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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmkraft 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmas 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmtoxicological 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm(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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmthe 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm(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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmthe 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmpathophysiological 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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.

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTITLE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmppm 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm[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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm18

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmhydrogen 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmwarning 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmRussia)]

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmeconomic 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTITLE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmFischer-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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmphosphatase, 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm39

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmConcentration-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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTITLE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmvalue (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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmcontribute 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmrespiratory 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmEffects 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmalso 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htminclude 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmPersistent 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmunusually 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm65

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAmplitude 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmthought 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmthe 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAUTHORS: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmLi 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 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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. 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm79

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmMeleason 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 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmupper 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmPol 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTITLE: [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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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: 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmJ 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmNeurosci 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmof 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmPicone 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmchanges 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmsodium 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmblocked 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmconcentrations ( < 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmLPS-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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAlthough 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htma 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAUTHORS: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmbrain 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmactivity. 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm30- 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmNitrite 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAUTHORS: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmsub-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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmexhibited 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmand 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmStudy 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmevaluations 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTITLE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmwas 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTITLE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmCOS 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmPhysiologically, 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmpore 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmLewis 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmduring 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmcolumns 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmapproach 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm(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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmYadav 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmextensively 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmas 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] 

### Pa g e 96 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAUTHORS: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTITLE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmwall. 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm[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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmDvoriantseva 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmby 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htma 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmLutsky 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm204

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm206

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmBACKGROUND: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm(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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm85 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmFormation 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAUTHORS:
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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmKenesariev 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmgroup. 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAUTHORS: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmcontrol 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmreliability 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmIrritancy 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmdemonstration 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTITLE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm0.25-0.50 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmsulfide 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmsulfide. 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmMcCallan 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmanimals, 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmand 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmThe 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmcurves 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmHydrogen 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmexposure 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmacute 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmaction. 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmfield-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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm263

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmHANNAH 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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 

### Pa g e 140 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmcharacteristically 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTITLE: 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 

### Pa g e 142 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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 

### Pa g e 143 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmOSEID 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmlocated 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmbetween 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmeffects 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmcompared 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAUTHORS:
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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm294

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmat 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmIglesias 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAUTHORS:

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmOSBORNE 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmconcomitant 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmindicators 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm(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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmproduct-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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAUTHORS: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmpoisoning, 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmpig, 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 

### Pa g e 164 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmand 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. 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT:

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 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAUTHORS:

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: 

### Pa g e 167 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmGIG 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmChallenges. 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmelevated 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmand 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmCarbon-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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmcompletion 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmDifferential 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmproposed 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmrooms 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmGovt 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmalso 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTITLE:

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT:

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. 

### Pa g e 182 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAUTHORS:

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 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmsignificantly 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm365

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. 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm368

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 

### Pa g e 186 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm(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: 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmDrinker 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmToxic 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 

### Pa g e 189 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm(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. 

### Pa g e 190 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm377

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: 

### Pa g e 191 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmJ 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 

### Pa g e 192 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTREUTLER 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmof 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 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmN-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 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmtime 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: 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAEROBIC 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: 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmPULMONARY 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmGIDROBIOL 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 

### Pa g e 199 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTITLE:

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmKOUTINAS 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 

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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmLewis 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 

### Pa g e 202 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmSOURCE:
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: 

### Pa g e 203 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmBIOSIS 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 

### Pa g e 204 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmCARBON 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 

### Pa g e 205 of 245

9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmgas, 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm422

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmFOMINA 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmperoxidase 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTITLE: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm432

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm434

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAUTHORS:
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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmability 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmon 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAgricultural 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmecchymoses 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmHeinz 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmaccidental 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAUTHORS: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmnitrogen 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmblood 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmconcentration 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmsulfide 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmchemicals 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAcute 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmde 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmPapers 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmthe 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm479

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmincluding 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmGCL, 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm486

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmthe 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmAmerican 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmcylinders; 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmABSTRACT: 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmpresented. 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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htm501

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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9/25/2008 file://G:\ASB Chemical Assessments\H y dro g en Sul p hide\References\TOXLINE 2007.htmTITLE: 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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