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AUTHORS: 

 AGRAWAL V 

 SHIVHARE P 

 GUPTA VK 

SOURCE: 

 FRESENIUS' J ANAL CHEM; 344 (7-8). 1992. 350-352. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. A spectrophotometric method has been 

 developed for the determination of Zineb in water and vegetables. The 

 method is based on the liberation of hydrogen sulphide from Zineb, which 

 is trapped in an absorbing solution of triethanolamine, sodium hydroxide 

 and ethylene-diamine tetraacetic acid. The absorbing solution is treated 

 with N-N-dimethyl-p-phenylene diamine sulphonate and ferric chloride to 

 form methylene blue. Beer's law is obeyed over the concentration range of 

 3-32 ppm. The method is simple and can be used for the determination of 

 Zineb in the presence of other dithiocarbamates. 

362 

TITLE: 

 Volatile compounds produced by meat Pseudomonas grown on beef at 

 refrigeration temperatures. 

AUTHORS: 

 INTARAPICHET K-O 

 BAILEY ME 

SOURCE: 

 ASEAN FOOD J; 8 (1). 1993. 14-21. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Seventy-three pseudomonad isolates were 

 recovered from spoiled commercial ground beef stored at 4ê C for 14 days. 

 These isolates included 27% fluorescent pseudomonad and 73% 

 non-fluorescent pseudomonads. A representative isolate from Pseudomonas 

 fluorescens and three isolates from non-fluorescent Pseudomonas along with 

 reference cultures were grown on sterile beef at 4ê C for 14 days. 

 Volatile compounds produced during microbial growth on beef were collected 

 on Tenax GC trap and subsequently identified by direct sampling GLC-MS. 

 Compounds of major sensory significance were sulfur containing compounds 

 including methanethiol, dimethylsulfide, dimethyldisulfide, 

 dimethylytrisulfide and methylthioacetate but not hydrogen sulfide. Esters 

 were not significant volatiles produced by strains of Pseudomonas growing 

 on beef. 

363 

TITLE: 

 Hazards in confinement housing--gases and dusts in confined animal houses 

 for swine, poultry, horses and humans. 

AUTHORS: 

 Pickrell J 

SOURCE: 

 Vet Hum Toxicol. 1991, Feb; 33(1):32-9. [Veterinary and human toxicology] 

ABSTRACT: 

 Indoor atmospheres in swine or poultry confinement buildings, horse stalls 

 or human dwellings contain gases, dusts and endotoxin in concentrations 

Page 183 of 245

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 significantly in excess of those in outdoor environments. Although 

 concentrations of such constituents differ appreciably between species, 

 many of such differences may be related to differences in indoor mass 

 loading and ventilation, or to the homogeneity of such ventilation. The 

 high protein content of these indoor dust particles suggest they are of 

 animal origin. Their ability to form bacterial colonies and to form or 

 bind endotoxin suggest that the smallest and most respirable particles 

 were manure particles containing enteric bacteria and endotoxin. 

 Respiratory disease in swine, poultry and horses and in the workers who 

 care for them may be caused by increased levels of carbon monoxide, 

 ammonia, hydrogen sulfide, or indoor dust particles from feed and manure. 

 The stagnant air of a well-insulated building causes the most active 

 individual to attract these stagnant pockets, while the tendency of young 

 animals to seek warmth may lead to the formation of additional pockets. 

 Increased ventilation is an expensive solution to the problems associated 

 with indoor air pollution. However, more thorough mixing of indoor air may 

 reduce the effects of these clouds of pollutants. 

364 

TITLE: 

 Response of Quercus pubescens leaves exposed to geothermal pollutant input 

 in southern Tuscany (Italy). 

AUTHORS: 

 Bussotti F 

 Tognelli R 

 Montagni G 

 Borghini F 

 Bruschi P 

 Tani C 

SOURCE: 

 Environ Pollut. 2003; 121(3):349-61. [Environmental pollution (Barking, 

 Essex : 1987)] 

ABSTRACT: 

 The paper reports a case of evident and widespread leaf damage on trees in 

 southern Tuscany (Central Italy) attributed to the input of pollutants 

 produced in a geothermal area. The main potentially phytotoxic substances 

 are boron and hydrogen sulphide. Trees affected are conifers as well as 

 both evergreen and deciduous broadleaves. In the present study the 

 possible impact of geothermal pollutants on Quercus pubescens leaves has 

 been considered. Leaf samples coming from three sampling locations (S1 

 inside the geothermal area; S2 on the margins; S3 outside) and three 

 consecutive dates (June, July and August) were analyzed for the following 

 parameters: sulphur and boron concentration; leaf area; leaf mass per 

 area; chlorophyll fluorescence (Fv/Fm); chlorophyll a, chlorophyll b and 

 carotenoid concentrations. Anatomical and ultrastructural observations 

 were also performed. In all sampling location sulphur and boron 

 concentrations are greater than the background values recorded in southern 

 Tuscany in a previous survey. The sulphur concentration in leaves was 

 higher in S1 than S2 and S3, but did not increase throughout the survey 

 period. Boron reached the greatest concentrations in S2 and showed a 

 continuous increase over the study period. Leaves subjected to a higher 

 load of pollutants were smaller in size (in terms of leaf area), but were 

 more sclerophyllous. Damaged chloroplasts and reduced Fv/Fm values were 

 observed at S1 and S2, but chlorophyll concentration values were higher at 

 S1. Such an apparent anomaly can possibly be explained by the onset of 

 compensation and recovery mechanisms. Foliar injuries appeared to be 

 related to boron concentration. 

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365 

TITLE: 

 ACTIVITIES OF SULFATE-REDUCING BACTERIA SRB IN RESPONSE TO MANIPULATION OF 

 DIETARY SULFATE IN ULCERATIVE COLITIS 

AUTHORS: 

 PITCHER M CL 

 MAGEE E AM 

 BEATTY ER 

 CUMMINGS JH 

SOURCE: 

 96TH ANNUAL MEETING OF THE AMERICAN GASTROENTEROLOGICAL ASSOCIATION AND 

 THE DIGESTIVE DISEASE WEEK, SAN FRANCISCO, CALIFORNIA, USA, MAY 19-22, 

 1996. GASTROENTEROLOGY; 110 (4 SUPPL.). 1996. A992. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM MEETING ABSTRACT DESULFOVIBRIO-SPP HUMAN 

 HYDROGEN SULFIDE SULFITE SULFATED POLYSACCHARIDE FOOD PRESERVATIVE 

 BUTYRATE OXIDATION COLONOCYTE METABOLISM DISEASE RELAPSE 

366 

TITLE: 

 HYDROGEN SULPHIDE A BACTERIAL TOXIN IN ULCERATIVE COLITIS? 

AUTHORS: 

 PITCHER M CL 

 CUMMINGS JH 

SOURCE: 

 GUT; 39 (1). 1996. 1-4. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM LITERATURE REVIEW HUMAN INFLAMMATION 

367 

TITLE: 

 Volatile fractions of landfill leachates and their effect on Chlamydomonas 

 reinhardtii: In vivo chlorophyll a fluorescence. 

AUTHORS: 

 BRACK W 

 ROTTLER H 

 FRANK H 

SOURCE: 

 ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY; 17 (10). 1998. 1982-1991. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. A method for identification of toxic 

 volatile constituents of landfill leachates is presented that combines 

 bioassay-compatible sample preparation, chemical analysis, and a bioassay 

 based on in vivo chlorophyll a fluorescence of the green alga 

 Chlamydomonas reinhardtii. Two major pathways of toxicity were identified 

 by comparing fluorescence patterns: specific toxicity of hydrogen sulfide, 

 and narcotic action of nonreactive organic compounds. For quantification, 

 the contributions of identified compounds were calculated using toxic 

 units. The ecotoxicologic relevance of volatile fractions from hazardous 

 waste leachates was shown. 

Page 185 of 245

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368 

TITLE: 

 Sulfur toxicity and media capacity for H2S removal in biofilters packed 

 with a natural or a commercial granular medium. 

AUTHORS: 

 Jones K 

 Martinez A 

 Rizwan M 

 Boswell J 

SOURCE: 

 J Air Waste Manag Assoc. 2005, Apr; 55(4):415-20. [Journal of the Air & 

 Waste Management Association (1995)] 

ABSTRACT: 

 Two types of media, a natural medium (wood chips) and a commercially 

 engineered medium, were evaluated for sulfur inhibition and capacity for 

 removal of hydrogen sulfide (H2S). Sulfate was added artificially (40, 65, 

 and 100 mg of S/g of medium) to test its effect on removal efficiency and 

 the media. A humidified gas stream of 50 ppm by volume H2S was passed 

 through the media-packed columns, and effluent readings for H2S at the 

 outlet were measured continuously. The overall H2S baseline removal 

 efficiencies of the column packed with natural medium remained >95% over a 

 2-day period even with the accumulated sulfur species. Added sulfate at a 

 concentration high enough to saturate the biofilter moisture phase did not 

 appear to affect the H2S removal process efficiency. The results of 

 additional experiments with a commercial granular medium also demonstrated 

 that the accumulation of amounts of sulfate sufficient enough to saturate 

 the moisture phase of the medium did not have a significant effect on H2S 

 removal. When the pH of the biofilter medium was lowered to 4, H2S removal 

 efficiency did drop to 36%. This work suggests that sulfate mass transfer 

 through the moisture phase to the biofilm phase does not appear to inhibit 

 H2S removal rates in biofilters. Thus, performance degradation for 

 odor-removing biofilters or H2S breakthrough in field applications is 

 probably caused by other consequences of high H2S loading, such as sulfur 

 precipitation. 

369 

TITLE: 

 Water, water everywhere, nor any drop to drink ,. ,. ,. ,. 

AUTHORS: 

 Ravera O 

SOURCE: 

 Eurospectra; 11(2): 34-46; 1972 ; (REF:20) 

ABSTRACT: 

 HAPAB When ascertaining the lower limits of human tolerance to 

 pollutants, an investigation of water pollution should include studies in 

 biology, morphometry, hydrology, water chemistry, and climatology, and 

 ones on the sedimentological characteristics of the polluted water. For 

 the specification of ''limits,'' the scope of the experiments should be 

 extended to identify organisms (or stages in their development) which are 

 highly sensitive, typical of various environments (e.g. littoral, 

 pelagic, and deep-water), and readily usable as toxicity indications. To 

 assess the noxiousness of an element in the environment, the overall 

 concentration, the concentration of its compounds, and its physical form 

Page 186 of 245

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 (in terms of oxidation potential) are needed. Proposed tolerance limits 

 for Italian waters are tabulated for various metals, oils, detergents, 

 free and combined chlorines, phosphorus derivatives, pesticides, arsenic, 

 cyanides, hydrogen sulfide, and carbon disulfide. The hazard due to a 

 pollutant depends on toxicity, concentration, and degradability. 1972 

370 

TITLE: 

 A CRITICAL REVIEW OF THE LITERATURE ON HYDROGEN SULFIDE TOXICITY 

AUTHORS: 

 BEAUCHAMP R O JR 

 BUS JS 

 POPP JA 

 BOREIKO CJ 

 ANDJELKOVICH DA 

 LEBER P 

SOURCE: 

 CRIT REV TOXICOL; 13 (1). 1984 (RECD. 1985). 25-97. 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. RRM HUMAN ANIMAL EYE IRRITATION PULMONARY 

 TOXICITY NEUROTOXICITY INHALATION AIR POLLUTION 

371 

TITLE: 

 Physiological responses to sulfide toxicity by the air-breathing catfish, 

 Hoplosternum littorale (Siluriformes, Callichthyidae). 

AUTHORS: 

 Affonso EG 

 Polez VL 

 Corrêa CF 

 Mazon AF 

 Araújo MR 

 Moraes G 

 Rantin FT 

SOURCE: 

 Comp Biochem Physiol C Toxicol Pharmacol. 2004, Dec; 139(4):251-7. 

 [Comparative biochemistry and physiology. Toxicology & pharmacology : CBP] 

ABSTRACT: 

 Hemolytic anemia accompanied by changes in the immunology system is one of 

 the sulfide intoxication harmful effects on Hoplosternum littorale. 

 Hematological parameters are considered as effective indicators of stress 

 caused by this hydrogen sulfide. During sulfide exposure, H. littorale 

 neither alters the methemoglobin concentration nor forms sulfhemoglobin in 

 the presence of high levels of dissolved sulfide in the water. Cytochrome 

 c oxidase shows little activity in the gills and blood of H. littorale 

 when exposed to sulfide. Alternative metabolic routes are suggested 

 through which the accumulation of pyruvate leads to the formation of an 

 end product other than lactate. 

372 

TITLE: 

 Maximum Allowable Concentration of Atmospheric Impurities 

AUTHORS: 

Page 187 of 245

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 Drinker P 

 Cook WA 

SOURCE: 

 Journal of Industrial Hygiene and Toxicology, Vol. 31, No. 1, pages 51-54, 

 11 references, 19491949 

ABSTRACT: 

 Maximum allowable concentrations of atmospheric impurities are considered 

 on the basis of variations in toxicity, with topics including: duration of 

 exposure, sensory reactions versus poisoning, zones of toxicity, and for 

 siliceous dusts, free silica (7631869) content. Maximum allowable 

 concentrations are suggested for acetone (67641), gasoline (8006619), 

 ethyl ether (60297), ethyl chloride (75003), ethyl alcohol (64175), methyl 

 alcohol (67561), toluene (108883), methyl ethyl ketone (78933), 

 trichlorethane (25323891), benzene (71432), butanol (71363), 

 carbon-tetrachloride (56235), carbon-monoxide (630080), hydrogen-sulfide 

 (7783064), carbon-disulfide (75150), tetrachloroethane (79345), 

 hydrochloric-acid, hydrocyanic-acid (74908), chlorine, phosgene (75445), 

 arsine (7784421), dimethyl-sulfate (77781), and radon (10043922) gas and 

 other radioactive gases. 

373 

TITLE: 

 Selenium-dependent enzymes. 

AUTHORS: 

 Stadtman TC 

SOURCE: 

 Annu Rev Biochem. 1980; 49:93-110. [Annual review of biochemistry] 

ABSTRACT: 

 Selenium, molecular weight 78.96, resembles sulfur in many of its chemical 

 properties and occurs in inorganic forms as H2Se, H2Se2O3, H2SeO3, and 

 H2SeO4 which are the analogues of hydrogen sulfide, thiosulfate, sulfite, 

 and sulfate, respectively. The commonly available radionuclide, 75Se, is a 

 gamma emitter (half-life 122 days) that is used extensively as a tracer in 

 biochemical studies and as a radiopharmaceutical agent for diagnostic 

 purposes. Organoselenium compounds, in general, are less stable and more 

 reactive than the corresponding sulfur analogues and these properties may 

 account for the toxicity of selenium when it is incorporated 

 indiscriminately in place of sulfur in cellular constituents. On the other 

 hand living systems may have exploited the greater reactivity of certain 

 types of organoselenium compounds in those instances where selenium is 

 specifically required as a component of an enzyme or other macromolecule. 

 Several enzymic processes that do not distinguish selenium from sulfur and 

 therefore may be important in selenium toxicity were discussed in some 

 detail in two earlier reviews on selenium biochemistry (1, 2) and this 

 aspect of the problem is not treated here. Rather, the information 

 currently available on the properties and catalytic functions of the four 

 known selenium-dependent enzymes is summarized. These enzymes are formate 

 dehydrogenases of Escherichia coli and several anaerobic bacteria, 

 clostridial glycine reductase, mammalian and avian glutathione peroxidase, 

 and nicotinic acid hydroxylase of Clostridium barkeri. Additional 

 selenoproteins whose catalytic activities are as yet unidentified are 

 mentioned. 

374 

TITLE: 

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 Toxic Hazards Research Unit Annual Technical Report: 1972 

AUTHORS: 

 MacEwen JD 

 Vernot EH 

SOURCE: 

 Aerospace Medical Research Laboratory, Air Force Systems Command, 

 Wright-Patterson Air Force Base, Ohio, Report No. AMRL-TR-72-62, NTIS 

 AD755-358, 162 pages, 37 references, 19721972 

ABSTRACT: 

 Work by the Toxic Hazards Research Unit from June 1971 through May 1972 is 

 reviewed. Acute inhalation studies performed with hydrogen-chloride 

 (7647010) (HCl), ethyl-bromide (74964) (EB), hydrogen-sulfide (7783064) 

 (HS), ammonia (7664417), chlorine (7782505), and silane (7803625) are 

 discussed. Subacute toxicity studies conducted on chlorine-pentafluoride 

 (13637633) (CF) and dichloromethane (75092) (DCM) are reported. HCl gas 

 and aerosol have the same toxic effects; primary target is the respiratory 

 tract. The major effect of EB inhalation is depression of the central 

 nervous system in both mice and rats. It is reported that 1 hour of 

 exposure to 800 parts per million (ppm) HS produced death in nine of ten 

 rats and eight of ten mice. Exposure to the highest concentrations of 

 ammonia produces mottling of the liver in rats and congestion of the liver 

 in mice. The most common finding in necropsied animals subjected to acute 

 chlorine exposure is mottling of the liver tissue. It is reported that 

 four of ten mice died after inhaling 9600ppm silane vapor for 4 hours and 

 that a 60 minute exposure to 10ppm CF produced pale livers and kidneys in 

 rats, and congested lungs in monkeys. Also discussed is exposure to 

 5000ppm DCM for 3 to 4 weeks; 50 percent of dogs and 30 percent of mice 

 died. 

375 

TITLE: 

 Chromium, Manganese, Nickel, And Other Elements 

AUTHORS: 

 Smith TJ 

 Blough S 

SOURCE: 

 Environmental and Occupational Medicine, pages 491-510, 96 references, 

 19831983 

ABSTRACT: 

 Occupational hazards associated with a number of elements are reviewed. 

 While trivalent chromium (7440473) compounds are not very toxic, 

 hexavalent compounds are irritants and corrosives, with acute symptoms and 

 a risk of lung cancer resulting from long term exposure. Manganese 

 (7439965) compounds are acute irritants and chronic exposure causes 

 pulmonary symptoms and neurological effects. Exposure to soluble nickel 

 (7440020) compounds can cause severe nasal damage. Chronic exposure is 

 associated with nasal and lung cancers. Yellow phosphorus (7723140) poses 

 risks of acute and chronic poisoning and phosphorus compounds have toxic 

 qualities requiring great care in their use. Compounds of selenium 

 (7782492) present occupational risks. Hydrogen-selenide is more toxic 

 than hydrogen-sulfide. Dusts of selenium-dioxide are irritants to eyes, 

 nose, and throat. There are acute hazards from exposure to silver 

 (7440224) compounds. Chronic ingestion of silver can result in deposition 

 of pigment in the body. The toxicology of compounds of tellurium 

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 (13494809) is quite similar to that of analogous compounds of selenium. 

 Tin (7440315) salts can be highly irritating and organic tin can cause 

 burns. Alkyl and aromatic tin compounds are potent neurotoxins. The 

 major problem associated with occupational exposure to tungsten (7440337) 

 is respiratory disease caused by cemented tungsten-carbide dust. Most 

 zinc (7440666) compounds have no important toxic properties, but 

 zinc-chloride is an exception, being highly corrosive to skin and the 

 respiratory tract. Symptoms of exposure to antimony (7440360) are often 

 confused with those of exposure to arsenic (7440382). Ingested cobalt 

 (7440484) has caused cases of cardiomyopathy. Cobalt has chronic effects 

 on several body systems. Whether toxicity is acute or chronic, the 

 mechanism of copper (7440508) toxicity is due to the inhibition of 

 sulfhydryl groups. Molybdenum (7439987), osmium (7440042), thallium 

 (7440280), and vanadium (7440622) have relatively few industrial uses but 

 each is toxic, and risk must be considered in their handling. 

376 

TITLE: 

 Low-Concentration Air Contaminants and Modeling of the Near Environment 

AUTHORS: 

 Hutter GM 

SOURCE: 

 Proceedings of the ASHRAE Conference: IAQ'86, Managing Indoor Air for 

 Health and Energy Conservation, April 20-23, 1986, Atlanta, Georgia, 

 American Society of Heating, Refrigerating and Air-Conditioning Engineers, 

 Inc., pages, 19861986 

 264-280, 31 references 

ABSTRACT: 

 The effects of exposure to low concentration air contaminants in the 

 workplace and surroundings upon personal health and property were 

 reviewed, and the utility of modeling studies designed to evaluate 

 existing emission sources, and the effects of past or future spills or 

 leaks was examined. The authors state that damage to personal health or 

 property may not be apparent until long after exposure. This often makes 

 it difficult to assess the contribution of low concentration air 

 contaminants to disease or damage processes. Steps which can be taken to 

 prevent this situation were said to include identification of suspect 

 exposure/emission sources, determination of personal exposure pathways, 

 inventory of materials and suspect pathways, monitoring, and construction 

 of an airborne contaminant transport model. Exposure concentration levels 

 and durations determine whether acute or chronic toxicity occurs. In some 

 cases, for example exposure to low levels of hydrogen-sulfide, long term 

 low level exposures are harmless, while high level short term exposures 

 can be quite toxic. Other gases, for example vinyl-chloride, are harmful 

 after long term low level exposure but appear to be harmless when 

 exposures are at a high level but are of short duration. The authors 

 describe work suggesting that adherence to current OSHA standards or NIOSH 

 recommended criteria for many solvents may not be sufficient to guarantee 

 health in the workplace. While the primary route of entry for most 

 airborne contaminants is through the lungs, secondary routes may include 

 mucous membranes, moist body areas susceptible to hygroscopic materials, 

 exposed and unprotected skin areas, and the mouth. Corrosive or galvanic 

 reactions are often involved in property damage induced by low level 

 airborne contaminants. Precedents, the theoretical basis for modeling 

 studies, and examples of current usage were also presented. 

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377 

TITLE: 

 Overview of Respiratory Health Risks in Agriculture 

AUTHORS: 

 Warren CPW 

SOURCE: 

 Principles of Health and Safety in Agriculture, J. A. Dosman and D. W. 

 Cockcroft, Editors; CRC Press, Inc., Boca Raton, Florida, pages 47-49, 23 

 references, 1989 

ABSTRACT: 

 An overview of respiratory health risks in agriculture and farming was 

 presented. Physicians often overlook farmer's lung in rural patients. 

 The prevalence of farmer's lung is uncertain, and it may leave sufferers 

 with permanent abnormalities. The use of silage as feed for cattle has 

 reduced farmer's lung, but has introduced new hazards, in particular, silo 

 filler's lung which is due to inhalation of oxides of nitrogen which form 

 in silage. Grain rarely produces farmer's lung, and it rarely causes 

 allergic alveolitis; it may cause chronic grain fever. Various molds that 

 are rare in grains may be allergens that produce allergic asthma in 

 farmers, including field fungi such as Cladosporium, Alternaria, and 

 Verticillium, and storage fungi such as Aspergillus and Penicillium. 

 Arthropods such as the mite Lepidoglyphus-destructor have been shown to 

 cause asthma in grain workers and farmers. The practices of modern animal 

 husbandry in closed confinement structures may also result respiratory 

 problems. Long term collection of manure results in release of large 

 amounts of hydrogen-sulfide (7783064) gas. At high concentrations, this 

 gas can not be detected by the olfactory system and the farmer will not be 

 aware of the danger. An unclear phenomenon often observed in farmers is 

 that allergic alveolitis is often more common in nonsmokers. The author 

 concludes that it is important that research on occupational disorders of 

 farmers be continued to ensure that the conditions that produce these 

 disorders on the farm do not occur and dust be kept to a minimum. 

378 

TITLE: 

 [Histo-enzymatic examinations of the lung in experimental hydrogen sulfide 

 poisoning] 

AUTHORS: 

 Jonek J 

 Konecki J 

SOURCE: 

 Med Pr. 1966; 17(4):329-35. [Medycyna pracy] 

379 

TITLE: 

 The metabolism of arylthioureas. III. (a) The toxicity of hydrogen 

 sulphide in relation to that of phenylthiourea. (b) The protection of rats 

 against the toxic effects of phenylthiourea, with 

 1-methyl-1-phenylthiourea. 

AUTHORS: 

 SMITH RL 

 WILLIAMS RT 

SOURCE: 

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 J Med Pharm Chem. 1961, Jul 1; 4:137-46. [Journal of medicinal and 

 pharmaceutical chemistry] 

380 

TITLE: 

 Health effects of airborne exposures from concentrated animal feeding 

 operations. 

AUTHORS: 

 Heederik D 

 Sigsgaard T 

 Thorne PS 

 Kline JN 

 Avery R 

 Bønløkke JH 

 Chrischilles EA 

 Dosman JA 

 Duchaine C 

 Kirkhorn SR 

 Kulhankova K 

 Merchant JA 

SOURCE: 

 Environ Health Perspect. 2007, Feb; 115(2):298-302. [Environmental health 

 perspectives] 

ABSTRACT: 

 Toxic gases, vapors, and particles are emitted from concentrated animal 

 feeding operations (CAFOs) into the general environment. These include 

 ammonia, hydrogen sulfide, carbon dioxide, malodorous vapors, and 

 particles contaminated with a wide range of microorganisms. Little is 

 known about the health risks of exposure to these agents for people living 

 in the surrounding areas. Malodor is one of the predominant concerns, and 

 there is evidence that psychophysiologic changes may occur as a result of 

 exposure to malodorous compounds. There is a paucity of data regarding 

 community adverse health effects related to low-level gas and particulate 

 emissions. Most information comes from studies among workers in CAFO 

 installations. Research over the last decades has shown that microbial 

 exposures, especially endotoxin exposure, are related to deleterious 

 respiratory health effects, of which cross-shift lung function decline and 

 accelerated decline over time are the most pronounced effects. Studies in 

 naïve subjects and workers have shown respiratory inflammatory 

 responses related to the microbial load. This working group, which was 

 part of the Conference on Environmental Health Impacts of Concentrated 

 Animal Feeding Operations: Anticipating Hazards-Searching for Solutions, 

 concluded that there is a great need to evaluate health effects from 

 exposures to the toxic gases, vapors, and particles emitted into the 

 general environment by CAFOs. Research should focus not only on nuisance 

 and odors but also on potential health effects from microbial exposures, 

 concentrating on susceptible subgroups, especially asthmatic children and 

 the elderly, since these exposures have been shown to be related to 

 respiratory health effects among workers in CAFOs. 

381 

TITLE: 

 [Stomach diseases due to subchronic carbon monoxide-hydrogen sulfide 

 effects in coal distillation plants.] 

AUTHORS: 

 LEOPOLD PG 

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 TREUTLER H 

SOURCE: 

 Dtsch Gesundheitsw. 1952, Jun 12; 7(24):764-9. [Das Deutsche 

 Gesundheitswesen] 

382 

TITLE: 

 Air pollution by hydrogen sulfide in Poza Rica, Mexico; an evaluation of 

 the incident of Nov. 24, 1950. 

AUTHORS: 

 McCABE LC 

 CLAYTON GD 

SOURCE: 

 A M A Arch Ind Hyg Occup Med. 1952, Sep; 6(3):199-213. [A. M. A. archives 

 of industrial hygiene and occupational medicine] 

383 

TITLE: 

 [Intoxications with hydrogen sulfide and their prevention.] 

AUTHORS: 

 CHERNIKOV AP 

SOURCE: 

 Feldsher Akush. 1952, Jul; 7:19-23. [Fel'dsher i akusherka] 

384 

TITLE: 

 Issues of human exposure to agents causing developmental toxicity. 

AUTHORS: 

 Tabacova S 

 Vukov M 

SOURCE: 

 Congenital Anomalies 1992;32(Suppl):S21-S30 

ABSTRACT: 

 The evaluation of human developmental toxicity is a complex process. 

 Specific examples are based on a study which assessed the relationship of 

 multiple environmental exposures and reproductive outcomes in areas 

 contaminated by industrial sources (e.g. metallurgy, chemical and 

 petrochemical industry). Rates of spontaneous abortions, malformations, 

 stillbirths, prematurity, maternal toxemia, and early neonatal morbidity 

 and mortality were determined for a 6-year retrospective period which 

 included 238,221 births and 30,579 spontaneous abortions. Exposures via 

 ambient air (SO2, NO2, H2S, particulates, lead aerosols), soil and water 

 (e.g. Pb, Cd, Cr, Mn, Zn) were studied in parallel. A multiple regression 

 analysis was used to assess the relationships among environmental and 

 reproductive parameters. Other known developmental hazards also were 

 considered (e.g. background radiation, rubella and varicella morbidity, 

 and pertinent disease states). It was found that the excess of heavy 

 metals (Pb, Cd, Cr, Mn), the deficit of essential elements (Zn, Cu, Ni), 

 and particularly the combination of both, had significant relations to the 

 rate of unfavorable reproductive outcomes. Air pollution by H2S, NO2, and 

 particulate matter was found to contribute, although to a lesser extent, 

 to some reproductive and developmental pathologies. Background morbidity 

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 of rubella, as well as of renal, cardiovascular and endocrine diseases was 

 also of importance. It is suggested that the interplay of various 

 environmental factors is essential in evaluating their role as 

 developmental hazards. 

385 

TITLE: 

 Mutagenicity of the reaction products of dibenzo-p-dioxin with nitrogen 

 oxides. 

AUTHORS: 

 Watanabe T 

 Kusumoto M 

 Ikeda M 

 Hirayama T 

SOURCE: 

 Mutat Res 1992 Apr;281(4):247-54 

ABSTRACT: 

 Dibenzo-p-dioxin (DD) was made to react with various concentrations of 

 nitrogen oxides in the dark. The mutagenicities of the reaction products 

 were tested using Salmonella typhimurium strains TA98, TA100, TA98NR and 

 TA98/1,8-DNP6 in the presence or absence of a mammalian metabolic 

 activation system (S9 mix). DD-NOx (molar ratios 1:3, 1:6 and 1:18) 

 reaction products exhibited mutagenic potency in strains TA98 and 

 TA98/1,8-DNP6 without S9 mix. In a gas chromatography/mass spectrometry 

 study, 2-nitrodibenzo-p-dioxin (NDD) was identified with authentic sample 

 in the mutagenic reaction products. DD-NOx (1:18) reaction products were 

 reduced by sodium hydrogen sulfide and the reduction mixture was analyzed 

 by HPLC. 2,7-Dinitrodibenzo-p-dioxin (DNDD) and 2,8-DNDD were identified 

 as corresponding diamino-DDs in the reduction mixture. 2-NDD, 2,7-DNDD and 

 2,8-DNDD were also mutagenic in strains TA98 and TA98/1,8-DNP6 without S9 

 mix and the mutagenicity of DD-NOx reaction products was largely accounted 

 for by the nitro-DDs. 

386 

TITLE: 

 Improved synthesis, antibacterial activity and potential carcinogenicity 

 of 5-amino-1 ,2,4-thiadiazol-3(2H)-one. 

AUTHORS: 

 Pískala A 

 Vachálková A 

 Masojídková M 

 Horváthová K 

 Ovesná Z 

 Paces V 

 Novotný L 

SOURCE: 

 Pharmazie. 2004, Oct; 59(10):756-62. [Die Pharmazie] 

ABSTRACT: 

 This paper reports on the preparation of 

 5-amino-1,2,4-thiadiazol-3(2H)-one, a sulfur-containing analogue of 

 cytosine with the -CH=CH- group between the positions 5 and 6 of the 

 pyrimidine ring replaced by the divalent sulfur (-S-). Improved procedures 

 for the preparation of thiobiuret, some of its methyl derivatives and 

 5-amino-1,2,4-thiadiazol-3(2H)-one are documented. Thiobiuret and its 

Page 194 of 245

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 N-methyl derivatives were obtained by addition of hydrogen sulfide to the 

 respective 1-cyanoureas. Subsequent oxidation of thiobiuret with hydrogen 

 peroxide in alkaline medium produced 5-amino-1,2,4-thiadiazol-3(2H)-one. 

 This substance was traced back converted to the starting thiobiuret by 

 reaction with cysteine hydrochloride. Alkaline degradation of thiadiazol 

 led to the formation of 1-cyanourea isolated as its silver salt. An 

 investigation of the thiadiazol biological activities has shown that it 

 inhibits the growth of E. coil by 10% at 8.5 microM concentrations, but 

 exhibited no cytostatic activity in L1210, HeLa S3 and HL-60 cell lines. 

 Potential carcinogenicity of the prepared compounds was determined by a DC 

 polarographic method. While the values of the parameter of carcinogenicity 

 for all intermediates indicate only marginal carcinogenic potential, the 

 value of the parameter of carcinogenicity for the thiadiazole indicates 

 possible carcinogenicity of this compound. 

387 

TITLE: 

 Acute toxicity of inhaled gases and particulates 

AUTHORS: 

 Mitchell CA 

 Carroll PA 

SOURCE: 

 Medical Journal of Australia 19 June 1989, Vol.150, No.12, p.717-720. 41 

 ref. 

ABSTRACT: 

 Review article on the prevention and treatment of acute poisoning due to 

 the inhalation of gases and particulates, with particular attention being 

 paid to carbon monoxide, cyanide and hydrogen sulfide. 

388 

TITLE: 

 90-DAY VAPOR INHALATION TOXICITY STUDY OF HYDROGEN SULFIDE IN FISCHER 344 

 RATS 

SOURCE: 

 EPA/OTS; Doc #FYI-OTS-0883-0255 

389 

TITLE: 

 A model for effective toxic load from fluctuating gas concentrations. 

AUTHORS: 

 HILDERMAN TL 

 HRUDEY SE 

 WILSON DJ 

SOURCE: 

 JOURNAL OF HAZARDOUS MATERIALS; 64 (2). 1999. 115-134. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. At any receptor position in a dispersing gas 

 plume there will be large fluctuations in concentration for the duration 

 of the exposure. The non-linearity of acute toxicity with exposure 

 concentration means that these fluctuations are important to evaluating 

 the overall effect of a release. In this paper, an effective toxic load 

 model with three receptor response parameters was proposed to provide a 

 realistic model of toxicity when applied to a fluctuating concentration 

Page 195 of 245

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 time series. The receptor response factors included were an uptake time 

 constant, a recovery time constant, and a saturation concentration. The 

 effective toxic load model was compared with the standard toxic load model 

 using simulated time series produced by a stochastic model. For a 

 realistic simulated hydrogen sulphide exposure, the effective toxic load 

 was found to provide more realistic estimates of fatalities than the 

 conventional exposure toxic load calculations. 

390 

TITLE: 

 EXPOSURE TO TOXIC AGENTS THE HEME BIOSYNTHETIC PATHWAY AND HEMOPROTEINS AS 

 INDICATOR 

AUTHORS: 

 MARKS GS 

 DE MATTEIS F 

SOURCE: 

 CRIT REV TOXICOL; 15 (2). 1985. 151-180. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM REVIEW HYDROGEN SULFIDE PESTICIDE 

 POLYCHLORINATED BIPHENYL METAL TOXICITY HEMOGLOBIN 

391 

TITLE: 

 AMBIENT LEVELS OF SELECTED GASES INSIDE SWINE CONFINEMENT BUILDINGS 

AUTHORS: 

 DONHAM KJ 

 POPENDORF WJ 

SOURCE: 

 AM IND HYG ASSOC J; 46 (11). 1985. 658-661. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM HUMAN WORKER FARMING INDUSTRY AIR 

 POLLUTION HAZARDOUS MATERIALS HAZARDOUS OCCUPATION THRESHOLD LIMIT VALUE 

 AMMONIA CARBON MONOXIDE CARBON DIOXIDE HYDROGEN SULFIDE ANIMAL AGE 

 PULMONARY TOXICITY ENVIRONMENTAL SURVEILLANCE SWINE WASTE HAZARDOUS WASTE 

392 

TITLE: 

 TOXICITY OF BLACK SEA DEEP WATER FOR BENTHOS AMPHIPODS GAMMARUS-OLIVII 

AUTHORS: 

 POLIKARPOV GG 

 TSYTSUGINA VG 

 TIMOSHCHUK VI 

 DEMINA NV 

 TERESHCHENKO NN 

SOURCE: 

 DOKL AKAD NAUK UKR SSR SER B GEOL KHIM BIOL NAUKI; 0 (8). 1985. 74-76. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM MORTALITY CONCENTRATION HYDROGEN SULFIDE 

 

393 

TITLE: 

Page 196 of 245

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 AEROBIC AND ANAEROBIC TREATMENT OF NEUTRAL SULFITE SEMICHEMICAL PROCESS 

 AND CHEMITHERMOMECHANICAL PULP EFFLUENT 

AUTHORS: 

 WILSON RW 

 MURPHY KL 

 FRENETTE EG 

SOURCE: 

 CANADIAN PULP AND PAPER ASSOCIATION. CONFERENCE SUR L'ENVIRONNEMENT; 1985 

 ENVIRONMENT CONFERENCE, TORONTO, ONT., CANADA, SEPT. 24-26, 1985. 

 III+157P. TECHNICAL SECTION, CANADIAN PULP AND PAPER ASSOCIATION: 

 MONTREAL, QUE., CANADA. ILLUS. PAPER. ISBN 0-919893-25-2.; 0 (0). 1985. 

 113-120. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM ACTIVATED SLUDGE ANAEROBIC FILTRATION 

 AERATED BASIN ANAEROBIC BASIN TOXICITY METHANE CARBON DIOXIDE OXYGEN ARGON 

 NITROGEN HYDROGEN SULFIDE 

394 

TITLE: 

 ADAPTATION TO HYDROGEN SULFIDE OF OXYGENIC AND ANOXYGENIC PHOTOSYNTHESIS 

 AMONG CYANOBACTERIA 

AUTHORS: 

 COHEN Y 

 JORGENSEN BB 

 REVSBECH NP 

 POPLAWSKI R 

SOURCE: 

 APPL ENVIRON MICROBIOL; 51 (2). 1986. 398-407. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM TOLERANCE SULFIDE TOXICITY 

 SULFIDE-DEPENDENT PHOTOSYNTHESIS ANOXYGENIC PHOTOSYNTHESIS 

395 

TITLE: 

 ROLE OF HYDROGEN SULFIDE IN METABOLISM AND TOXICITY OF CYSTEINE 

 S-CONJUGATES IN RAT KIDNEY 

AUTHORS: 

 BANKI K 

 ELFARRA AA 

 LASH LH 

 ANDERS MW 

SOURCE: 

 76TH ANNUAL MEETING OF THE AMERICAN SOCIETY OF BIOLOGICAL CHEMISTS, 

 WASHINGTON, D.C., USA, JUNE 8-12, 1986. FED PROC; 45 (6). 1986. 1930. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM ABSTRACT S-2-CHLORO-1 1 

 2-TRIFLUOROETHYL-L-CYSTEINE S-1 2 DICHLOROVINYL-L-CYSTEINE S-1 2 

 DICHLOROVINYL-L-HOMOCYSTEINE NEPHROTOXIN 

396 

TITLE: 

Page 197 of 245

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 PULMONARY EDEMA OF ENVIRONMENTAL ORIGIN NEWER CONCEPTS 

AUTHORS: 

 CORDASCO EM 

 DEMETER SR 

 KESTER L 

 CORDASCO MA 

 LAMMERT G 

 BEEREL F 

SOURCE: 

 ANGIOLOGY; 37 (6). 1986. 440-447. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM HUMAN CHEMICAL BLOCKING AGENTS PHOSGENE 

 INTOXICATION HYDROGEN SULFIDE TOXICITY TOXIC GAS EXPLOSIONS CONSTANT 

 POSITIVE PRESSURE BREATHING FIBEROPTIC BRONCHOSCOPY 

397 

TITLE: 

 REDOX ACTIVITIES AS ADDITIONAL CAUSATIVE FACTORS IN THE GENERATION OF 

 GULLY EROSION IN THE AGULU-NANKA AREA OF NIGERIA 

AUTHORS: 

 EGBOKA B CE 

 ORAJAKA IP 

 NWOSU VC 

SOURCE: 

 SCI TOTAL ENVIRON; 53 (3). 1986. 217-232. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM VEGETATION GROUND WATER SURFACE WATER 

 TOXICITY FREE ACIDS HYDROGEN SULFIDE 

398 

TITLE: 

 ASPHYXIANT GASES 

AUTHORS: 

 BRANDS A 

SOURCE: 

 HALEY, T. J. AND W. O. BERNDT (ED.). HANDBOOK OF TOXICOLOGY. XIV+697P. 

 HEMISPHERE PUBLISHING CORP.: NEW YORK, NEW YORK, USA; CAMBRIDGE, ENGLAND, 

 UK. ILLUS. ISBN 0-89116-403-0.; 0 (0). 1987. 472-503. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM HUMAN ANIMAL AMMONIA CARBON MONOXIDE 

 ETHYLENE OXIDE FLUOROCARBONS FORMALDEHYDE HYDROGEN CYANIDE HYDROGEN 

 SULFIDE ISOCYANATES NITROGEN DIOXIDE NITROUS OXIDE SULFUR DIOXIDE 

399 

TITLE: 

 EFFECT OF HYDROGEN SULFIDE ON THE SURVIVAL OF SOME FISHES UNDER HYPOXIA 

AUTHORS: 

 TAIL FT 

SOURCE: 

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 GIDROBIOL ZH; 23 (3). 1987. 99-104. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM POMATOSCHISTUS-MICROPS 

 PROTERORHINUS-MARMORATUS NEOGOBIUS-CEPHALARGES TOXICITY RESISTANCE 

400 

TITLE: 

 INVESTIGATION OF HYDROGEN SULFIDE TOXICITY IN MOUSE NEUROBLASTOMA CELLS 

 USING PATCH-CLAMP TECHNIQUE 

AUTHORS: 

 WARENYCIA MW 

 STEELE JA 

 KARPINSKI E 

 REIFFENSTEIN RJ 

SOURCE: 

 17TH ANNUAL MEETING OF THE SOCIETY FOR NEUROSCIENCE, NEW ORLEANS, 

 LOUISIANA, USA, NOVEMBER 16-21, 1987. SOC NEUROSCI ABSTR; 13 (1). 1987. 

 94. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM ABSTRACT OCCUPATIONAL HAZARD RESPIRATORY 

 FAILURE NEUROTOXICITY ION CHANNEL 

401 

TITLE: 

 CONCENTRATION-TIME INTERACTIONS IN HYDROGEN SULFIDE TOXICITY IN RATS 

AUTHORS: 

 PRIOR MG 

 SHARMA AK 

 YONG S 

 LOPEZ A 

SOURCE: 

 CAN J VET RES; 52 (3). 1988. 375-379. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM PULMONARY EDEMA SEX MORTALITY 

402 

TITLE: 

 WRACK BREAKDOWN ON SANDY BEACHES ITS IMPACT ON INTERSTITIAL MEIOFAUNA 

AUTHORS: 

 MCGWYNNE LE 

 MCLACHLAN A 

 FURSTENBERG JP 

SOURCE: 

 MAR ENVIRON RES; 25 (3). 1988. 213-232. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM PLOCAMIUM-CORALLORHIZA HYPNEA-ROSEA 

 BACTERIA NEMATODE COPEPOD OLIGOCHAETE TURBELLARIA AMMONIUM HYDROGEN 

 SULFIDE NUTRIENT ANALYSIS BIOMASS OXYGEN AVAILABILITY TOXICITY 

403 

Page 199 of 245

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TITLE: 

 AN ELECTROPHYSIOLOGICAL STUDY OF HYDROGEN SULFIDE TOXICITY IN FROG 

 SYMPATHETIC GANGLIA 

AUTHORS: 

 KOMBIAN SB 

 ZIDICHOUSKI J 

 KEHOE M 

 REIFFENSTEIN RJ 

SOURCE: 

 18TH ANNUAL MEETING OF THE SOCIETY FOR NEUROSCIENCE, TORONTO, ONTARIO, 

 CANADA, NOVEMBER 13-18, 1988. SOC NEUROSCI ABSTR; 14 (2). 1988. 1083. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM ABSTRACT 

404 

TITLE: 

 A QUALITATIVE AND QUANTITATIVE ANALYSIS OF THE SEDIMENT GAS AND DIETHY-L 

 ETHER EXTRACT OF THE SEDIMENT FROM SALMON FARMS 

AUTHORS: 

 SAMUELSEN OB 

 ERVIK A 

 SOLHEIM E 

SOURCE: 

 AQUACULTURE; 74 (3-4). 1988. 277-286. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM WATER QUALITY METHANE CARBON DIOXIDE 

 HYDROGEN SULFIDE TOXICITY AQUACULTURE 

405 

TITLE: 

 THE CAPACITY OF SUBGINGIVAL MICROBIOTAS TO PRODUCE VOLATILE SULFUR 

 COMPOUNDS IN HUMAN SERUM 

AUTHORS: 

 PERSSON S 

 CLAESSON R 

 CARLSSON J 

SOURCE: 

 ORAL MICROBIOL IMMUNOL; 4 (3). 1989. 169-172. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM DIMETHYL SULFIDE DIMETHYL DISULFIDE 

 HYDROGEN SULFIDE PROTEIN DEGRADATION TOXICITY 

406 

TITLE: 

 EFFECT OF HIGH SULFITE CONTENTS ON ANAEROBIC DIGESTION OF RAISIN-FINISHING 

 WASTEWATER 

AUTHORS: 

 ATHANASSOPOULOS N 

 KOUINIS J 

 PAPADIMITRIOU A 

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 KOUTINAS AA 

SOURCE: 

 BIOL WASTES; 30 (1). 1989. 53-60. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM SLUDGE BED REACTOR CHEMICAL OXYGEN 

 DEMAND REMOVAL EFFICIENCY HYDROGEN SULFIDE METHANE FERMENTATION BIOGAS 

 TOXICITY FRUITS WASTEWATER TREATMENT FOOD PROCESSING INDUSTRY 

407 

TITLE: 

 Ditiocarb: decomposition in aqueous solution and effect of the volatile 

 product on its pharmacological use. 

AUTHORS: 

 Martens T 

 Langevin-Bermond D 

 Fleury MB 

SOURCE: 

 J Pharm Sci. 1993, Apr; 82(4):379-83. [Journal of pharmaceutical sciences] 

ABSTRACT: 

 The kinetic profile for the decomposition of ditiocarb sodium salt in 

 aqueous solution was achieved with UV-visible absorption spectrometry. The 

 kinetic profile indicates that the decomposition reaction is hydrogen 

 ion-catalyzed over the entire 4-10 pH range and enables the determination 

 of the value of the acid-base equilibrium constant (Ka = 4.0.10(-4) at 5 

 degrees C). Decomposition of ditiocarb produces volatile carbon disulfide, 

 exclusive of hydrogen sulfide, as shown with electrochemical methods. This 

 feature is of interest from a toxicological point of view. 

408 

TITLE: 

 HYDROGEN SULFIDE INHIBITS RAT HIPPOCAMPAL CA1 PYRAMIDAL CELLS AND SYNAPTIC 

 POTENTIALS IN-VITRO MECHANISM OF TOXICITY 

AUTHORS: 

 BALDELLI RJ 

 REIFFENSTEIN RJ 

 COLMERS WF 

SOURCE: 

 19TH ANNUAL MEETING OF THE SOCIETY FOR NEUROSCIENCE, PHOENIX, ARIZONA, 

 USA, OCTOBER 29-NOVEMBER 3, 1989. SOC NEUROSCI ABSTR; 15 (2). 1989. 1348. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM ABSTRACT 

409 

TITLE: 

 Exposure assessment methods for a study of mortality and cancer morbidity 

 in relation to specific petroleum industry exposures. 

AUTHORS: 

 Drummond I 

 Murray N 

 Armstrong T 

 Schnatter AR 

Page 201 of 245

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 Lewis RJ 

SOURCE: 

 J Occup Environ Hyg. 2006, Oct; 3(10):513-20. [Journal of occupational and 

 environmental hygiene] 

ABSTRACT: 

 In 1987 a Canadian company implemented an exposure tracking and health 

 information system. The exposure tracking method aligned closely with 

 published concepts for describing workplace exposure, with over 1800 

 similar exposure groups being used to describe occupational exposures. The 

 database has been actively maintained and is subject to a number of 

 quality checks. Recently, the company initiated a cancer morbidity study, 

 with one objective being to examine whether the exposure tracking data 

 could be used to reconstruct exposure estimates for the cohort. Five 

 agents--hydrogen sulfide, petroleum coke/spent catalyst, hydrocarbon 

 solvents and fuels, hydrocarbon lubricants, and an index for exposure to 

 operations derived from noise exposure--were selected for development of 

 occupational exposure estimates for each cohort member. The cohort 

 consisted of workers first employed between January 1964 and December 1994 

 and who were employed for at least 1 year. Work history records were 

 associated with a similar exposure group, using human resources data and 

 knowledge of local industrial hygienists. Only employees with >90% 

 duration of their work history assigned were kept in the cohort (25,292 

 people out of a possible 25,617). For each similar exposure group 

 inventory, the substances were identified that contributed to each of the 

 five agents being studied. Exposure estimates before 1987 were modified 

 using historic occupational exposure limits. Rules were created to sum the 

 exposure from multiple substances found in any one similar exposure group. 

 The validity of exposure estimates was tested via comparison with results 

 documented in industrial hygiene survey reports. Industrial hygienists who 

 were unaware of the derived exposure estimates evaluated several hundred 

 industrial hygiene surveys and prepared benchmark information. The two 

 lists were then evaluated for concordance, which was found to be 

 significantly different from that occurring by chance. We conclude that 

 the process described can create valid exposure estimates for use in 

 epidemiology studies. 

410 

TITLE: 

 HYDROGEN SULFIDE A CORROSIVE METABOLITE 

AUTHORS: 

 EDYVEAN R GJ 

SOURCE: 

 INT BIODETERIOR; 27 (2). 1991. 109-120. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM REVIEW MICROORGANISM MARINE CORROSION 

 TOXICITY STRESS FATIGUE 

411 

TITLE: 

 ISSUES OF HUMAN EXPOSURE TO AGENTS CAUSING DEVELOPMENTAL TOXICITY 

AUTHORS: 

 TABACOVA S 

 VUKOC M 

Page 202 of 245

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SOURCE: 

 THE THIRTY-FIRST ANNUAL MEETING OF THE TERATOLOGY SOCIETY, BOCA RATON, 

 FLORIDA, USA, JUNE 22-27, 1991 AND THE THIRD MEETING OF THE INTERNATIONAL 

 FEDERATION OF TERATOLOGY SOCIETIES, BOCA RATON, FLORIDA, USA, JUNE 24-25, 

 1991. TERATOLOGY; 43 (5). 1991. 410. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM ABSTRACT SULFUR DIOXIDE NITROGEN DIOXIDE 

 HYDROGEN SULFIDE LEAD CADMIUM CHROMIUM MANGANESE ZINC 

412 

TITLE: 

 Lung dysfunction in animal confinement workers--chairman's report to the 

 Scientific Committee of the Third International Symposium: issues in 

 health, safety and agriculture, held in Saskatoon, Saskatchewan, Canada, 

 May 10-15, 1992. 

AUTHORS: 

 Donham KJ 

 Zejda JE 

SOURCE: 

 Pol J Occup Med Environ Health. 1992; 5(3):277-9. [Polish journal of 

 occupational medicine and environmental health] 

ABSTRACT: 

 The session traced the course of health hazards in livestock confinement 

 from anticipation of an emerging health hazard in 1974 to its full 

 recognition as a significant health hazard in 1992. The session documented 

 the major health hazards including hydrogen sulfide toxicity, bronchitis, 

 non-allergic asthma, organic dust toxic syndrome, and mucus membrane 

 irritation. In regard to exposures, bioaerosols seem to be the most 

 significant hazard, with endotoxin evident as at least one of the major 

 specific atiologic agents. Other agents were suspected, as newly 

 recognized agents, specifically 1,3 beta-glucan. Previous epidemiological 

 studies have revealed mild decrements in pulmonary function, however 

 symptoms have always been excessively prevalent relative to controls. 

 Recent results of a longitudinal observation showed a 12% drop out of 

 workers with profound decrement in pulmonary function. In summary, the 

 health hazard of livestock confinement workers is now well substantiated 

 in North America and Europe and further work regarding prevention is 

 highly indicated. 

413 

TITLE: 

 SYSTEMATIC APPLICATION OF WATER FLOW AND CHEMICAL FERTILIZATION TO CONTROL 

 HYDROGEN SULFIDE TOXICITY AND NITROGEN-PHOSPHORUS DEFICIENCY IN THE WATER 

 OF COMMERCIAL GROW-OUT PONDS STOCKED WITH PENAEUS-VANNAMEI 

AUTHORS: 

 AYALA-B LB 

 HIRONO Y 

 VALENCIA F 

SOURCE: 

 22ND ANNUAL CONFERENCE AND EXPOSITION OF THE WORLD AQUACULTURE SOCIETY, 

 SAN JUAN, PUERTO RICO, JUNE 16-20, 1991. J WORLD AQUACULT SOC; 22 (3). 

 1991. 13A-14A. 

ABSTRACT: 

Page 203 of 245

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 BIOSIS COPYRIGHT: BIOL ABS. RRM ABSTRACT 

414 

TITLE: 

 ASPECTS OF LIFE DEVELOPMENT AT DEEP SEA HYDROTHERMAL VENTS 

AUTHORS: 

 GAILL F 

SOURCE: 

 FASEB (FED AM SOC EXP BIOL) J; 7 (6). 1993. 558-565. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM RIFTIA-PACHYPTILA VESTIMENTIFERA 

 CHEMOAUTOTROPHIC BACTERIAL SYMBIOSIS HYDROGEN SULFIDE TOXICITY COLLAGEN 

 TEMPERATURE EFFECTS PRESSURE EFFECTS 

415 

TITLE: 

 Sulfide toxicity: Mechanical ventilation and hypotension determine 

 survival rate and brain necrosis. 

AUTHORS: 

 BALDELLI RJ 

 GREEN F HY 

 AUER RN 

SOURCE: 

 J APPL PHYSIOL; 75 (3). 1993. 1348-1353. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Occupational exposure to hydrogen sulfide is 

 one of the leading causes of sudden death in the workplace, especially in 

 the oil and gas industry. High-dose exposure causes immediate neurogenic 

 apnea and death; lower doses cause "knockdown" (transient loss of 

 consciousness, with apnea). Because permanent neurological sequelae have 

 been reported, we sought to determine whether sulfide can directly kill 

 central nervous system neurons. Ventilated and unventilated rats were 

 studied to allow administration of higher doses of sulfide and to 

 facilitate physiological monitoring. It was extremely difficult to produce 

 cerebral necrosis with sulfide. Only one of eight surviving unventilated 

 rats given high-dose sulfide (a dose that was lethal in \ 50% of animals) 

 showed cerebral necrosis. Mechanical ventilation shifted the dose that was 

 lethal in 50% of the animals to 190 mg/kg from 94 mg/kg in the 

 unventilated rats. Sulfide was found to potently depress blood pressure. 

 Cerebral ne 

416 

TITLE: 

 KUWAITI OIL FIRES AIR QUALITY MONITORING 

AUTHORS: 

 AMIN MB 

 HUSAIN T 

SOURCE: 

 ATMOSPHERIC ENVIRONMENT; 28 (13). 1994. 2261-2276. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM RESEARCH ARTICLE HUMAN SULFUR DIOXIDE 

Page 204 of 245

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 CARBON MONOXIDE HYDROGEN SULFIDE CARBON DIOXIDE NITROGEN OXIDES GASEOUS 

 POLLUTANTS PARTICULATE MATTER AIR POLLUTION HEALTH HAZARD VEGETATION 

 TOXICITY KUWAIT SAUDI ARABIA 

417 

TITLE: 

 Stimulation of constituent processes of anaerobic degradation of organic 

 matter by the "methane" model. 

AUTHORS: 

 VAVILIN VA 

 VASILIEV VB 

 RYTOV SV 

SOURCE: 

 ANTONIE VAN LEEUWENHOEK; 69 (1). 1996. 15-23. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. The model of anaerobic digestion described 

 earlier by the authors was used for analysis of the different phases of 

 the process. It was shown that at the glucose conversion a coexistence of 

 hydrogen-producing acidogenic bacteria and hydrogen-utilizing 

 non-methanogenic bacteria causes a hydrogen partial pressure decrease at 

 an increase of solids retention time (i), the intensity of the negative 

 feed-back effect in sulfate-reduction through hydrogen sulfide formation 

 is regulated by the pH level during an oscillation dynamics in 

 acetate/sulfate system (ii), under the toxicity influence the processes of 

 methanogenesis and acetogenesis together with hydrolysis may be 

 rate-limiting steps in the anaerobic system with particulate substrate 

 degradation (iii). 

418 

TITLE: 

 Correlations between virulence and other characters of Clostridium 

 perfringens type A. 

AUTHORS: 

 Forget A 

 Paquette G 

 Roy A 

 Fredette V 

SOURCE: 

 Appl Microbiol. 1969, Oct; 18(4):668-76. [Applied microbiology] 

ABSTRACT: 

 The correlation analysis which has already proved its value in ecology has 

 not yet been applied to the determination of virulence indicators. Its 

 application to a group of Clostridium perfringens type A strains has 

 brought out some characters that may be considered as virulence 

 indicators. This study suggests that the toxicity of the culture 

 supernatant fluids for mice is significantly correlated with the virulence 

 for mice and guinea pigs. A significant correlation was found between the 

 virulence of the fluid cultures for mice or guinea pigs and the 

 coagulation of milk, production of gas (in deep agar), hydrogen sulfide 

 production, and fermentation of glucose, sucrose, maltose, and levulose. 

419 

TITLE: 

 Modern aspects of mechanisms underlying effects of multi-component natural 

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 gas, its toxicity and selectivity. 

AUTHORS: 

 SETKO NP 

SOURCE: 

 MEDITSINA TRUDA I PROMYSHLENNAYA EKOLOGIYA; 0 (1). 1996. 12-16. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. Experiments on animals included acute, 

 subacute and chronic inhalation of natural gas containing hydrogen 

 sulfide. The multi-component natural gas was proved to induce more 

 intensive toxic effects, than its components do. When inhaled in 

 concentrations equal to the MACs for its components, the gas induces 

 higher permeability of cellular membranes, compromised biocatalysis 

 systems, 2 times increased lipid peroxidation, disturbed thioldisulfide 

 balance. Mechanism underlying primary effect of the natural gas is 

 associated mostly with activated free radicals, methylation and oxidation 

 of sulfurous compounds and their interaction with proteins containing 

 sulfides and metals. 

420 

TITLE: 

 SULFATE REDUCING BACTERIA AND ULCERATIVE COLITIS 

AUTHORS: 

 LEVINE J 

 ELLIS CJ 

 FURNE JK 

 SPRINGFIELD JR 

 LEVITT MD 

SOURCE: 

 96TH ANNUAL MEETING OF THE AMERICAN GASTROENTEROLOGICAL ASSOCIATION AND 

 THE DIGESTIVE DISEASE WEEK, SAN FRANCISCO, CALIFORNIA, USA, MAY 19-22, 

 1996. GASTROENTEROLOGY; 110 (4 SUPPL.). 1996. A949. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM MEETING ABSTRACT HUMAN HYDROGEN SULFIDE 

 INFECTION TOXICITY 

421 

TITLE: 

 SULFIDE TOLERANCE OF FOUR MARINE SPECIES USED TO EVALUATE SEDIMENT AND 

 PORE-WATER TOXICITY 

AUTHORS: 

 KNEZOVICH JP 

 STEICHEN DJ 

 JELINSKI JA 

 ANDERSON SL 

SOURCE: 

 BULLETIN OF ENVIRONMENTAL CONTAMINATION AND TOXICOLOGY; 57 (3). 1996. 

 450-457. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM RESEARCH ARTICLE 

 STRONGYLOCENTROTUS-PURPURATUS MYTILUS-EDULIS RHEPOXYNIUS-ABRONIUS 

 EOHAUSTORIUS-ESTUARIUS HYDROGEN SULFIDE 

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422 

TITLE: 

 Evaluation of sulcular sulphide level monitoring using a portable sensor 

 system. 

AUTHORS: 

 Gleissner C 

 Springborn I 

 Willershausen B 

SOURCE: 

 Eur J Med Res. 2002, Nov 25; 7(11):491-501. [European journal of medical 

 research] 

ABSTRACT: 

 PURPOSE: Volatile sulphur compounds (VSC) such as hydrogen sulphide and 

 methyl mercaptan are toxic bacterial metabolites considered to contribute 

 to the progression of periodontitis. However, the quantitative 

 determination of sulcular VSC concentration requires costly time-consuming 

 laboratory methods limiting its evaluation in large clinical trials. 

 Recently, a portable monitor with a sulphide microsensor has been 

 developed to measure sulcular VSC levels (SU). This cross-sectional study 

 evaluated 1) the clinical usage of the sulphide sensor system, 2) the 

 reproducibility of SU-measurements, 3) the distribution of SU-values in 

 periodontal health and disease and 4) the relationship between SU and 

 clinical parameters documenting periodontal disease severity. METHODS: The 

 specificity, the measuring range and the reproducibility of the sensor 

 system were tested with reference solutions in vitro. 10 probands with 

 healthy gingiva, 23 patients with gingivitis and 30 patients with chronic 

 periodontitis were examined recording periodontal parameters (clinical 

 attachment loss, CAL, probing depth, PD, bleeding on probing intensity BI, 

 plaque and gingival index PI, GI) and sulcular sulphide level (SU) 

 measured by the portable monitor as a digital score ranging from 0.0 ( < 

 10 superset -6 M of S2-) to 5.0 (10 superset -2 M of S superset 2-) in 

 increments of 0.5. RESULTS: The in vitro testing confirmed the sensor s 

 specificity for sulphide ions. The intraexaminer agreement (Pearson 

 correlation coefficient) was 0.91 between two measurements (p < 0.05). 

 However, positive SU-values decreased with measurement repetition due to 

 the volatility of the sulphur compounds. SU and the percentage of positive 

 SU-values per patient were correlated with disease severity. There were no 

 positive SU-values in healthy probands, a mean SU of 0.11 +/- 0.08 in 

 gingivitis and of 0.22 +/- 0.15 in periodontitis (p < 0.001). SU was 

 significantly correlated with PD in gingivitis, PD and CAL in 

 periodontitis and the bleeding index in the analysis of all data. 

 CONCLUSION: The portable sulphide monitor is a reliable method for the 

 chairside determination of sulcular sulphide level in periodontal disease 

 and in spite of its limitations a valuable supplementation of traditional 

 clinical examination methods. It offers the possibility of relating in 

 vitro results on the toxicity of VSC to clinical findings and might 

 provide new insight into the impact of sulcular sulphide on the 

 pathophysiology of periodontitis. 

423 

TITLE: 

 Effects of some xenobiotics of peroxidase-dependent immunity in plants. 

AUTHORS: 

 ROGOVIN VV 

 MUSHTAKOVA VM 

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 FOMINA VA 

SOURCE: 

 IZVESTIYA AKADEMII NAUK SERIYA BIOLOGICHESKAYA (MOSCOW); 0 (5). 1996. 

 613-617. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. The effects of fabric dyes (16 items), heavy 

 metal ions (Cd2+, Pb2+, Sn2+, Hg2+, and Cu2+) and gaseous waste of steam 

 power plants (H2S, SO2, NO, NH3) on the peroxidase-dependent immunity in 

 Pisum sativum were studied using the method of luminol-enhanced 

 chemiluminescence. Copper compares to mercury according to its toxicity. 

 The fabric dyes at 10-5 M decrease the chemiluminescence of plants by 50%. 

 Hydrogen sulfide is the most toxic among gaseous wastes. Since the 

 peroxidase system plays an important role in the struggle of plants 

 against various infections, it is necessary to monitor the effects of 

 xenobiotics dissolved in water on plant immunity. 

424 

TITLE: 

 OKOTOKS SOUR GAS PLANT DECOMMISSIONING SITE DESCRIPTION AND RECLAMATION 

 PLANNING 

AUTHORS: 

 CHOLLAK DF 

SOURCE: 

 TWENTY-THIRD ANNUAL AQUATIC TOXICITY WORKSHOP, CALGARY, ALBERTA, CANADA, 

 OCTOBER 7-9, 1996. CANADIAN TECHNICAL REPORT OF FISHERIES AND AQUATIC 

 SCIENCES; 0 (2144). 1997. 1. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM MEETING ABSTRACT TOXICOLOGY GAS PLANT 

 DECOMMISSIONING OKOTOKS SOUR GAS PLANT CANADIAN OCCIDENTAL PETROLEUM 

 LIMITED HYDROGEN SULFIDE GAS POLLUTANT POLLUTION PROCESS WASTES RISK 

 ASSESSMENT COMPANY-ORGANIZATION ALBERTA CANADA 

425 

TITLE: 

 Estimation of xenobiotic effects on the peroxidase-dependent plant 

 immunity as a means of ecological control. 

AUTHORS: 

 ROGOVINE VV 

 MUSHTAKOVA VM 

 FOMINA VA 

SOURCE: 

 WATER QUALITY RESEARCH JOURNAL OF CANADA; 32 (4). 1997. 829-837. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. The effect of various dyes, ions of heavy 

 metals (Cd2+, Pb2+, Sn2+, Hg2+, Cu2+) and gaseous waste from thermal power 

 stations (H2S, SO2, NO, NH3) on the peroxidase-dependent immunity of pea 

 roots (Pisum sativum) has been studied by luminol-enhanced 

 chemiluminescence. It has been found that copper toxicity could be 

 comparable to that of mercury. Fabric dyes dis-azodye "direct" red and 

 "vat" violet at concentrations of 10-5 M reduced plant chemiluminescence 

 as much as 50%. Hydrogen sulfide turned out to be the most toxic among 

 the gases of the industrial gaseous waste. Considering the importance of 

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 peroxidase system activity in plants against various infections, it is 

 necessary to control the possibility of impairment of plant immunity by 

 xenobiotics dissolved in water. 

426 

TITLE: 

 THE EFFECT OF VARYING WATER SULFATE CONTENT ON H-2S GENERATION AND HEALTH 

 OF FEEDLOT CATTLE 

AUTHORS: 

 LONERAGAN GH 

 GOULD DH 

 WAGNER JJ 

 GARRY FB 

 THOREN M 

SOURCE: 

 89TH ANNUAL MEETING OF THE AMERICAN SOCIETY OF ANIMAL SCIENCE, NASHVILLE, 

 TENNESSEE, USA, JULY 29-AUGUST 1, 1997. JOURNAL OF ANIMAL SCIENCE; 75 

 (SUPPL. 1). 1997. 272. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM MEETING ABSTRACT CATTLE STEER MALE 

 SULFATE WATER CONTENT HYDROGEN SULFIDE TOXIN GENERATION ANIMAL HEALTH 

 THIAMIN THIAMIN DEFICIENCY POLIOENCEPHALOMALACIA POLYENCEPHALOMALACIA 

 PULMONARY DAMAGE RUMEN NUTRITION VETERINARY MEDICINE FEEDLOT PERFORMANCE 

 ANIMAL HUSBANDRY AGRICULTURE NUTRITIONAL DISEASE NERVOUS SYSTEM DISEASE 

 RESPIRATORY SYSTEM DISEASE TOXICITY DIGESTIVE SYSTEM 

427 

TITLE: 

 MECHANISMS OF SULFIDE TOXICITY 

AUTHORS: 

 ARP A 

SOURCE: 

 Crisp Data Base National Institutes of Health 

ABSTRACT: 

 No subproject abstract available. See parent grant. 

428 

TITLE: 

 Three cases of toxic lung caused by ammonia and hydrogen sulfide vapors. 

AUTHORS: 

 COUTURIER Y 

 BARBOTIN M 

 BOBIN P 

 DERRIEN JP 

SOURCE: 

 BULL SOC MED AFR NOIRE LANG FR; 16 (2). 1971 250-252 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. One case of inhalation toxicity was fatal. 

 The other 2 cases ran disturbed but favorable courses. 

429 

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TITLE: 

 On relationships in action between carbon disulfide and hydrogen sulfide. 

AUTHORS: 

 BITTERSOHL G 

SOURCE: 

 MED LAV; 62 (12). 1971 554-556 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. Several industrial processes are complicated 

 with regard to the potential health hazard, due to a simultaneous exposure 

 to CS2 and H2S. Autoxidation of H2S by a free radical mechanism was 

 detected. Since CS2 has a selective action on the brain and nerves and 

 because of reports that simultaneous exposure to CS2 and H2S produce more 

 severe intoxications than each substance alone. CS2 toxicity may also be 

 explained by a free radical reaction. 

430 

TITLE: 

 EXPERIMENTAL STUDIES ON THE EFFECT OF HYDROGEN SULFIDE ON LIMNIC AND 

 MARINE BOTTOM ANIMALS 

AUTHORS: 

 CASPERS H 

SOURCE: 

 SLADECEK, V. (ED.). INTERNATIONALE VEREINIGUNG FUR THEORETISCHE UND 

 ANGEWANDTE LIMNOLOGIE. INTERNATIONAL ASSOCIATION OF THEORETICAL AND 

 APPLIED LIMNOLOGY. ASSOCIATION INTERNATIONALE DE LIMNOLOGIE THEOREQUE ET 

 APPLIQUEE. VOL. 18, PARTS 1 & 2. VERHANDLUNGEN, PROCEEDINGS. TRAVAUX. 

 LENINGRAD, USSR, 1971. 562P. (PART 1). ILLUS. MAPS. 694P. (PART 2). ILLUS 

 MAPS. E. SCHWEIZERBART'SCHE VERLAGSBUCHHANDLUNG: STUTTGART, WEST GERMANY; 

 (DIST. IN U.S.A. BY JOHN WILEY & SONS, INC.: NEW YORK, N.Y.).; 1972 (RECD 

 1973) 946-954 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. NEREIS-SUCCINEA NASSA-RETICULATA 

 GAMMARUS-PULEX TOXICITY 

431 

TITLE: 

 Chronic toxicity of hydrogen sulfide to Gammarus pseudolimnaeus. 

AUTHORS: 

 OSEID DM 

 SMITH L L JR 

SOURCE: 

 TRANS AM FISH SOC; 103 (4). 1974 819-822 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. Gammarus pseudolimnaeus from 2 trout streams 

 were exposed to various levels of H2S from 0.0007-0.0192 mg/1 in a 

 flow-through apparatus for periods of 65, 95 and 105 days in 4 tests. 

 Results indicate that 0.002 mg/1 of H2S is the maximum safe concentration 

 for Gammarus, but below this level there is increased reproduction or 

 survival. Mean 96-h LC50 for Gammarus from the same populations was 0.022 

 mg/1 of H2S or approximately 10 times the safe level. 

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432 

TITLE: 

 Free radical biology and medicine: it's a gas, man! 

AUTHORS: 

 Pryor WA 

 Houk KN 

 Foote CS 

 Fukuto JM 

 Ignarro LJ 

 Squadrito GL 

 Davies KJ 

SOURCE: 

 Am J Physiol Regul Integr Comp Physiol. 2006, Sep; 291(3):R491-511. 

 [American journal of physiology. Regulatory, integrative and comparative 

 physiology] 

ABSTRACT: 

 We review gases that can affect oxidative stress and that themselves may 

 be radicals. We discuss O(2) toxicity, invoking superoxide, hydrogen 

 peroxide, and the hydroxyl radical. We also discuss superoxide dismutase 

 (SOD) and both ground-state, triplet oxygen ((3)O(2)), and the more 

 energetic, reactive singlet oxygen ((1)O(2)). Nitric oxide ((*)NO) is a 

 free radical with cell signaling functions. Besides its role as a 

 vasorelaxant, (*)NO and related species have other functions. Other 

 endogenously produced gases include carbon monoxide (CO), carbon dioxide 

 (CO(2)), and hydrogen sulfide (H(2)S). Like (*)NO, these species impact 

 free radical biochemistry. The coordinated regulation of these species 

 suggests that they all are used in cell signaling. Nitric oxide, nitrogen 

 dioxide, and the carbonate radical (CO(3)(*-)) react selectively at 

 moderate rates with nonradicals, but react fast with a second radical. 

 These reactions establish "cross talk" between reactive oxygen 

 (ROS) and reactive nitrogen species (RNS). Some of these species can react 

 to produce nitrated proteins and nitrolipids. It has been suggested that 

 ozone is formed in vivo. However, the biomarkers that were used to probe 

 for ozone reactions may be formed by non-ozone-dependent reactions. We 

 discuss this fascinating problem in the section on ozone. Very low levels 

 of ROS or RNS may be mitogenic, but very high levels cause an oxidative 

 stress that can result in growth arrest (transient or permanent), 

 apoptosis, or necrosis. Between these extremes, many of the gasses 

 discussed in this review will induce transient adaptive responses in gene 

 expression that enable cells and tissues to survive. Such adaptive 

 mechanisms are thought to be of evolutionary importance. 

433 

TITLE: 

 EFFECT OF HYDROGEN SULFIDE ON VENTILATORY CONTROL IN THE CHICKEN 

AUTHORS: 

 KLENTZ RD 

 FEDDE MR 

SOURCE: 

 TRANS KANS ACAD SCI; 79 (1/2). 1976 (1977) 66-67 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. ABSTRACT RESPIRATORY FREQUENCY TIDAL VOLUME 

 MINUTE VENTILATION TOXICITY 

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434 

TITLE: 

 Behavioral studies on toxicity of hydrogen sulfide by means of conditioned 

 avoidance responses in rats. 

AUTHORS: 

 HIGUCHI Y 

SOURCE: 

 FOLIA PHARMACOL JPN; 73 (3). 1977 307-320 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. Few studies have been done on the response of 

 the living body to H2S at a sublethal concentration (under 500 ppm). The 

 effects of H2S at various concentrations (100ined on conditioned avoidance 

 response. Discriminated avoidance response was significantly inhibited 

 immediately after exposure to 200 ppm at the minimum, but significant 

 inhibition of Sidman-type avoidance response was observed after exposure 

 to 300 ppm. There was no correlation between the inhibitory intensity and 

 the response rate on the behavioral baseline. The extinction of 

 Sidman-type avoidance response was significantly accelerated only when the 

 animal was exposed to a concentration over 500 ppm. In case of exposure to 

 300iminated the Sidman-type avoidance responses were inhibited at a rate 

 and intensity which paralleled the concentrations. At 1 h after forced 

 ventilation, the initial response level was restored, but in case of 

 exposure to higher concentrations, the inhibitory effect sometimes 

 persisted until the next day. With other rats placed under almost the same 

 conditions, blood pressure, respiration and heart rates were determined 

 without anesthesia, following the exposure to 100 showed only transient 

 deflections for about 5 min immediately after the exposure, but remained 

 relatively stable for 1 h. It was consequently assumed that inhibition of 

 conditioned avoidance responses after exposure to H2S might be due to a 

 depressive effect on the CNS. 

435 

TITLE: 

 NUTRIENTS HYDROGEN SULFIDE AND DRY MATTER PRODUCTION OF 

 SPARTINA-ALTERNIFLORA IN 3 SALT MARSHES 

AUTHORS: 

 CARLSON P R JR 

SOURCE: 

 ASB (ASSOC SOUTHEAST BIOL) BULL; 24 (2). 1977 41-42 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. ABSTRACT TOXICITY SEWAGE EFFLUENT 

436 

TITLE: 

 Nitrite as an antidote for acute hydrogen sulfide intoxication? 

AUTHORS: 

 BECK JF 

 BRADBURY CM 

 CONNORS AJ 

 DONINI JC 

SOURCE: 

 AM IND HYG ASSOC J; 42 (11). 1981. 805-809. 

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ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. The detoxification of H2S by a heme catalyzed 

 oxidation was examined as part of an on-going study of human occupational 

 H2S toxicity. Interlocking O2 absorption and sulfide depletion data 

 indicated that HbO2 and methemoglobin were effective catalytic agents. 

 Although the latter was more efficacious, the life time of excess sulfide 

 in the presence of O2 and either agent was of the order of min. It was 

 also established that the formation of methemoglobin following nitrite 

 administration occurred preferentially under O2 poor conditions. Under an 

 atmospheric or O2 enriched environment, which favored sulfide depletion, 

 the nitrite retarded sulfide oxidation. Nitrite as an antidote for acute 

 H2S intoxication was only effective within the 1st few min after exposure, 

 at which time resuscitation and/or ventilation of the victim was likely to 

 produce conditions in which the nitrite actually slowed sulfide removal. 

437 

TITLE: 

 EFFECTS OF THE ANIONIC ENVIRONMENT ON THE TRANSFER OF METHYL GROUPS TO 

 INORGANIC MERCURY 

AUTHORS: 

 COMPEAU G 

 BARTHA R 

SOURCE: 

 82ND ANNUAL MEETING OF THE AMERICAN SOCIETY FOR MICROBIOLOGY, ATLANTA, 

 GA., USA, MARCH 7-12, 1982. ABSTR ANNU MEET AM SOC MICROBIOL; 82 (0). 

 1982. ABSTRACT Q111. 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. ABSTRACT METHYLATING MICROBES DEMETHYLATING 

 MICROBES ESTUARINE SEDIMENT SALINITY SODIUM CHLORIDE HYDROGEN SULFIDE 

 SULFATE CHLORIDE MERCURY TOXICITY 

438 

TITLE: 

 Physiological and biochemical effects of acute exposure of fish to 

 hydrogen sulfide. 

AUTHORS: 

 TORRANS EL 

 CLEMENS HP 

SOURCE: 

 COMP BIOCHEM PHYSIOL C COMP PHARMACOL; 71 (2). 1982. 183-190. 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. Exposure of channel catfish to 0.5 mg/l H2S at 

 20ê C resulted in hyperpnea, followed by apnea and respiratory arrest. 

 Catfish brain cytochrome oxidase activity was inhibited in vitro 18% by 

 10-7 M H2S, 64% by 10-6 M H2S and 100% by 10-4 M H2S. When channel catfish 

 were exposed to 0.1 mg/l H2S at 20 C for 30 min, the cytochrome oxidase 

 activity of the brain was inhibited 40% and that of the gill was inhibited 

 74%, while blood lactate rose from 11.6 to 38.1 mg/100 ml. Catfish with 

 nitrite-induced methemoglobinemia showed less inhibition of brain and gill 

 cytochrome oxidase when exposed to H2S than did control fish. 

 Sulfide-inhibited brain cytochrome oxidase recovered from 50% inhibition 

 to control levels in channel catfish after 6 h in freshwater at 10ê C. 

 Management practices were recommended which may help the commercial fish 

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 farmer alleviate the problem of the toxicity of sulfide to fish during 

 harvest operations. 

439 

TITLE: 

 Effects of sulfur dioxide on ascorbic acid in crop plants. 

AUTHORS: 

 VARSHNEY S RK 

 VARSHNEY CK 

SOURCE: 

 ENVIRON POLLUT SER A ECOL BIOL; 35 (4). 1984. 285-290. 

ABSTRACT: 

 HEEP COPYRIGHT: BIOL ABS. The effects of low levels of SO2 (78.6, 131 

 and 262 mug m-3) on ascorbic acid were evaluated in 3 crop plant spp., 

 namely Brassica nigra L., Phaseolus radiatus L. and Zea mays L. Z. mays, 

 which is relatively SO2-resistant, possesses a comparatively high amount 

 of ascorbic acid. The ascorbic acid contents of B. nigra and P. radiatus, 

 which are relatively SO2-sensitive spp., decreased markedly within 1 wk 

 following SO2 fumigation. Fumigation of Z. mays with SO2 was accompanied 

 by a significant reduction in ascorbic acid only after 6 wk of fumigation 

 with 131 and 262 mug m-3 of SO2. The results of this investigation 

 indicate a positive correlation between ascorbic acid content and SO2 

 sensitivity of plants. The ascorbic acid acts as a powerful reductant and 

 seems to mediate the reduction of sulfite to hydrogen sulfide, thereby 

 reducing the toxicity of SO2. Apparently, Z. mays is relatively resistant 

 to SO2 because initially it has a high ascorbic acid content. It is 

 unlikely that the ascorbic acid in plants plays an important role in 

 determining their relative resistance to SO2 pollution. 

440 

TITLE: 

 Dangerous Gases in Distillation and Refining Processes 

AUTHORS: 

 Herbert Ele Q 

SOURCE: 

 Journal of the Institute of Petroleum, Vol. 25, No. 188, pages 323-346, 29 

 references, 19391939 

ABSTRACT: 

 The hazards of petroleum vapors and other gases encountered in the 

 distillation and refining of petroleum are reviewed. The distillation 

 processes which produce the vapors and the safety precautions which must 

 be taken because of their toxicity and flammability are discussed. 

 Special attention is given to the characteristics, sources, and 

 physiological effects of hydrogen-sulfide (7783064) which is usually found 

 in admixture with the petroleum vapors and fixed gases resulting from 

 distillation. Because of the anesthetic, poisonous, and flammable nature 

 of these gases, the author recommends that considerable care be taken by 

 those who may come in contact with them. 

441 

TITLE: 

 Anti-inflammatory and gastrointestinal effects of a novel diclofenac 

 derivative. 

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AUTHORS: 

 Li L 

 Rossoni G 

 Sparatore A 

 Lee LC 

 Del Soldato P 

 Moore PK 

SOURCE: 

 Free Radic Biol Med. 2007, Mar 1; 42(5):706-19. [Free radical biology & 

 medicine] 

ABSTRACT: 

 S-diclofenac (2-[(2,6-dichlorophenyl)amino]benzeneacetic acid 

 4-(3H-1,2,dithiol-3-thione-5-yl)phenyl ester; ACS 15) is a novel molecule 

 comprising a hydrogen sulfide (H2S)-releasing dithiol-thione moiety 

 attached by an ester linkage to diclofenac. S-diclofenac administration 

 inhibited lipopolysaccharide-induced inflammation (as evidenced by reduced 

 lung and liver myeloperoxidase activity) and caused significantly less 

 gastric toxicity than diclofenac. S-diclofenac did not affect blood 

 pressure or heart rate of the anesthetized rat. S-diclofenac 

 administration downregulated expression of genes encoding enzymes which 

 synthesize nitric oxide, prostanoids, and H2S; reduced plasma 

 IL-1beta/TNF-alpha; and elevated plasma IL-10. Reduced liver NF-kappaB p65 

 and AP-1/c-fos DNA-binding activity was also observed. These effects were 

 mimicked in large part by a combination of diclofenac plus an 

 H2S-releasing moiety (ADT-OH). Incubation of S-diclofenac (100 microM) 

 with rat plasma or liver homogenate caused a time-dependent release of 

 H2S, which was inhibited by sodium fluoride (10 mM). Administration of 

 S-diclofenac (47.2 micromol/kg, i.p.) to conscious rats significantly 

 increased plasma H2S concentration (at 45 min and 6 h). We propose that 

 H2S release from S-diclofenac in vivo contributes to the observed effects. 

442 

TITLE: 

 Developmental changes in the metabolism of 3-methylthiopropionate in the 

 rat. 

AUTHORS: 

 Finkelstein A 

 Benevenga NJ 

SOURCE: 

 J Nutr. 1984, Sep; 114(9):1622-9. [The Journal of nutrition] 

ABSTRACT: 

 The oxidation of 3-methylthiopropionate (MTP), a product in the 

 transamination pathway of methionine metabolism, was measured in rats from 

 1 to 400 days of age. The metabolic capacity of liver homogenates to 

 produce volatile sulfur compounds (methanethiol and/or hydrogen sulfide) 

 from [35S]MTP increased sixfold during the first week of life, remained at 

 that level through weaning, then gradually decreased to essentially the 

 value observed in the 1-day-old rat by 400 days of age. This pattern is 

 not altered when the data are expressed in relation to tissue O2 

 consumption. This implies that the greater ability of young rats to 

 produce volatile sulfur compounds is not simply a reflection of their 

 greater metabolic rate (kilocalorie/kilogram per day). In contrast to 

 experiments in vitro, the ability to convert a tracer dose of [35S]MTP to 

 urinary sulfate increased from 50% of the dose in the 15-day-old rat to 

 80% in the 24-, 50- and 400-day-old rats. This difference between the 

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 ability to produce volatile sulfur compounds and to excrete them as 

 sulfate may explain the toxicity of methionine in young animals. 

443 

TITLE: 

 The evolution of bioluminescent oxygen consumption as an ancient oxygen 

 detoxification mechanism. 

AUTHORS: 

 Timmins GS 

 Jackson SK 

 Swartz HM 

SOURCE: 

 J Mol Evol. 2001, Apr; 52(4):321-32. [Journal of molecular evolution] 

ABSTRACT: 

 Endogenous reductants such as hydrogen sulfide and alkylthiols provided 

 free radical scavenging systems during the early evolution of life. The 

 development of oxygenic photosynthesis spectacularly increased oxygen 

 levels, and ancient life forms were obliged to develop additional 

 antioxidative systems. We develop here the hypothesis of how 

 "prototypical" bioluminescent reactions had a plausible role as 

 an ancient defense against oxygen toxicity through their 

 "futile" consumption of oxygen. As oxygen concentrations 

 increased, sufficient light would have been emitted from such systems for 

 detection by primitive photosensors, and evolutionary pressures could then 

 act upon the light emitting characteristics of such systems independently 

 of their use as futile consumers of oxygen. Finally, an example of 

 survival of this ancient mechanism in present-day bioluminescent bacteria 

 (in the Euprymna scolopes-Vibrio fischeri mutualism) is discussed. Once 

 increasing ambient oxygen levels reached sufficiently high levels, the use 

 of "futile" oxygen consumption became too bioenergetically 

 costly, so that from this time the evolution of bioluminescence via this 

 role was made impossible, and other mechanisms must be developed to 

 account for the evolution of bioluminescence by a wide range of organisms 

 that patently occurred after this (e.g., by insects). 

444 

TITLE: 

 Investigation Of Toxic Gases From Mexican And Other High-Sulphur 

 Petroleums And Products 

AUTHORS: 

 Sayers RR 

 Smith NAC 

 Fieldner AC 

 Mitchell CW 

 Jones GW 

 Yant WP 

 Stark DD 

 Katz SH 

 Bloomfield JJ 

 Jacobs WA 

SOURCE: 

 U.S. Bureau of Mines, Bulletin No. 231, pages 1-8, 19251925 

ABSTRACT: 

 The presence of toxic components in Mexican crude oil is discussed, based 

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 on the findings of a study done by the Bureau of Mines and the Public 

 Health Service under a cooperative agreement with the American Petroleum 

 Institute. The general scope of the study is described, including both 

 field and laboratory investigations, and the main findings are summarized. 

 The processes involved in the production, marketing, and refining of light 

 Mexican crude oil are reviewed. The chemical and physical characteristics 

 of typical high sulfur (7704349) crudes marketed in the United States are 

 described, with special note of the generation of hydrogen-sulfide 

 (7783064) (H2S). The products found in laboratory distilled oil are 

 reviewed, and the generation of H2S gas over time is described. H2S 

 hazards associated with each phase of the distillation process are 

 described. Symptoms associated with exposure to the gas given off during 

 storage and refining of light Mexican crude are discussed, and safety 

 precautions used at the refineries to prevent exposures are noted, 

 including inspections, ventilation, closed and automated systems, and 

 ample work space. H2S toxicity symptoms in laboratory animals are 

 reviewed, along with methods of treatment of poisoning. Types of 

 respirators used by refinery workers are described. The authors recommend 

 that all gases and vapors from Mexican crude should be confined to closed 

 systems and properly vented tanks; employees should be instructed about 

 the hazards of H2S exposure and appropriate first aid measures; and hose 

 masks or oxygen breathing apparatus should be readily available and 

 workers should be trained to use these devices properly. 

445 

TITLE: 

 Chemical Exposures In The Plant 

AUTHORS: 

 Olson CM 

SOURCE: 

 National Safety Congress Transactions, Chemical; Fertilizer Industries; 

 Research and Development, Vol. 5, pages 23-30, 19701970 

ABSTRACT: 

 Typical accidents in a chemical manufacturing facility are reviewed. 

 Generalized use of carbon-tetrachloride (56235) before knowledge of its 

 toxicity is described. Safety precautions when working with phosphorus 

 (7723140) are considered. Regular laundering of specially provided 

 laboratory wear is recommended. Dangers of oxidizing agents are examined. 

 Cases involving carbon-monoxide (630080), hydrogen-sulfide (7783064), 

 phosphine (7803512), and phosgene (75445) poisoning are described. 

 Accidents involving mishandling of chemicals that hydrolyze with evolution 

 of heat are considered. Repeated training and regular reminders of safe 

 courses of action are suggested to help prevent panic in the event of 

 accidents. Immediate and prolonged flushing with water is recommended as 

 the best initial treatment of any chemical burn. Destruction of clothes 

 contaminated with corrosive chemicals is also suggested, as burns may 

 develop when the clothes are worn again. Poor technique in loading or 

 moving dangerous chemicals is responsible for many accidents in chemical 

 manufacturing facilities. The author concludes that exposure to chemicals 

 can be by drips, leaks, spillage, splashes, poor housekeeping, inadequate 

 facilities, malfunctions, deviations from or lack of standard operating 

 procedures, absence of emergency procedures, failure to provide or use 

 adequate protective equipment, and haphazard training. Books on 

 occupational safety and accident prevention are recommended. 

446 

TITLE: 

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 Agricultural lung diseases. 

AUTHORS: 

 Kirkhorn SR 

 Garry VF 

SOURCE: 

 Environ Health Perspect. 2000, Aug; 108 Suppl 4:705-12. [Environmental 

 health perspectives] 

ABSTRACT: 

 Agriculture is considered one of the most hazardous occupations. Organic 

 dusts and toxic gases constitute some of the most common and potentially 

 disabling occupational and environmental hazards. The changing patterns of 

 agriculture have paradoxically contributed to both improved working 

 conditions and increased exposure to respiratory hazards. Animal 

 confinement operations with increasing animal density, particularly swine 

 confinement, have contributed significantly to increased intensity and 

 duration of exposure to indoor air toxins. Ongoing research has implicated 

 bacterial endotoxins, fungal spores, and the inherent toxicity of grain 

 dusts as causes of upper and lower airway inflammation and as immunologic 

 agents in both grain and animal production. Animal confinement gases, 

 particularly ammonia and hydrogen sulfide, have been implicated as 

 additional sources of respiratory irritants. It has become evident that a 

 significant percentage of agricultural workers have clinical symptoms 

 associated with long-term exposure to organic dusts and animal confinement 

 gases. Respiratory diseases and syndromes, including hypersensitivity 

 pneumonitis, organic dust toxic syndrome, chronic bronchitis, mucous 

 membrane inflammation syndrome, and asthmalike syndrome, result from 

 ongoing acute and chronic exposures. In this review we focus upon the 

 emerging respiratory health issues in a changing agricultural economic and 

 technologic environment. Environmental and occupational hazards and 

 exposures will be emphasized rather than clinical diagnosis and treatment. 

 Methods of prevention, from both engineering controls and personal 

 respiratory perspectives, are also addressed. 

447 

TITLE: 

 On The Effect And Toxicity Of Dimethyl Sulfide, Dimethyl Disulfide And 

 Methyl Mercaptan 

AUTHORS: 

 Ljunggren G 

 Norberg B 

SOURCE: 

 Acta Physiologica Scandinavica, Vol. 5, pages 248-255, 14 reference, 

 19431943 

ABSTRACT: 

 The toxic effects produced by exposure to dimethyl-sulfide (75183), 

 dimethyl-disulfide (624920), and methyl-mercaptan (74931) were studied in 

 rats. Female white-rats underwent gas chamber exposures to 

 dimethyl-sulfide, dimethyl-disulfide, and methyl-mercaptan at 

 concentrations of 3 to 140, 7.1 to 26, and 1 to 20 milligrams per liter, 

 respectively, for periods of 30 to 35 minutes. Dimethyl-sulfide irritated 

 the mucous membranes, as well as paralyzing the voluntary and respiratory 

 muscles, with a 15 minute exposure at 5 percent by volume causing death. 

 Dimethyl-disulfide produced a higher degree of local irritation than 

 dimethyl-sulfide, resulting in convulsions and macroscopically visible 

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 ecchymoses in the lungs. Paralysis of locomotion and external respiration 

 occurred, with a 15 minute exposure at 0.5 percent by volume causing 

 death. Methyl-mercaptan resulted in the more or less pronounced paralysis 

 of locomotion of respiration, with signs of local irritation being found 

 in the lungs at autopsy. Exposure to methyl-mercaptan for a period of 15 

 minutes at a concentration of 0.5 percent by volume caused death. The 

 authors conclude that the toxic effects of the sulfides tested are 

 primarily the same as those of hydrogen-sulfide, with dimethyl-disulfide 

 being the most toxic, followed by methyl-mercaptan, and dimethyl-sulfide. 

448 

TITLE: 

 Safety Aspects in the Design of an Organic Insecticide Plant 

AUTHORS: 

 Curwen KM 

SOURCE: 

 Chemistry and Industry (Paper presented at the Safety in the Chemical 

 Industry Symposium of the Chemical Engineering Group and the London 

 Section at the Royal Institution, October 14, 1957),, 19581958 

 August 23, 1958 issue, pages 1096-1101, 17 references 

ABSTRACT: 

 Safety aspects in the design of an organic insecticide plant for 

 manufacturing an organophosphorus product are listed and discussed. The 

 manufacturing process consists basically of the formation of a 

 thiophosphoric-acid by reaction of an alcohol on a slurry of 

 phosphorus-pentasulfide (1314803) in an organic solvent, with the 

 evolution of hydrogen-sulfide (7783064). The excess 

 phosphorus-pentasulfide (1314803) is removed by filtration and the acid is 

 then condensed with an ester, followed by removal of the solvent under 

 vacuum. A crude product is then purified by washing and stream stripping 

 under vacuum. The planning approach utilized is to go through various 

 stages of design noting probable hazards and indicating methods for 

 counteracting these hazards. First principles of design apparent from the 

 probable hazards discovered include flameproofing, ventilation of toxic 

 vapors, and explosion release mechanisms. Procedures for design and 

 planning are described in detail, and discussions of the procedures (with 

 the author's replies to questions) are included. 

449 

TITLE: 

 Adaptation of pregnant ewes to an exclusive onion diet. 

AUTHORS: 

 Knight AP 

 Lassen D 

 McBride T 

 Marsh D 

 Kimberling C 

 Delgado MG 

 Gould D 

SOURCE: 

 Vet Hum Toxicol. 2000, Feb; 42(1):1-4. [Veterinary and human toxicology] 

ABSTRACT: 

 A diet consisting entirely of cull onions fed to pregnant ewes produced 

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 Heinz body hemolytic anemia in all sheep after 21 d. After 28 d of daily 

 consumption of 20 kg of onions/ewe, the anemia stabilized, and for the 

 remaining 74 d the packed cell volume increased in the majority of sheep, 

 although it did not return to normal. Compared to control ewes fed an 

 alfalfa and grain diet, the onion-fed ewes had comparable body condition 

 scores and fleece weights. There was no significant difference (alpha = 

 0.05) in pregnancy or lambing rate, number of lambs born/ewe exposed, or 

 number of lambs born/ewe lambing. Greater numbers of sulfate-reducing 

 bacteria (Desulfovibrio spp) and more ruminal hydrogen sulfide were 

 present in onion-fed sheep compared to controls. Although an average 27% 

 reduction in packed cell volume and Heinz body anemia developed in the 

 onion-fed ewes, on the basis of this study it appears that pregnant ewes 

 may be fed a pure onion diet with minimal detrimental effects. This 

 adaptation to a pure onion diet is in part likely due to the apparent 

 ability of the sheep's rumen to quickly develop a population of 

 sulfate-reducing bacteria that decrease the toxicity of onion disulfides. 

450 

TITLE: 

 Clinical Findings in Industrial Poisonings 

AUTHORS: 

 Kulkow AE 

SOURCE: 

 Zeitschrift fuer die Gesamte Neurologie und Psychiatrie, Vol. 103, pages 

 435-454, 19261926 

ABSTRACT: 

 A large number of cases were viewed where poisoning resulted from 

 industrial exposure to toxic substances such as lead (7439921), benzene 

 (71432), carbon-disulfide (75150), and aniline. The cases have been 

 divided into three groups: cases of lead intoxication with stable 

 disorders of the peripheral nervous system, (16 cases); cases of benzene 

 poisoning which displayed the picture of a neurosis (hysterical 

 condition); and cases of poisoning from a mixture of carbon-disulfide and 

 hydrogen-sulfide (7783064), which cause similar stable disorders in the 

 peripheral nervous system and also in the central nervous system. The 

 cases of benzene poisoning experienced general toxicity symptoms, and 

 there were also cases with a clearly pronounced neurosis evidence by 

 hysterical attacks, which makes it justifiable to classify benzene as an 

 absolutely active factor in the development of these neuroses. (German; 

 English translation available) 

451 

TITLE: 

 Pulmonary Edema of Environmental Origin 

AUTHORS: 

 Cordasco EM 

 Stone FD 

SOURCE: 

 Chest, Vol. 64, No. 2, pages 182-185, 27 references, 19731973 

ABSTRACT: 

 The effects of poisoning with diborane (19287457), hydrogen-sulfide 

 (7783064) (H2S), chlorine (7782505), phosgene (75445), carbon-monoxide 

 (630080), or antimony-pentachloride (7647189) were examined in 55 patients 

 with pulmonary edema. Most of the cases of intoxication resulted from 

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 accidental acute exposure to gaseous agents in industrial settings. 

 Chlorine gas in low concentrations induced damage to the mucosa of the 

 nose and throat because of the solubility of the gas in water. Greater 

 concentrations gave rise to severe pulmonary congestion and edema due to 

 the hydrolysis of chlorine to hydrochloric-acid in the parenchymal lung 

 tissue. Phosgene produced irritation of the conjunctiva, nasal, and 

 pharyngeal membranes at low concentrations. At higher exposures, 

 bronchial, bronchiolar, and alveolar inflammatory reactions ensued. At 

 low exposures to H2S, damage occurred in the conjunctiva, cornea, and 

 pharyngeal membranes. A more prolonged exposure to low concentrations 

 evoked damage to the respiratory tract and produced pulmonary edema. 

 Following high exposure to H2S, central nervous system depression 

 developed with respiratory and olfactory paralysis. All patients with 

 diborane intoxication survived; there were two deaths from H2S poisoning 

 and two deaths from antimony-pentachloride poisoning. All patients 

 received oxygen therapy (at 60 to 80 percent), usually with intermittent 

 positive pressure breathing. The authors conclude that narcotic agents 

 should not be administered to patients with respiratory depression. 

 Victims of poisonings such as those described should be treated in 

 intensive care units. 

452 

TITLE: 

 Sulphur Metabolism and Excretion Studies in Ruminants. X. Sulphide 

 Toxicity in Sheep 

AUTHORS: 

 Bird PR 

SOURCE: 

 Australian Journal of Biological Sciences, Vol. 25, No. 5, pages 

 1087-1098, 36 references, 19721972 

ABSTRACT: 

 The effects of sodium-sulfate (7757826) or sodium-sulfide (1313822) (Na2S) 

 on food and water consumption and on ruminant activity were examined in 

 sheep. In six experiments, sheep were given continuous duodenal or 

 ruminal infusions of sodium-sulfate, single infusions of Na2S, continuous 

 infusions of Na2S, infusions of hydrogen-sulfide (7783064) (H2S) into the 

 ileum, or infusions of Na2S into the ileum. Ruminal infusions of Na2S 

 were able to completely inhibit ruminal movements, during which time the 

 sheep exhibited activity of the peripheral musculature suggestive of 

 sympathetic stimulation. Decreased food intake was associated with 

 ruminal infusions of Na2S. The effect of sulfide on the nervous system 

 was not immediately reversible; there appeared to be an accumulative 

 effect of H2S infusion over time. Changes in respiration and heart rate 

 when H2S was infused were consistent with those found in nonruminant 

 species. Ruminal infusions of 4 grams (g) of sodium-sulfate per day did 

 not adversely affect the sheep, nor did duodenal infusions of up to 6g of 

 sodium-sulfate per day. The author concludes that the toxic effect of 

 sulfide on the nervous system is mediated via eructation of H2S from the 

 rumen and absorption through the lungs. A daily intake by sheep of 

 sulfur, in any form, should not exceed 4g, which is more than required for 

 optimal ruminal protein synthesis but less than is likely to reduce food 

 intake. 

453 

TITLE: 

 Coal Mine Combustion Products: Ingredients Of Conveyor Belts 

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AUTHORS: 

 Christos T 

 Forshey DR 

 Hartstein AM 

SOURCE: 

 U.S. Department of the Interior, Bureau of Mines Report of Investigations 

 No. RI-8235, 18 pages, 7 references, 19771977 

ABSTRACT: 

 The thermal oxidative degradation products of materials used in coal mine 

 conveyor belts were investigated. Samples of cured and uncured 

 styrene/butadine rubber, neoprene, nylon, dacron polyester, rayon, 

 tritolyl-phosphate (1330785), tri-p-tolyl-phosphate (78320), 

 tributyl-phosphate (126738), tris(dichloropropyl)-phosphate (26604513), 

 di(2-ethylhexyl)-sebacate (122623), and 2-mercaptobenzothiazole (149304) 

 were decomposed in a sealed system at 370 or 420 degrees-C. All volatile 

 products were quantitated by gas chromatography/mass spectrometry. The 

 concentrations (expressed as milligrams per gram) of volatile components 

 of all materials were tabulated. The raw styrene/butadiene rubber 

 produced only traces of sulfur compounds. Toxic products from the cured 

 samples included carbon-disulfide (75150), hydrogen-sulfide (7783064), 

 phenol (108952), and cresols, all at concentrations below their threshold 

 limit values (TLVs). Neoprene produced hydrogen-chloride (7647010) at 

 concentrations in excess of its TLV value. At 370 degrees, dacron 

 decomposed slightly, producing only carbon-monoxide and formaldehyde. At 

 420 degrees, decomposition of dacron produced acrolein (107028). Aromatic 

 phosphate esters showed only a slight degree of degradation. The 

 aliphatic phosphate ester produced butene (25167673) and the chlorinated 

 esters produced acrolein, vinyl-chloride (75014), and hydrogen-chloride. 

 The authors conclude that styrene/butadiene rubber reinforced with dacron 

 appears to be the best combination of conveyor belt materials from the 

 standpoint of potential toxicity. 

454 

TITLE: 

 Toxicity Of Oxygen Mixed With Helium 

AUTHORS: 

 Troshikhin GV 

 Donina ZhA 

SOURCE: 

 Kosmicheskaya Biologiya i Aviakosmicheskaya Meditsina, No. 3, pages 54-58, 

 18 references, 19791979 

ABSTRACT: 

 The toxic effect of oxygen mixed with helium was investigated in male 

 white CC57-mice. Animals were placed in two pressure chambers of 150 

 liter capacity. Each chamber was equipped with rubber sleeves and gloves, 

 and an autonomous system for air regeneration. Temperature in the 

 chambers was kept at a constant 24 to 26 degrees-C, or it was raised by an 

 electric heater. A gas analyzer and oxygen analyzer were used to monitor 

 the gas composition. Concentrations of harmful admixtures, including 

 ammonia (7664417), hydrogen-sulfide (10034932), carbon-monoxide (630080), 

 and nitrogen oxides, were in the range of hygienic standards adopted for 

 humans. Oxygen uptake was determined daily for 6 to 8 hours, 3 to 4 times 

 a day. An electric thermometer was used to measure rectal temperature 

 directly in the chamber. Mice were kept for 1 day in the air, then the 

 chambers were filled with an 80 percent hyperoxic mixture, one diluted in 

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 nitrogen and the other, helium. Animals were exposed to these mixtures 

 for 2 and 3 days. Twenty control mice were kept in a chamber filled with 

 air for 3 days. Animals were sacrificed after the experiments. The toxic 

 effect of oxygen on the mice was about the same in an 80 percent 

 oxygen/helium and oxygen/nitrogen mixture at the same ambient temperature. 

 Removal of the cooling effect of helium in the 80 percent oxygen/helium 

 atmosphere resulted in earlier decline of gas exchange values, faster 

 development of inflammatory signs in the lungs, and earlier mortality, 

 compared with atmospheres at room temperature. The authors conclude that 

 the mechanism of this phenomenon may be attributable to the correlation 

 between the toxic effect of oxygen and ambient temperature. (Russian) 

455 

TITLE: 

 Potential Ecological Hazards Of H-Coal Liquefaction 

AUTHORS: 

 Eddlemon GK 

 Sigal LL 

SOURCE: 

 Trace Substances in Environmental Health-XVI (Proceedings of University of 

 Missouri's 16th Annual Conference), pages 28-38, 25 references, 19821982 

ABSTRACT: 

 The ecological hazards of hard coal (8002059) liquefaction were 

 investigated. Five principal waste streams were identified as potential 

 hazards because of their likelihood for release into the environment: 

 atmospheric emissions; cooling tower blow down; coal pile leachates; solid 

 waste leachates; and product spills. The estimated release rates for 

 individual contaminants were used to calculate post dilution 

 concentrations in a model receiving atmosphere, soil, and river. The post 

 dilution concentration for each contaminant was compared to environmental 

 and toxicological bench marks as an indication of relative ecological 

 hazard. The relative hazard potential of the contaminants was determined 

 by ranking the contaminant to benchmark ratios. Sulfur dioxides, nitrogen 

 oxides, and hydrogen-sulfide (7783064) were found to have the greatest 

 potential to effect the environment. More than 90 percent of particles 

 larger than 50 micrometers with selected trace elements were predicted to 

 fall out with 400 meters (m) of release. Deposition of most of the 

 selected trace elements beyond 2,000m was not found to have significant or 

 detectable effects on the chemical composition of soil and vegetation 

 during early fallout. Among the organics for which source terms and 

 toxicity data was available, aromatic amines were rated first as a 

 potential hazard, followed by phenols and polycyclic aromatic 

 hydrocarbons. The authors conclude that a hard coal facility can impose 

 significant short and long term adverse effects on ecosystems unless 

 properly designed and operated. 

456 

TITLE: 

 Inhalation Of Irritant Gases 

AUTHORS: 

 Summer W 

 Haponik E 

SOURCE: 

 Clinics in Chest Medicine, Vol. 2, No. 2, pages 273-287, 74 references, 

 19811981 

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ABSTRACT: 

 The health effects from inhaling irritant gases are reviewed. The 

 inhalation of toxic gases and mists such as smoke inhalation by a fire 

 fighter or the accidental drenching of a chemical worker causes a wide 

 variety of symptoms and provides a spectrum of problems in management. 

 The mechanism of injury may be asphyxiation, systemic toxicity, or 

 immunological effects. In some instances, direct mucosal and alveolar 

 damage may be the cause. The ill effects of acute massive exposure to 

 chlorine (7782505), acrolein (107028), acrylonitrile (107131), ammonia 

 (7664417), cadmium (7440439), carbon-monoxide (630080), copper (7440508), 

 formaldehyde (50000), hydrogen-chloride (7647010), hydrogen-cyanide 

 (74908), hydrogen-sulfide (7783064), and magnesium-oxide (1309484) are 

 discussed. Effects of low dose exposure to a number of chemical vapors 

 and fumes are summarized. Therapeutic management of adverse health 

 effects caused by these agents is outlined. The prognosis of patients 

 with acute injury is discussed. The authors conclude that various gases, 

 mists, and fumes represent an important cause of lung injury. 

457 

TITLE: 

 Neurotoxicity Of Industrial Chemicals And Contaminants: Aspects Of 

 Biochemical Mechanisms And Effects 

AUTHORS: 

 Savolainen H 

SOURCE: 

 Archives of Toxicology, Supplement 5, pages 71-83, 113 references, 

 19831983 

ABSTRACT: 

 Neurotoxicity of industrial chemicals and contaminants is reviewed. 

 Transfer of xenobiotics in the brain is discussed. It is noted that the 

 adult central nervous system displays a functional barrier toward blood 

 borne chemicals (the blood brain barrier) so that water soluble chemicals 

 having molecular weights greater than 100 are directly prevented from 

 entering the brain. Lipophilic chemicals can enter the brain more easily 

 than ionic compounds. For example, isopropanol (67630) enters the brain 3 

 times more effectively than water. Hypoxia and histotoxic hypoxia are 

 discussed. The nervous system depends on having an adequate supply of 

 oxygen. Chemical agents that reduce oxygen availability at the cellular 

 level by inhibiting mitochondrial respiration cause effects that are 

 similar to hypoxia. Hydrogen-sulfide (7783064) and the cyanide (57125) 

 and formate (1838591) ions are examples of substances that inhibit the 

 cytochrome a/a3 complex in the mitochondrial respiration chain. Acute 

 solvent effects and tolerance are discussed. Acute harmful effects are 

 caused by lipophilic organic solvents. The lipid soluble molecules pass 

 the blood brain barrier rapidly and depress the nerve cell membrane 

 functions, which result in inhibiting the formation of action potentials. 

 Nerve neurons can acquire tolerance toward membrane depressant effects. 

 Chronic toxicity is discussed. It is noted that chronic nerve 

 degeneration due to solvent inhalation can occur without acute 

 intoxication. Chronic toxic effects may be due to the formation of 

 biologically reactive metabolites. The typical degeneration seen in 

 carbon-disulfide (75150) or n-hexane (110543) induced disease may result 

 from binding of reactive metabolites to the affected organelles. Metal 

 ions do not penetrate the blood brain barrier as readily as organic 

 materials. This may explain the low incidence of central nervous system 

 effects in adults exposed to lead (7439921). Children, with an immature 

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 blood brain barrier, are more vulnerable to the effects of lead. 

458 

TITLE: 

 Sewers 

AUTHORS: 

 Bell JH 

SOURCE: 

 Encyclopaedia of Occupational Health and Safety, Vol. 2, pages 2019-2021, 

 6 references, 19831983 

ABSTRACT: 

 Sewers are discussed. The duties of sewer workers consist of inspection, 

 silt removal, and repair of the subterranean channels to ensure the free 

 flow of sewage. Sewage is a chemically complex mixture of liquids of 

 domestic and industrial origin. In addition to domestic wastes, sewage 

 may contain such materials as mineral oils, acids, alkalis, soaps, 

 ammoniacal liquors, tar and phenol derivatives, cyanides, sand and cement 

 from building operations, and organic matter from tanners, and dye and gut 

 works. The working environment inside sewers is described. Temperature, 

 humidity, air movement, and atmospheric toxicity vary widely from sewer to 

 sewer and from minute to minute. Lethal amounts of toxic gases such as 

 carbon-monoxide, methane, hydrogen-sulfide and ammonia can be generated by 

 the interaction of wastes in poorly ventilated sewers. Work procedures 

 are enumerated. Hazards of sewer work are discussed. Gassing, 

 immersions, and injuries from accidents have occurred. Health risks 

 include infectious diseases, cardiovascular degeneration, lumbar spine 

 lesions, dermatitis, and conjunctivitis. A Danish survey showed a 

 significant increase of cancer of the pancreas in sewer workers. Safety 

 and health measures are considered. These include providing adequate 

 general ventilation, using toxic and combustible gas detectors, 

 preemployment and periodic medical examinations, health and safety 

 education, and vaccination against such diseases as leptospirosis, 

 tetanus, and typhoid fever. 

459 

TITLE: 

 Viscose 

AUTHORS: 

 Elattal MM 

SOURCE: 

 Encyclopaedia of Occupational Health and Safety, Vol. 2, pages 2263-2264, 

 4 references, 19831983 

ABSTRACT: 

 Hazards, safety, and health requirements while using viscose are reviewed. 

 The viscose process is the method often used for the manufacture of 

 synthetic silk and transparent paper. Principal raw materials used are 

 wood pulp cellulose, sodium-hydroxide (1310732), carbon-disulfide (75150), 

 and sulfuric-acid (7664939). Cellulose is steeped in sodium-hydroxide, 

 shredded, and aged. Shredded cellulose is treated with carbon-disulfide 

 to become cellulose-xanthate. This is dissolved in sodium-hydroxide to 

 form viscose, which is extruded into sulfuric-acid to form filaments or 

 film. Principal toxic hazards are from carbon-disulfide and 

 hydrogen-sulfide (7783064) toxicity. All possible measures must be taken 

 to keep concentrations of both below safe exposure limits. Total 

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 concentration of the two compounds should not exceed 20 parts per million, 

 the threshold limit value of each separately. Personal protective 

 equipment is required for many operations in the process. Efficient 

 exhaust ventilation is a necessity in the processing room. A reduction in 

 the number of hours workers may be exposed to carbon-disulfide has been 

 proposed to a total of 5 hours a day and no more than 2.5 hours 

 consecutively. Measures against fire and explosion hazards are required, 

 including exclusion of sources of heat and the use of non sparking tools. 

 Suitable protective clothing should be worn by workers where there is risk 

 of contamination from sodium-hydroxide or sulfuric-acid. Preemployment 

 and periodic physical examinations are required for all workers, with 

 special attention to neurological and psychological tests. The author 

 concludes that the protection of worker health should rely basically on 

 observance of acceptable working exposure limits. 

460 

TITLE: 

 Clostridium difficile: isolation and characteristics. 

AUTHORS: 

 Hafiz S 

 Oakley CL 

SOURCE: 

 J Med Microbiol. 1976, May; 9(2):129-36. [Journal of medical microbiology] 

ABSTRACT: 

 Clostridium difficile can be grown readily in Reinforced Clostridial 

 Medium (RCM) containing 0-1-0-4% of o-, m- or p-cresol, or phenol. We 

 recommend 0-2% of phenol or p-cresol in RCM for the isolation of this 

 organism. The characteristic "cornfield" growth in RCM in 25-ml 

 Universal containers is described. Glucose, fructose, galactose, mannose, 

 raffinose, aesculin and mannitol are fermented with production of acid and 

 gas; maltose, sucrose, glycogen, soluble starch and sorbitol are fermented 

 with production of acid only. Lactose and rice starch are not fermented by 

 any strain, and DL-methionine is not attacked. Nitrate is reduced to 

 nitrite. Hydrogen sulphide and indole are not produced. Gelatin is 

 attacked by all strains, but in some cases prolonged incubation is 

 required. Hyaluronidase is produced, but not deoxyribonuclease. A lethal 

 toxin appears to be produced. Strains possess shared and strain-specific 

 antigens. 

461 

TITLE: 

 [Study of Vibrio strains isolated from swine] 

AUTHORS: 

 Semov P 

 Georgiev S 

SOURCE: 

 Vet Med Nauki. 1975; 12(10):29-34. [Veterinarno-meditsinski nauki] 

ABSTRACT: 

 Antigen and biochemical studies were carried out of nine Vibrio strains 

 isolated from pigs, testing their pathogenicity and toxicity for 

 experimental animals. According to their biochemical behaviour six of the 

 strains were shown to belong to type I, three--to subtype I, and on the 

 grounds of their antigenic characteristics six belonged to type I and 

 three--to type II. It was found that the strains producing hydrogen 

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 sulfide were more weakly pathogenic and toxic. No substantial differences 

 were found between the strains isolated from miscarrying and normally 

 farrowing sowa originating from pig breeding farms with a record of 

 vibriosis. 

462 

TITLE: 

 Estimating Worker Exposure To Gases And Vapors Leaking From Pumps And 

 Valves 

AUTHORS: 

 Powell RW 

SOURCE: 

 American Industrial Hygiene Association Journal, Vol. 45, No. 11, pages 

 A7-A15, 16 references, 19841984 

ABSTRACT: 

 Methods to estimate the concentration of a toxic material in a worker's 

 breathing zone caused by leaking process equipment are described. The 

 method is designed primarily for pumps with leaks around valves and seals. 

 It makes use of an evaporation model and a dispersion model and involves 

 computer calculation to estimate concentrations. The fraction of material 

 vaporized from liquids and the vapor or gas concentration at a worker 

 location is calculated from the concentration of a toxic material in a 

 process stream, the process stream properties, and an estimate of the leak 

 potential of the equipment. When a leak rate is known, potential exposure 

 is derived by calculating the amount of vaporized liquid and the 

 concentration of contaminant in the vapor and estimating the dispersion 

 concentration of the contaminant downwind of the leak. When the vapor 

 emission rate is known or estimated, exposure is calculated from the 

 concentration of the contaminant in the vapor and an estimate of the vapor 

 dispersion. For equipment that is out of service, exposure is calculated 

 by first estimating the evaporation rate of the material, then determining 

 the dispersion of the vapor. Sample calculations are presented for 

 hydrogen-sulfide (7783064) leaking from a pump seal, a liquid hydrocarbon 

 mixture leaking from a pump seal, a gas mixture leaking from a valve, and 

 a hydrocarbon mixture evaporating from a pump withdrawn from service for 

 maintenance. Knowledge of leak potential can help in the design of better 

 controlled process equipment. For pumps, engineering controls may include 

 use of auxiliary packing, dual seals, tandem seals, or double mechanical 

 seals. Permanent drain and flushing connections could be designed into 

 the equipment to reduce exposure during maintenance. 

463 

TITLE: 

 Concentration-Time Mortality Response Relationship of Irritant and 

 Systemically Acting Vapours and Gases 

AUTHORS: 

 ten Berge WF 

 Zwart A 

 Appelman LM 

SOURCE: 

 Journal of Hazardous Materials, Vol. 13, No. 3, pages 301-309, 26 

 references, 19861986 

ABSTRACT: 

 Concentration time mortality response relationships of volatile industrial 

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 chemicals were evaluated. Raw data from previously published acute 

 inhalation toxicity studies of 20 volatile industrial chemicals having 

 local irritant or systemic effects were reevaluated by a probit analysis 

 procedure. The procedure was based on the assumption that mortality 

 response, when plotted against the logarithm of the concentration or the 

 logarithm of the exposure time, had the shape of a cumulative normal 

 distribution. Using the method of Maximum Likelihood, regression 

 coefficients were derived from the raw data. Results were tested against 

 Haber's rule, which states that mortality response depends on the product 

 of the exposure concentration and exposure time, both to the first power. 

 Values of the regression coefficients for each chemical and for each 

 animal species tested were tabulated. Only two compounds, 

 hydrogen-chloride (7647010) and dibutylhexamethylenediamine, obeyed 

 Haber's rule. A concentration time product in which the concentration was 

 raised to an exponent other than 1.0 fit the data well. For example, the 

 mortality response of hydrogen-sulfide (7783064) was best expressed by 

 raising the concentration to the 2.2 power. The authors note that the 

 data indicate that mice are more sensitive than other mammals. 

 Experiments using mice probably do not provide an appropriate basis for 

 predicting quantitatively the mortality response in humans. 

464 

TITLE: 

 Toxicology: Relationship to Occupational Health Nursing 

AUTHORS: 

 Kilburn GG 

SOURCE: 

 Proceedings of the National Occupational Health Nursing Symposium: State 

 of the Art and Directions for the Future, Cincinnati, Ohio, June 1-3, 

 1983, I. A. Horvitz, Editor; Cincinnati, Ohio, NIOSH, pages 139-141, 

 19871987 

ABSTRACT: 

 Toxicology and its relationship to occupational health nursing were 

 discussed. Toxicology is defined as the study of the adverse effects of 

 chemical and physical agents on a biological system. Toxicity refers to 

 the ability of a substance to cause injury to a biological tissue or 

 system. Inhalation, skin absorption, and ingestion are the most common 

 routes of entry of chemical toxins into the body. More than half of the 

 deaths attributed to industrial toxins are due to respiratory failure. 

 Although the lungs are frequently the target organ for industrial toxins, 

 they also provide entry for substances that can cause injury to other 

 organs, such as the liver and kidney. Factors important in influencing 

 respiratory exposure include particle size and solubility of the inhaled 

 substance in body fluids. Sources of information about chemical exposures 

 useful to occupational health nurses were discussed. The major source of 

 information is considered to be the worker himself. In emergency 

 situations, it is considered imperative to know exactly what the worker 

 was exposed to so that appropriate treatment can be given. Material data 

 sheets are also sources of information. Identifying an occupational 

 illness depends on obtaining a work history, clinical testing, and a 

 physical examination. Clinical signs of exposure to a variety of chemical 

 agents including carbon-monoxide (630080), organophosphates, lead 

 (7439921), mercury (7439976), organic solvents, formaldehyde (50000), and 

 hydrogen-sulfide (7783064) were summarized. 

465 

TITLE: 

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 Acute Intoxications during Work 

AUTHORS: 

 de Kort WL 

 Sangster B 

SOURCE: 

 Veterinary and Human Toxicology, Vol. 30, No. 1, pages 9-11, 2 references, 

 19881988 

ABSTRACT: 

 An attempt was made to evaluate the occurrence of acute intoxications in 

 the work environment in the Netherlands. Acute intoxication was defined 

 as the occurrence of unwanted health effects resulting from exposure to 

 chemicals. Exposure had to be short lasting and effects had to occur 

 immediately or within a few hours or days. Of 6856 calls made to the 

 Netherlands Poison Control Center (NPCC) during the 12 year time period of 

 study, 301 incidents occurred in a work situation and involved 385 men and 

 21 women. Most often pesticides, lung irritants, and solvents were 

 involved, accounting for 51 percent of calls. The primary contact site in 

 54 percent was the respiratory tract; it was the skin in 27 percent. 

 Occupations frequently involved included agricultural and market gardening 

 sectors and the public authorities, mainly police, fire brigade, local 

 authority employees and defense workers, together accounting for about 30 

 percent of incidents. During 1984 the Directorate General of Labour 

 received 58,070 industrial accident reports, 0.73 percent (395 incidents) 

 of which involved chemical substances. Usually corrosive substances, 

 detergents and disinfectants, and solvents were involved. Dermal contact 

 occurred first in 53 percent of cases, eyes in 33 percent, and respiratory 

 tract in 14 percent. Eight of these reports overlapped with reports to 

 the NPCC. Five deaths were reported, one from hydrogen-cyanide (74908), 

 one from carbon-dioxide (124389), and three from hydrogen-sulfide 

 (7783064). Statistics from the Center for Health Care Information (CHCI) 

 and the Occupational Health Service also indicated corrosive substances, 

 cleaning agents, asphyxiants, solvents, and lung irritant gases as causes. 

 Fourteen deaths occurred among 477 relevant hospitalization reports to the 

 CHCI, although occupational cause was not established. The authors 

 conclude that there is considerable underreporting in official statistics 

 for work related acute intoxications. 

466 

TITLE: 

 The toxicity of hydrogen sulphide and other sulphides. 

AUTHORS: 

 Evans CL 

SOURCE: 

 Q J Exp Physiol Cogn Med Sci. 1967, Jul; 52(3):231-48. [Quarterly journal 

 of experimental physiology and cognate medical sciences] 

467 

TITLE: 

 Nephrotoxicity of Mercapturic Acids of Three Structurally Related 

 2,2-Difluoroethylenes in the Rat. Indications for Different Bioactivation 

 Mechanisms 

AUTHORS: 

 Commandeur JNM 

 Brakenhoff JPG 

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 de Kanter FJJ 

 Vermeulen NPE 

SOURCE: 

 Biochemical Pharmacology, Vol. 37, No. 23, pages 4495-4504, 37 references, 

 19881988 

ABSTRACT: 

 The nephrotoxic effects of the mercapturic acids of tetrafluoroethylene 

 (116143) (TFE), 1,1-dichloro-2,2-difluoroethylene (79356) (DCDFE), and 

 1,1-dibromo-2,2-difluoroethylene (430853) (DBDFE) were compared with 

 regard to dose dependent relationships and the influence of beta halogen 

 substitution. Male Wistar-rats were given intraperitoneal injections of 

 mercapturic acids of the N-acetyl-cysteine (NAC) conjugates of TFE, DCDFE, 

 or DBDFE at doses of 25, 50, 75, and 100 micromoles per kilogram body 

 weight (micromol/kg) and maintained in metabolism cages for 48 hours post 

 treatment for assessment of urinary toxicochemical parameters. The 

 animals were sacrificed at 48 hours for blood analysis, measurement of 

 kidney to body weight ratios, and assessment of the in-vitro metabolism of 

 the cysteine conjugates and dihaloacetic acids in renal cytosolic 

 preparations. Treatment with the mercapturic acids of TFE-NAC, DCDFE-NAC, 

 and DBDFE-NAC produced significant increases in plasma urea, urinary 

 protein, urinary glucose, and relative kidney weights. Kidney toxic 

 actions were first apparent at doses of 50, 75, and 100micromol/kg for 

 TFE-NAC, DCDFE-NAC, and DBDFE-NAC respectively. Urine analysis by gas 

 chromatography mass spectrometry revealed considerable amounts of 

 difluoroacetic-acid (DFAA) in animals treated with TFE-NAC, but the 

 corresponding halogenated acetic acids were not observed in the urine of 

 rats treated with either DCDFE-NAC or DBDFE-NAC. The incubation of rat 

 kidney cytosolic preparations with TFE, DCDFE, and DBDFE yielded 

 significant quantities of pyruvic-acid, indicative of metabolism by 

 cytosolic beta-lyase. Incubation with TFE but not DCDFE or DBDFE also 

 produced significant amounts of hydrogen-sulfide, thiosulfate, and DFAA. 

 The results were discussed in relation to possible bioactivation 

 mechanisms for kidney damage and fluoride ion excretion. 

468 

TITLE: 

 [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] 

AUTHORS: 

 Kamiński M 

 Mikolajczyk P 

SOURCE: 

 Med Pr. 1967; 18(1):42-6. [Medycyna pracy] 

469 

TITLE: 

 Chemical Hazards to Agricultural Workers 

AUTHORS: 

 Shaver CS 

 Tong T 

SOURCE: 

 Occupational Medicine: State of the Art Reviews, Vol. 6, No. 3, pages 

 391-413, 87 references, 1991 

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ABSTRACT: 

 Potential chemical hazards to agricultural workers were reviewed. 

 Potential hazards associated with fertilizer use were considered. 

 Problems associated with applying anhydrous ammonia (7664417) were 

 discussed. Vaporization of anhydrous ammonia can cause freezing burns of 

 the skin and eyes. Aqueous solutions can cause severe burns of the skin, 

 mucous membranes, and eyes. Inhalation can cause respiratory distress 

 syndrome, bronchiolitis obliterans, and chronic bronchiectasis. Problems 

 associated with groundwater contamination by nitrate fertilizers were 

 considered. Potential exposures associated with using and repairing farm 

 equipment were discussed. These included exposure to fuel, organic 

 solvents, paint thinners and strippers, and metal fumes as a result of 

 welding. Potential hazards presented by sterilization and fumigation of 

 agricultural products were reviewed. Common fumigants and sterilants 

 include a number of compounds having significant toxicity such as 

 halogenated hydrocarbons, epoxides, aldehydes, hydrogen-cyanide (74908), 

 coumarins, and indandiones. Feed associated illnesses were summarized. 

 Bronchiolitis obliterans induced by exposure to nitrogen oxides formed by 

 fermentation of feeds stored in silos under anaerobic conditions was 

 mentioned. Animal confinement hazards included exposure to ammonia, 

 carbon-monoxide (630080), carbon-dioxide (124389), methane (74828), 

 hydrogen-sulfide (7783064), toxic dusts from animal dander and fecal 

 material, and microorganisms. Acute and chronic pulmonary problems were 

 the most common health effects associated with animal confinement. 

 Pesticide contamination on farms was discussed. Most acute pesticide 

 poisonings resulted from improper use of organophosphates and carbamates. 

 Treatments for pesticide poisoning were summarized. Preventing chemical 

 related occupational diseases in farmers was discussed. These include 

 preventive, personal protective, and decontamination procedures, which 

 were outlined. 

470 

TITLE: 

 Hydrogen sulfide intoxication. Review of the literature and report of 

 unusual accident resulting in two cases of nonfatal poisoning. 

AUTHORS: 

 MILBY TH 

SOURCE: 

 J Occup Med. 1962, Aug; 4:431-7. [Journal of occupational medicine. : 

 official publication of the Industrial Medical Association] 

471 

TITLE: 

 Sulfide enhancement of PMN apoptosis. 

AUTHORS: 

 Mariggiò MA 

 Minunno V 

 Riccardi S 

 Santacroce R 

 De Rinaldis P 

 Fumarulo R 

SOURCE: 

 Immunopharmacol Immunotoxicol. 1998, Aug; 20(3):399-408. 

 [Immunopharmacology and immunotoxicology] 

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ABSTRACT: 

 Hydrogen sulfide is a toxic metabolite released by several bacterial 

 agents under anaerobic conditions. In the present paper, we investigated 

 the effects of sulfide on polymorphonuclear cell (PMN) apoptosis, a 

 mechanism suggested for limiting the toxic potential of neutrophils in 

 inflammatory sites. We showed that 1 mM sulfide (concentration not 

 conditioning PMN viability) is able to enhance the apoptotic fate of human 

 granulocytes by increasing: i) the number of cells containing pyknotic 

 nuclei, ii) the internucleosomal cleavage, and, iii) the intensity of 

 tubulin immunofluorescence staining. The sulfide effect is partially 

 prevented by ionomycin and this finding is consistent with the hypothesis 

 of the inhibiting role played by high levels of cytosolic calcium in PMN 

 apoptosis modulating. 

472 

TITLE: 

 Gases 

AUTHORS: 

 Becker CE 

SOURCE: 

 Occupational Medicine, J. LaDou, Editor; Appleton and Lange, Norwalk, 

 Connecticut, pages 432-442, 18 references, 1990 

ABSTRACT: 

 This chapter reviewed the noxious gases that pose health risks to humans. 

 Gases and fumes can pose a hazard of injury to the lung in five different 

 ways, and each of the mechanisms was discussed. The asphyxiant noxious 

 gases carbon-dioxide (124389), methane (74828), and nitrogen (7727379) 

 simply displace oxygen from inspired air and cause asphyxia. The chemical 

 asphyxiants carbon-monoxide (630080), cyanide (57125), and 

 hydrogen-sulfide (7783064) may be absorbed into the systemic circulation, 

 interfering with the process of oxygen transport and utilization. The 

 systemic toxicants arsine (7784421), phosphine (7803512), paraquat 

 (4685147), metal fumes, cause systemic toxicity without affecting oxygen 

 delivery. The irritant noxious gases chlorine (7782505), ammonia 

 (7664417), formaldehyde (50000), hydrogen-fluoride (7664393), and ozone 

 (10028156) cause direct respiratory tract irritation or injury. The 

 allergic lung reactions may damage the lung directly or impair gaseous 

 exchange. 

473 

TITLE: 

 [On the mechanism of the toxic effect of hydrogen sulfide.] 

AUTHORS: 

 ZBURZHINSKII VK 

SOURCE: 

 Gig Sanit. 1962, Jul; 27:64-7. [Gigiena i sanitariia] 

474 

TITLE: 

 Gases, Vapors, Liquids, and Drugs 

AUTHORS: 

 Popendorf W 

SOURCE: 

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 Papers and Proceedings of the Surgeon General's Conference on Agricultural 

 Safety and Health, April 30-May 3, 1991, Des Moines, Iowa, M. L. Myers, R. 

 F. Herrick, S. A. Olenchock, J. R. Myers, J. E. Parker, D. L. Hard, and 

 K. Wilson, Editors; -=NIOSH, U.S. Depar, 1992 

ABSTRACT: 

 Some toxic agricultural liquids, gases and vapors, their sources on the 

 farm, and some of the limitations of controlling these hazards either at 

 their source, along the pathway of the exposure route, or at the receiver, 

 were reviewed. Sources of agricultural toxicity included ammonia 

 (7664417), carbon-dioxide (124389), carbon-monoxide (630080), 

 hydrogen-sulfide (7783064), nitrogen-dioxide (10102440), oxygen depletion, 

 pesticides, welding, fuel storage, fuel and waste oil, liquified propane 

 (74986) gas, and liquified anhydrous ammonia. Pesticides commonly used 

 include organophosphates, carbamates, and organochlorines. Herbicides 

 frequently encountered included phenoxy-aliphatic acids, bipyridyls, and 

 triazines. Thiocarbamates were frequently used as fungicides along with 

 dicarboximides. Exposure to veterinary drugs on the farm causes risk of 

 either accidental inoculation or splashing of the product into the eyes, 

 mucous membrane or broken skin. The author urges that anticipation, 

 recognition, evaluation and control of hazards in the agricultural 

 community become more of a priority. 

475 

TITLE: 

 [On changes in the oxygen requirement of the organism under the influence 

 of hydrogen sulfide.] 

AUTHORS: 

 SINITSYN SN 

SOURCE: 

 Farmakol Toksikol. 1962 May-Jun; 25:364-5. [Farmakologiia i toksikologiia] 

476 

TITLE: 

 Other Important and Widely Encountered Chemicals 

AUTHORS: 

 Cowell J 

 Johnston D 

 Zenz C 

 Beaumont JJ 

 Cordasco EM 

 Hogstedt C 

 Petsonk EL 

 Poitrast BJ 

 Schutte NP 

 Stayner L 

 Ward E 

SOURCE: 

 Occupational Medicine, Third Edition, C. Zenz, O. B. Dickerson, and E. P. 

 Horvath, Jr., Editors; Mosby-Year Book, Inc., St. Louis, pages 661-718, 

 501 references, 1994 

ABSTRACT: 

 The production, uses, and health effects of chemical agents widely used in 

 diverse, small workshops were reviewed. Due to expanding technology the 

 production of new materials has been rapidly increasing thereby raising 

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 the number of workers potentially exposed to hazardous agents. The 

 toxicity, occupational exposures to, medical treatment of, and exposure 

 prevention of commonly used agents were described. These agents included 

 ammonia (7664417), chlorine (7782505) and its compounds, hydrogen-fluoride 

 (7664393), hydrogen-sulfide (7783064), nitric-acid (7697372), 

 nitrogen-dioxide (10102440), nitrogen-oxide (10024972), sulfuric-acid 

 (7664939), hydrogen-cyanide (74908) and cyanide salts, sodium-hydroxide 

 (1310732), sulfur-dioxide (7446095), formaldehyde (50000), ozone 

 (10028156), ethylene-glycol-dinitrate (628966), nitroglycerin (55630), 

 hydrazines, methyl-isocyanate (624839), phosgene (75445), phosphorus 

 (7723140) and its compounds, phosphoric-acid (7664382), alpha-chlorinated 

 toluenes, polybrominated biphenyls, polychlorinated biphenyls, naphthalene 

 (91203), polychlorinated naphthalenes, 2-nitropropane (79469), o-toluidine 

 (95534), benzidine derived dyes, chloroethanes, cresols, disulfiram 

 (97778), ethyl-ether (60297), monohalomethanes, amines, vinyl-acetate 

 (108054), and petroleum based solvents. 

477 

TITLE: 

 [Data for the establishment of permissible concentrations of hydrogen 

 sulfide in air.] 

AUTHORS: 

 TUAN FJ 

SOURCE: 

 Gig Sanit. 1959, Oct; 24:12-7. [Gigiena i sanitariia] 

478 

TITLE: 

 meso-2,3-Dimercaptosuccinic Acid Mono-N-Alkylamides: Syntheses and 

 Biological Activity as Novel in Vivo Cadmium Mobilizing Agents 

AUTHORS: 

 Singh PK 

 Jones MM 

SOURCE: 

 Chemical Research in Toxicology, Vol. 9, No. 6, pages 965-969, 25 

 references, 1996 

ABSTRACT: 

 Three meso-2,3-dimercaptosuccinic-acid mono-N-alkylamides were prepared 

 via a synthetic route using the sulfhydryl (SH) protected anhydride in an 

 effort to determine whether the monoamides might be more effective and 

 less toxic than the monoesterase cadmium (7440439) mobilizing agents. In 

 the preparation, 

 2,2-dimethyl-1,3-dithiolane-4,5-cis-dicarboxylic-acid-anhydride was opened 

 up with the corresponding amine to produce the SH protected monoamide. 

 Deblocking of the vicinal dithiol functionality was achieved by converting 

 the dithiolane into the mercury complex followed by reaction with 

 hydrogen-sulfide to produce the target molecule. The cadmium mobilizing 

 efficacy of the compounds was tested in-vivo in cadmium loaded female 

 albino-rats. N-Benzyl-D-glucamine-N-carbodithioate was used as the 

 standard drug. The new compounds were equally or more effective than the 

 standard drug at decreasing hepatic cadmium retention, while mostly less 

 effective in decreasing renal cadmium. Even though the new compounds were 

 shown to be effective as cadmium mobilizing agents, the specific compounds 

 examined did not possess optimized structures in terms of the balance 

 between effectiveness and toxicity. 

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479 

TITLE: 

 [Poisoning by hydrogen sulfide. Its effective treatment with ACTH.] 

AUTHORS: 

 REMOLAR JM 

 MULLER FE 

SOURCE: 

 Prensa Med Argent. 1959, Mar 20; 46:693-7. [Prensa medica argentina] 

480 

TITLE: 

 [How to avoid poisoning due to losses of hydrogen sulfide in analytical 

 laboratories.] 

AUTHORS: 

 PAOLI AR 

SOURCE: 

 Sem Med. 1959, Sep 17; 115:460-71. [La Semana medica] 

481 

TITLE: 

 [Exposure to carbon disulfide and hydrogen sulfide in the manufacture of 

 rayon by the viscose process in the state of Sao Paulo.] 

AUTHORS: 

 RIBEIRO BA 

 STETTINER HM 

 BEDRIKOW B 

 LAMBERT MI 

SOURCE: 

 Arq Fac Hig Saude Publica Univ Sao Paulo. 1959, Jun; 13:219-41. [Arquivos 

 da Faculdade de Higiene e Saude Publica da Universidade de Sao Paulo] 

482 

TITLE: 

 Abnormal features of Macoma balthica (Bivalvia) in the Baltic Sea: 

 alerting symptoms of environmental adversity? 

AUTHORS: 

 Sokołowski A 

 Wołowicz M 

 Hummel H 

 Smolarz-Górska K 

 Fichet D 

 Radenac G 

 Thiriot-Quiévreux C 

 Namieśnik J 

SOURCE: 

 Mar Pollut Bull. 2004, Jul; 49(1-2):17-22. [Marine pollution bulletin] 

ABSTRACT: 

 Recent studies of the Baltic clam Macoma balthica (L.) from the southern 

 Baltic (the Gulf of Gdansk) have revealed striking morphological, 

 histological and cytogenetic features. Strong deformation of the shell, 

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 including elongation of the posterior end and the appearance of an easily 

 visible flexure in this part, has been recorded. The population 

 contribution of the deformed blunt shelled ("irregular") clams 

 ranged from 0% to 65% and tended to increase with depth. The 

 morphologically "irregular" clams had higher accumulated tissue 

 concentrations of trace metals (As, Ag, Cd, Pb, Cu and Zn), indicating a 

 different metal handling ability. Adverse conditions in deeper water 

 regions of the Gulf (e.g. hypoxia, hydrogen sulphide, elevated 

 bioavailability of contaminants) have been suggested as inducers of the 

 phenotypical changes (morphological deformation) in part of the population 

 and, in parallel, of the specific physiological adaptations that result in 

 higher metal accumulation in the "irregular" clams. Cytogenetic 

 and histological analyses showed the presence of tumours in gill cells and 

 digestive system of the affected clams, the prevalence of disseminated 

 neoplasia ranging from 0% to 94% depending on the site. The disease was 

 manifested by a modified karyotype (i.e. an abnormal number and morphology 

 of chromosomes), a higher activity of nucleolar organizer regions 

 (AgNORs), and tissue lesions (enlarged cells, actively proliferative with 

 pleomorphic nuclei). Bottom sediments showed acute toxicity and have been 

 proposed as a source of an initialising carcinogenic factor. However, none 

 of the ecotoxicological studies provided was successful in the clear 

 demonstration of a single (or multifactorial) agent that can account for 

 the disseminated neoplasia. 

483 

TITLE: 

 Mammalian cysteine metabolism: new insights into regulation of cysteine 

 metabolism. 

AUTHORS: 

 Stipanuk MH 

 Dominy JE Jr 

 Lee JI 

 Coloso RM 

SOURCE: 

 J Nutr. 2006, Jun; 136(6 Suppl):1652S-1659S. [The Journal of nutrition] 

ABSTRACT: 

 The mammalian liver tightly regulates its free cysteine pool, and 

 intracellular cysteine in rat liver is maintained between 20 and 100 

 nmol/g even when sulfur amino acid intakes are deficient or excessive. By 

 keeping cysteine levels within a narrow range and by regulating the 

 synthesis of glutathione, which serves as a reservoir of cysteine, the 

 liver addresses both the need to have adequate cysteine to support normal 

 metabolism and the need to keep cysteine levels below the threshold of 

 toxicity. Cysteine catabolism is tightly regulated via regulation of 

 cysteine dioxygenase (CDO) levels in the liver, with the turnover of CDO 

 protein being dramatically decreased when intracellular cysteine levels 

 increase. This occurs in response to changes in the intracellular cysteine 

 concentration via changes in the rate of CDO ubiquitination and 

 degradation. Glutathione synthesis also increases when intracellular 

 cysteine levels increase as a result of increased saturation of 

 glutamate-cysteine ligase (GCL) with cysteine, and this contributes to 

 removal of excess cysteine. When cysteine levels drop, GCL activity 

 increases, and the increased capacity for glutathione synthesis 

 facilitates conservation of cysteine in the form of glutathione (although 

 the absolute rate of glutathione synthesis still decreases because of the 

 lack of substrate). This increase in GCL activity is dependent on 

 up-regulation of expression of both the catalytic and modifier subunits of 

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 GCL, resulting in an increase in total catalytic subunit plus an increase 

 in the catalytic efficiency of the enzyme. An important role of cysteine 

 utilization for coenzyme A synthesis in maintaining cellular cysteine 

 levels in some tissues, and a possible connection between the necessity of 

 controlling cellular cysteine levels to regulate the rate of hydrogen 

 sulfide production, have been suggested by recent literature and are areas 

 that deserve further study. 

484 

TITLE: 

 Toxic gases. 

AUTHORS: 

 Mitchell CS 

 Kuhnen AE 

 Dailey VA 

 Weaver VM 

 Schwartz BS 

SOURCE: 

 Reproductive Hazards of the Workplace 1998;:276-88 

485 

TITLE: 

 Effect of cadmium, copper and mercury on antioxidant enzyme activities and 

 lipid peroxidation in the gills of the hydrothermal vent mussel 

 Bathymodiolus azoricus. 

AUTHORS: 

 Company R 

 Serafim A 

 Bebianno MJ 

 Cosson R 

 Shillito B 

 Fiala-Médioni A 

SOURCE: 

 Mar Environ Res. 2004 Aug-Dec; 58(2-5):377-81. [Marine environmental 

 research] 

ABSTRACT: 

 Metals are known to influence lipid peroxidation and oxidative status of 

 marine organisms. Hydrothermal vent mussels Bathymodiolus azoricus live in 

 deep-sea environments with anomalous conditions, including high metal 

 concentrations. Although B. azoricus are aerobic organisms they possess 

 abundant methano and thioautotrophic symbiotic bacteria in the gills. The 

 enzymatic defences (superoxide dismutase (SOD), catalase (CAT), total 

 glutathione peroxidase (Total GPx) and selenium-dependent glutathione 

 peroxidase (Se-GPx)) and lipid peroxidation were determined in the gills 

 of B. azoricus exposed to Cd (0.9 microM), Cu (0.4 microM) and Hg (0.1 

 microM) with different times of exposure. The experiments were performed 

 in pressurized containers at 9+/-1 degrees C and 85 bars. Results show 

 that vent mussels possess antioxidant enzymatic protection in the gills. 

 Cd and Cu had an inhibitory effect in the enzymatic defence system, 

 contrarily to Hg. These enzymatic systems are not completely understood in 

 the B. azoricus, since reactive oxygen species might be produced through 

 other processes than natural redox cycling, due to hydrogen sulphide and 

 oxygen content present. Also the symbiotic bacteria may play an important 

 contribution in the antioxidant protection of the gills. 

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486 

TITLE: 

 Final Performance Report for Ventilation Control To Reduce Airborne 

 Contaminants. 

AUTHORS: 

 O'Shaughnessy PT 

 Thorne PS 

 Donham KJ 

 Smith TF 

 Hoff SJ 

SOURCE: 

 Govt Reports Announcements & Index (GRA&I), Issue 25, 2003 

ABSTRACT: Final rept. 1 Apr 99-31 Mar 02. 

 Studies have shown conclusively that airborne contaminant levels in swine 

 confinements are typically of a sufficient level to pose a health hazard 

 to workers in that occupation. In addition to a particulate component that 

 can reach levels of 26 mg/m, gases present in confinements in high amounts 

 include methane, hydrogen sulfide, ammonia, and carbon dioxide. Recognized 

 respiratory diseases of swine farmers include upper airway inflammation, 

 an asthma-like syndrome, and chronic airflow limitations. Ventilation 

 systems associated with swine confinements are largely designed a 

 comfortable climate for the pigs. However, because confinements are 

 operated on a for-profit basis, costs associated with operating the 

 ventilation system are typically kept to a minimum by minimizing fan 

 usage, which results in maintaining high airborne contaminant levels. This 

 research involved the analysis of continuous readings of two environmental 

 parameters, temperature and relative humidity, and air quality parameters, 

 airborne dust and ammonia, relative to measurements taken by sampling 

 methods. 

487 

TITLE: 

 Characterization of Emissions from Motor Vehicles Designed for Low N0x 

 Emissions 

AUTHORS: 

 Smith LR 

SOURCE: 

 Govt Reports Announcements &amp; Index (GRA&I), Issue 12, 1981 

ABSTRACT: 

 TD3: Tailpipe emissions were characterized for four advanced low NOx 

 catalyst equipped passenger cars under a variety of cyclic driving 

 conditions. All of the vehicles had three-way catalysts, three with 

 feedback carburetors and exhaust gas recirculation, and two with oxidation 

 catalysts following the three-way catalysts. The emission rates of several 

 unregulated pollutants including aldehydes, organic amines, sulfur 

 dioxide, nitrous oxide, several individual hydrocarbons (including 

 benzene), hydrogen sulfide, cyanide, organic sulfides, nickel carbonyl, 

 ammonia, sulfate, trace metals, and N-nitrosodimenthylamine were 

 determined. Additionally, the emission rates of the regulated pollutants, 

 total hydrocarbons, carbon monoxide, and oxides of nitrogen were 

 determined along with carbon dioxide and oxygen. Using three test fuels of 

 varying sulfur content, the emissions were examined at an initial mileage 

 and at 5,000-mile intervals to 15,000 miles. Using a toxicity criteria, 

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 the most significant emissions 

488 

TITLE: 

 Hazardous materials section 

AUTHORS: 

 ANON 

SOURCE: 

 Dangerous Properties of Industrial Materials Reports July-Aug. 1981, 

 Vol.1, No.6, p.15-96. Illus. Bibl. 

ABSTRACT: 

 This section provides nomenclature, physical and chemical data, 

 computerised structural formulas and new toxicity and hazard information 

 about abietic acid, acetic anhydride, adiponitrile, aflatoxin G1, 

 americium, ammonium ferrocyanide, ammonium sulfate, arsenic, barium 

 carbonate, barium chloride, barium cyanide, barium hydroxide, barium 

 nitrate, beryllium chloride, butyl mercaptan, cadmium, chloramine-T, 

 chlorosulfonic acid, m-cresol, 2,2'-dichloroethyl ether, 

 2,4-dichlorophenoxyacetic acid, diisobutyl ketone, ethylene glycol, ehtyl 

 ether, ferbam, heptane, hexane, hydrocyanic acid, hydrofluoric acid, 

 hydrogen peroxide, hydrogen sulfide, isodecanol, indole, iron, isoprene, 

 isopropyl acetone, lactic acid, lead fluoborate, lithium chloride, 

 magnesium, magnesium sulfate, malathion, maltose, m-nitrophenol, phenyl 

 methyl ketone, beta-propiolactone, crystalline and amorphous silica. 

489 

TITLE: 

 Dose-Response Relationships of Acute Exposure to Sulfur Dioxide. 

AUTHORS: 

 Englehardt FR 

 Holliday MG 

SOURCE: 

 Govt Reports Announcements &amp; Index (GRA&I), Issue 14, 1983 

ABSTRACT: 

 TD3: Acute toxicity effects of sulphur dioxide are reviewed, and the 

 derivation of a dose-lethality curve (presented as LC sub 50 vs. time) for 

 human exposure to sulphur dioxide is attempted for periods ranging from 

 ten seconds to two hours. As an aid to assessment of the hazards involved 

 in operating heavy water manufacturing facilities, the fact that sulphur 

 dioxide would be produced by the combustion of hydrogen sulphide was 

 briefly considered in an appendix. It is suggested that sulphuric acid, a 

 much more toxic substance than sulphur dioxide, may also be formed in such 

 an event. It is concluded, therefore, that an overall hazard evaluation 

 may have to address the contributory effects of sulphuric acid. (Atomindex 

 citation 13:659414) 

490 

TITLE: 

 Hydrogen sulfide generation and detection system 

AUTHORS: 

 Ackley MW 

SOURCE: 

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 American Industrial Hygiene Association Journal July 1983, Vol.44, No.7, 

 p.475-479. Illus. 12 ref. 

ABSTRACT: 

 This dynamic system can be used for calibration at low (1-26ppm) and high 

 (0.05-2%) concentrations. A HNU photoionisation analyser is used for 

 measuring H[2]S concentrations. The low concentration configuration uses a 

 syringe pump to control the H[2]S/air mixture ratio. The high 

 concentration mixture is controlled by calibrated mass flowmeters for 

 H[2]S and air. Interfering moisture is removed by a drying train using 

 hygroscopic ion exchange membranes. This system can be used to test the 

 efficiency of H[2]S removal by various granular sorbents, to evaluate 

 passive dosimeters and sorbent tubes, to measure respirator cartridge or 

 canister breakthrough times, and for toxicity testing. 

491 

TITLE: 

 Arsine in air - Colorimetric field method using silver 

 diethyldithiocarbamate in the presence of excess silver nitrate 

SOURCE: 

 Health and Safety Executive, Health and Safety Executive Sales Point, St. 

 Hugh's House, Stanley Precinct, Bootle, Merseyside L20 3QZ, United 

 Kingdom, Dec. 1983. 4p. 6 ref. 

ABSTRACT: 

 Occurrence, toxicity and first-aid information are given for arsine. 

 Determination method: sampling through a midget impinger containing a 

 solution of silver diethyldithiocarbamate, with an excess of silver 

 nitrate, in pyridine. The magenta-coloured complex produced is compared 

 with coloured standards. A lead acetate-impregnated cotton-wool filter 

 traps hydrogen sulfide, preventing its interference. Scope: suitable for 

 field use in all circumstances where the release of arsine is suspected. 

 Analytical limits: 0.025-0.1ppm (with sampling at 1L/min over 10min), 

 greater sensitivity for longer sampling times. Accuracy: |0.025ppm. Some 

 substances react with the reagent, but the colours produced are different 

 from that of the arsine complex. 

492 

TITLE: 

 Safe handling of hazardous chemicals 

AUTHORS: 

 Rohatgi AK 

SOURCE: 

 J.K. Enterprises, 13, New Nandu Industrial Estate, Mahakali Caves Road, 

 Andheri (East), Bombay 400 093, India, 1986. 372p. Illus. 83 ref. 

ABSTRACT: 

 This detailed manual provides information on physical and chemical 

 properties (including lists of safety reminders presented in a 

 point-by-point format), toxicity, symptoms of poisoning and first aid 

 connected with 21 common industrial chemicals: chlorine, ammonia, sulfur 

 dioxide, phosgene, hydrogen cyanide, hydrogen sulfide, bromine, carbon 

 monoxide, hydrogen fluorine, ethylene oxide, butadiene, benzene, methyl 

 bromide, vinyl chloride, ethyl alcohol, acetylene, caustic soda, sulfuric 

 acid, hydrochloric acid, nitric acid, phosphoric acid. There are also 

 chapters devoted to: personal respiratory protection; cylinders used for 

 hazardous chemicals; recommendations for the safe handling of such 

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 cylinders; hazardous chemicals in bulk storage tanks (handling and 

 storage); leak detection, neutralisation and disposal; emergencies and 

 their management; transportation of hazardous chemicals; release 

 calculations; prevention of emergencies and disasters; emergency control 

 and disaster planning. Relevant Indian laws and regulations are cited 

 throughout. Labelling requirements. 

493 

TITLE: 

 Treatment of acute and chronic poisoning in agriculture and industry 

SOURCE: 

 Fondazione Carlo Erba, Sezione di Medicina del Lavoro e Igiene Ambientale, 

 Via Cino del Duca 8, 20122 Milano, Italy, 1987. 110p. Illus. Bibl. 

ABSTRACT: 

 Proceedings of a meeting held at Milan (Italy), 21 Feb. 1986. Papers: role 

 of poison centres in providing first aid for poisoning in the workplace; 

 first aid in agriculture for pesticide poisoning; first aid in industry 

 for poisoning by cyanides, nitriles or hydrogen sulfide; first aid for 

 poisoning by carbon monoxide nitrous fumes, arsine or freons; antidotes; 

 special detoxification methods; treatment of metal poisoning by chelating 

 agents; treatment of metallic mercury poisoning; treatment of poisoning by 

 mercury fumes and by organic and inorganic mercury compounds; two case 

 studies of treatment of acute lead poisoning; treatment of thallium 

 poisoning; treatment of poisoning by solvents; the role of poison centres 

 in the acquisition of data on human toxicology. Information on toxicity 

 and symptoms is provided for most substances discussed. A list of 

 addresses and telephone numbers of poison centres in Italy is appended. 

494 

TITLE: 

 Sodium sulfide 

AUTHORS: 

 ANON 

SOURCE: 

 Indian Chemical Manufacturing Association, India Exchange, India Exchange 

 Place, Calcutta 700 001, India, 1986. 1p. 

ABSTRACT: 

 Chemical safety information sheet. Toxicity: irritation of skin and 

 digestive tract; corrosive; decomposes to hydrogen sulfide and free 

 alkali. 

495 

TITLE: 

 Dosis-Wirkungsbeziehungen fuer phytotoxische Luftschadstoffe fuer die 

 keine Immissionswerte festgelegt sind. Entscheidungshilfen fuer die 

 Pruefung in Sonderfaellen (TA Luft, Nr. 2.2.1.3.). 

 (Dose-response-relationships for phytotoxic air pollutants, where no air 

 quality standards have been establishe 

AUTHORS: 

 Schulze E 

SOURCE: 

 Govt Reports Announcements &amp; Index (GRA&I), Issue 21, 1990 

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ABSTRACT: 

 TD3: Since 1983 'the Technical Instruction for maintaining air purity' has 

 required, in the case of plant construction permits, an examination of 

 whether potentially polluting substances for which no environmental 

 standards exist could cause adverse environmental effects. The available 

 scientific literature was reviewed and evaluated for 15 pollutant 

 substances: ammonia, chlorine gas, gaseous hydrochloric acid, ethylene, 

 formaldehyde, hydrogen sulphide, carbon disulphide, hydrogen cyanide, 

 tetrachlorethene, tetrachloroethylene, dichloroethene, trichloroethene, 

 trichloroethylene and the aromatics benzene, toluene and o-xylene. 

 Literature is available only for the first six; the results are summarized 

 in tables of effects scales (Tables 1-4 and 6). The most important biotic, 

 abiotic and anthropogenic factors to be taken into account when assessing 

 pollution risks are indicated. (orig.). (Copyright (c) 1990 by FIZ. 

 Citation no. 90:081342.) In German. With 97 refs., 6 tabs., 1 fig. 

496 

TITLE: 

 Simultaneous Gas-Chromatographic Determination of Four Toxic Gases 

 Generally Present in Combustion Atmospheres. 

AUTHORS: 

 Endecott BR 

 Sanders DC 

 Chaturvedi AK 

SOURCE: 

 Govt Reports Announcements &amp; Index (GRA&I), Issue 03, 1995 

ABSTRACT: 

 TD3: Measurement of combustion gases produced by burning aircraft cabin 

 materials poses a continuing limitation for smoke toxicity research. Since 

 toxic effects of gases depend on both their concentrations and duration of 

 exposures, frequent atmosphere sampling is necessary to define the 

 concentration-time curve. A gas chromatographic method was developed for 

 the simultaneous analyses of carbon monoxide (CO), hydrogen sulfide (H2S), 

 sulfur dioxide (SO2), and hydrogen cyanide (HCN). The method utilized an 

 MTI M200 dual-column gas chromatograph (GC) equipped with 4-m molecular 

 sieve-5A and 8-m PoraPlot-U capillary columns and two low-volume, 

 high-sensitivity thermal conductivity detectors. Detectability 

 (ppm)/retention times (seconds) for the gases were: CO (100/28); H2S 

 (50/26); SO2 (125/76); HCN (60/108). The method was effective for 

 determining these gases in mixtures and in the combustion atmospheres 

 generated by burning wool (CO, HCN, and H2S) and modacrylic (CO and HCN) 

 fabrics. Common atmospheri 

497 

TITLE: 

 General evaluation of risk associated with the use of pesticides and other 

 chemical substances on animal breeding and plant production farms 

AUTHORS: 

 Pomorska K 

SOURCE: 

 International Journal of Occupational Safety and Ergonomics 1999, Vol.5, 

 No.3, p.449-457. 17 ref. 

ABSTRACT: 

 The general characteristics of chemical risk on farms in Poland are 

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 presented. The paper describes the risk associated with the natural 

 occurrence of chemicals (such as ammonia and hydrogen sulfide) in the 

 process of animal breeding and the risk connected with the use of 

 artificial fertilizers and pesticides. Pesticides are briefly described 

 taking into consideration toxicity classes and toxic effects. Exposure to 

 pesticides is presented for individual methods and related activities. 

 Finally, the risk of exposure to pesticides in orchards and greenhouses is 

 discussed. 

498 

TITLE: 

 THE EFFECTS OF CHRONIC EXPOSURE TO SULFONATED HYDROGEN; THE EFFECT OF 

 CHRONIC EXPOSURE TO HYDROGEN SULFIDE (AND WITH CARBON DISULFIDE, WITH 

 COVER LETTER DATED 05/11/94 

SOURCE: 

 EPA/OTS; Doc #86940000854 

499 

TITLE: 

 The novel function of giant hemoglobins from tubeworms and annelids. 

AUTHORS: 

 ZAL F 

 GOTOH T 

 TOULMOND A 

SOURCE: 

 FIFTH INTERNATIONAL CONGRESS OF COMPARATIVE PHYSIOLOGY AND BIOCHEMISTRY, 

 CALGARY, ALBERTA, CANADA, AUGUST 23-28, 1999.YCOMPARATIVE BIOCHEMISTRY AND 

 PHYSIOLOGY PART A MOLECULAR & INTEGRATIVE PHYSIOLOGY; 124 (SUPPL.). 1999. 

 S16. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM THE NOVEL FUNCTION OF GIANT HEMOGLOBINS 

 FROM TUBEWORMS AND ANNELIDSYMEETING ABSTRACT ARENICOLA MARINA ALVINELLA 

 POMPEJANA PONTODRILUS MATSUSHIMENSIS RIFTIA PACHYPTILA LUMBRICUS 

 TERRESTRIS PERINEREIS AIBUHITENSIS HYDROGEN SULFIDE TOXICITY 

 DETOXIFICATION HEMOGLOBINS TOXICOLOGY FREE CYSTEINES 

500 

TITLE: 

 Air emissions from oilfield waste landfarm facilities. 

AUTHORS: 

 PARDUE JH 

 VALSARAJ KT 

 SHIN W 

SOURCE: 

 218TH NATIONAL MEETING OF THE AMERICAN CHEMICAL SOCIETY, PARTS 1 AND 2, 

 NEW ORLEANS, LOUISIANA, USA, AUGUST 22-26, 1999.YABSTRACTS OF PAPERS 

 AMERICAN CHEMICAL SOCIETY; 218 (1-2). 1999. ENVR 66. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. RRM AIR EMISSIONS FROM OILFIELD WASTE 

 LANDFARM FACILITIESYMEETING ABSTRACT POLLUTION TOXICOLOGY ENVIRONMENTAL 

 POLLUTION OILFIELD WASTE LANDFARM FACILITIES AIR POLLUTION VOLATILE 

 ORGANIC COMPOUNDS TOXICITY POLLUTANT HYDROGEN SULFIDE LANDFARM ACTIVITIES 

 ASSESSMENT AIR EMISSIONS LOUISIANA USA 

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501 

TITLE: 

 Treatment characteristics of high strength fermentation wastewater 

 consisting of high sulfate and ammonia by UAHB process. 

AUTHORS: 

 IMAI T 

 UKITA M 

 SEKINE M 

 NAKANISHI H 

 FUKAGAWA M 

SOURCE: 

 WATER SCIENCE AND TECHNOLOGY; 38 (8-9). 1998. 377-384. 

ABSTRACT: 

 BIOSIS COPYRIGHT: BIOL ABS. In this study, the formation process of 

 granules and treatment characteristics were discussed for an Upflow 

 Anaerobic Hybrid Blanket (UAHB) reactor, adding water absorbing polymer 

 particles (WAP) for treating a fermentation process wastewater consisting 

 of high sulfate and ammonia. Sulfide toxicity to methanogenic bacteria and 

 the TOC42- ratio that was usually used as an index of inhibition to 

 methanogenesis were also examined. The results indicated that the granules 

 could be developed in an UAHB process, in which a filter was installed in 

 the upper part of reactor and WAP were also added into inoculum, for 

 treating sulfide- and ammonia-rich wastewater, and inhibition caused by 

 sulfide did not occurred when free hydrogen sulfide concentration was less 

 than 200 mgl-1. Therefore, the UAHB process in the presence of adding WAP 

 was shown to have a better stability for treating the refractory 

 wastewater. The results also showed that total dissolved sulfide 

 concentration had 

502 

TITLE: 

 Simulation of constituent processes of anaerobic degradation of organic 

 matter by the "methane" model. 

AUTHORS: 

 Vavilin VA 

 Vasiliev VB 

 Rytov SV 

SOURCE: 

 Antonie Van Leeuwenhoek. 1996, Jan; 69(1):15-23. [Antonie van Leeuwenhoek] 

ABSTRACT: 

 The model of anaerobic digestion described earlier by the authors was used 

 for analysis of the different phases of the process. It was shown that at 

 the glucose conversion a coexistence of hydrogen-producing acidogenic 

 bacteria and hydrogen-utilizing non-methanogenic bacteria causes a 

 hydrogen partial pressure decrease at an increase of solids retention time 

 (i), the intensity of the negative feed-back effect in sulfate-reduction 

 through hydrogen sulfide formation is regulated by the pH level during an 

 oscillation dynamics in acetate/sulfate system (ii), under the toxicity 

 influence the processes of methanogenesis and acetogenesis together with 

 hydrolysis may be rate-limiting steps in the anaerobic system with 

 particulate substrate degradation (iii). 

503 

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TITLE: 

 Dimethylthioarsinic anhydride: a standard for arsenic speciation. 

AUTHORS: 

 Fricke M 

 Zeller M 

 Cullen W 

 Witkowski M 

 Creed J 

SOURCE: 

 Anal Chim Acta. 2007, Jan 30; 583(1):78-83. [Analytica chimica acta] 

ABSTRACT: 

 Dimethylthioarsinic acid (DMTA(V)) has recently been identified in 

 biological, dietary and environmental matrices. The relevance of this 

 compound to the toxicity of arsenic in humans is unknown and further 

 exposure assessment and metabolic studies are difficult to conduct because 

 of the unavailability of a well characterized standard. The synthesis of 

 DMTA(V) was accomplished by the reaction of dimethylarsinic acid (DMA(V)) 

 with hydrogen sulfide. The initial reaction product produced is DMTA(V) 

 but multiple products over the course of the reaction are also observed. 

 Therefore, a chromatographic separation was developed to monitor the 

 reaction progress via LC-ICP-MS. In this synthesis, conversion of DMA(V) 

 to DMTA(V) was not taken to completion to avoid the production of side 

 products. The product was isolated from the starting material by standard 

 organic techniques. Single crystal diffraction demonstrated that solid 

 DMTA(V) is present in the form of the oxygen-bridged dimethylthioarsinic 

 anhydride. Dissolution of the anhydride in water produces the acid form of 

 DMTA(V) and the aqueous phase DMTA(V) provided a characteristic molecular 

 ion of m/z 155 by LC-ESI-MS. The synthesis and isolation of 

 dimethylthioarsinic anhydride provides a stable crystalline standard 

 suitable for identification, toxicological study and exposure assessment 

 of dimethylthioarsinic acid. 

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