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SECTION 1. CHEMICAL IDENTIFICATION

CHEMINFO Record Number: 313
CCOHS Chemical Name: Hydrogen sulfide

Synonyms:
Acide sulfhydrique
H2S
Hydrogen sulphide
Hydrogene sulfure
Hydrosulfuric acid
Sewer gas
Sour gas
Stink damp
Sulfur hydride
Dihydrogen monosulfide
Dihydrogen sulfide
Sulfureted hydrogen

Chemical Name French: Sulfure d'hydrogené
Chemical Name Spanish: sulfuro de hidrogeno
CAS Registry Number: 7783-06-4
UN/NA Number(s): 1053
RTECS Number(s): MX1225000
EU EINECS/ELINCS Number: 231-977-3
Chemical Family: Inorganic gas / inorganic sulfide / hydrogen sulfide
Molecular Formula: H2-S
Structural Formula: H-S-H

SECTION 2. DESCRIPTION

Appearance and Odour:
Colourless gas. Colourless liquid at extremely low temperatures or under very high pressure. Odour of rotten eggs at very low concentrations.(1,20,58) Sickening sweet odour at 30-100 ppm.(1) The ability to smell H2S can begin to dull at 50 ppm and can be completely lost.(20)

Odour Threshold:
Values vary widely. Range of acceptable values: 0.001-0.13 ppm (detection). Geometric mean air odour thresholds: 0.0094 ppm (detection); 0.0045 ppm (recognition).(59) Loss of ability to smell H2S begins at 50 ppm (20); exposures above 100 ppm may rapidly (2-15 minutes) deaden the sense of smell.(1,33) Reduced ability to smell (olfactory fatigue) may also result from prolonged exposure to concentrations below 100 ppm.(60)

Warning Properties:
POOR - Detection through odour is not reliable. Olfactory fatigue may result from prolonged exposure to concentrations below 100 ppm. The sense of smell is deadened above 100 ppm.

Composition/Purity:
Hydrogen sulfide (H2S) is most commonly encountered occupationally as an environmental contaminant (see Uses and Occurrences). However, it is also available commercially in grades of 99-99.99 mole% minimum H2S (liquid phase). Most H2S is made and used captively (i.e. at the site of production) or transported over several kilometres by pipeline. It is also transported in authorized cylinders, tank cars and cargo tanks (tank trucks) as a flammable liquefied compressed gas under its own vapour pressure.(1,20,60) It is also available as a mixture in nitrogen or hydrogen gases. Special steel or stainless steel suitable for use with H2S can be used for transportation, storage vessels and pipes, pipelines and oil and natural gas wells.(20,61) Since H2S can react with iron in the presence of moisture, the steel used must be chosen carefully.(20)

Uses and Occurrences:
H2S is encountered most commonly as an environmental contaminant. It occurs naturally in crude petroleum, natural gas, sour gases, in salt mines, in volcanic gases, hot sulfur springs, lakes, salt water ponds, undersea vents, marine sediments, swamps, stagnant bodies of water, and as an occluded gas in some minerals. It is formed as a result of bacterial breakdown of organic matter containing sulfur and can be formed by bacteria in the digestive tract. It can be found in sewage treatment facilities and in livestock barns and manure.(1,20,33) It is also a by-product of many industrial operations, such as petroleum refineries, petrochemical plants, natural gas plants, Kraft paper mills, iron smelters, coke ovens, food processing plants and tanneries.(1,33)
The major industrial use of H2S is in the production of elemental sulfur and sulfuric acid. It is also used for the production of thioorganic compounds and sodium sulfide and sodium hydrosulfide; for purification of hydrochloric and sulfuric acids; to replenish sulfide content in Kraft pulping; for the purification of ores by selective flotation; in metallurgy to precipitate copper, nickel and cobalt sulfides from ores; in the removal of copper, cadmium and titanium from spent catalysts; for catalyst activation, such as presulfiding petroleum cracking catalysts, and catalyst poisoning; in the production of extreme pressure lubricants; in the formulation of rare earth phosphors for use in colour television tubes; for treatment of metal surfaces; for passivation of the walls of reactors operating at high temperatures in petroleum operations; to form a layer of sulfide on the surface of steel wires or plates that are to be coated with paint or plastic; in the production of heavy water for the nuclear industry; in analytical chemistry; and as an additive in cutting oils.(1,20,33,60,61)
Historically, H2S was used as an agricultural disinfectant.(33)


SECTION 3. HAZARDS IDENTIFICATION

EMERGENCY OVERVIEW:
Colourless gas. Colourless liquid at extremely low temperatures or under very high pressure. Odour of rotten eggs at very low concentrations. Sickening sweet odour at 30-100 ppm. The ability to smell H2S can begin to dull at 50 ppm and can be completely lost. EXTREMELY FLAMMABLE GAS. Forms explosive mixtures with air over a wide concentration range. Very low ignition energy. Gas is heavier than air and may hug the ground. Distant ignition and flashback are possible. During a fire, irritating/toxic sulfur dioxide may be generated. Confined space hazard. Can accumulate in confined spaces, especially in low-lying, poorly ventilated areas, producing a fire/toxicity/explosion hazard. COMPRESSED GAS. Cylinders and closed containers may rupture violently if heated, releasing large amounts of flammable gas or may cause cylinder to rocket. May ignite in contact with some metal oxides and oxidants. VERY TOXIC. May be fatal if inhaled. EYE IRRITANT. Gas may be severely irritating to the eyes and respiratory tract. Causes lung injury-effects may be delayed. Inhalation of high concentrations may cause respiratory paralysis, irregular heartbeat, collapse and death. May cause nervous system effects. Liquefied escaping from cylinder can cause frostbite.



POTENTIAL HEALTH EFFECTS

Effects of Short-Term (Acute) Exposure

Inhalation:
Hydrogen sulfide (H2S) is a very toxic gas at normal temperatures. It poses a very serious inhalation hazard.
There is a large amount of information on human exposures. However, in most cases, the exposure levels and exposure durations are unknown or crudely estimated. Effects at various exposure levels are believed to be as follows: 0.001-0.13 ppm - odour threshold (highly variable); 1-5 ppm - moderately offensive odour, possibly with nausea, or headaches with prolonged exposure; 20-50 ppm - nose, throat and lung irritation, digestive upset and loss of appetite, sense of smell starts to become "fatigued", odour cannot be relied upon as a warning of exposure; 100 -200 ppm - severe nose, throat and lung irritation, ability to smell odour completely disappears; 250-500 ppm - potentially fatal build-up of fluid in the lungs (pulmonary edema) in the absence of central nervous system effects (headache, nausea, dizziness), especially if exposure is prolonged; 500 ppm - severe lung irritation, excitement, headache, dizziness, staggering, sudden collapse ("knockdown"), unconsciousness and death within 4-8 hours, loss of memory for period of exposure; 500-1000 ppm - respiratory paralysis, irregular heart beat, collapse, and death.(2,6,12,13,24) It is important to note that the symptoms of pulmonary edema, such as chest pain and shortness of breath, can be delayed for up to 48 hours after exposure.
Prolonged exposure (for several hours or days) to concentrations as low as 50-100 ppm can cause a runny nose, cough, hoarseness, and shortness of breath. Prolonged exposure to higher concentrations can produce bronchitis, pneumonia and a potentially fatal build-up of fluid in the lungs (pulmonary edema).(2,13,35)
There are numerous case reports of deaths, especially in the petroleum industry, sewage maintenance, and farmers.(2,16) Most fatalities have occurred in relatively confined spaces (e.g. sewers, sludge tanks, cesspools, or H2S collecting in pits or dips on open land or in buildings).(33) In many cases, multiple deaths have occurred at a single site. Rescuers, attempting to save an unconscious co-worker, have entered a confined area without respiratory protection or safety lines. They, in turn, have been overcome by H2S.
Workers who survive a serious short-term H2S exposure may recover completely (12,13) or may experience long-term effects. Nervous system and respiratory effects have been described in small human population studies or case reports. Permanent or persistent nervous system effects have included fatigue, anxiety, irritability, intellectual decline, reduced attention span, impaired learning and memory, altered sense of smell, and motor deficits.(6,21,29,30,32,33,54) Some of the nervous system effects may be due to a lack of oxygen reaching the brain cells during a severe H2S exposure.(2,12,30) Respiratory effects have included symptoms (shortness of breath upon exertion, chest tightness or wheezing) consistent with hypersensitivity of the airways (Reactive Airways Dysfunction) (28); permanent lung damage (pulmonary fibrosis) (31) and significant reductions in residual volume (one measure of lung function) (39).

Skin Contact:
Direct contact with liquefied H2S escaping from a cylinder can cause frostbite (freezing of the tissue). Symptoms of frostbite include numbness, prickling and itching of the affected area. The skin may become white or yellow. In severe cases there may be blistering and tissue death (necrosis). Any skin contact will also involve significant inhalation exposure. Refer to "Inhalation" above.
H2S gas has only limited potential to be absorbed through the skin and skin absorption does not contribute significantly to exposure.(2,24,25)

Eye Contact:
The most commonly reported effect of H2S exposure is eye irritation.(13,17,35) Inflammation and irritation of the eyes has been reported at very low airborne concentrations, sometimes below 10 ppm.(2,6,24) However, eye irritation at these low concentrations seems to result from combined exposures, in particular with carbon disulfide.
There is little reliable information about the irritancy of H2S at concentrations below 100 ppm.(82) "Gas eyes" or "sore eyes" with scratchiness, irritation, tearing, burning, sensitivity to light, rainbow-like halos around lights, blurred vision and ulceration are reported in many cases of exposure. However the concentrations at which this happens are not well defined and the changes are usually reversible.(17,83,84,85) Male volunteers exposed to 100-150 ppm for as little as 2-15 minutes experienced eye irritation, and after 1-4 hours the pain was reported as sharp.(86) H2S appears to dull the sensory nerves, so pain cannot be relied upon as a warning of exposure.
Direct contact with liquefied H2S escaping from a cylinder can freeze the eye and cause severe damage or blindness.

Ingestion:
Ingestion is not an applicable route of exposure for gases.

Effects of Long-Term (Chronic) Exposure

Long-term H2S exposure has mainly been associated with nervous and respiratory system and eye effects. However, controversy exists as to whether or not long-term exposure to H2S causes any significant health effects.(2,22) The disagreement centres on the quality of the research and the nature of some of the reported symptoms, which include fatigue, headache, dizziness, irritability, and loss of appetite. These symptoms are not specific to H2S exposure and could be due to a number of other causes.
There are a few studies that have evaluated the potential effects of long-term environmental exposure to H2S. These studies are not reviewed here, since they are limited by factors such as concurrent exposures to many other chemicals, and self-reporting biases.

Nervous System:
Firm conclusions cannot be drawn from limited studies that describe neurobehavioural effects following long-term exposure.
Thirteen former employees and 22 residents living downwind from a crude oil processing plant were studied. The former employees had been employed for 1.5-3 years. Environmental exposures outside of the plant showed a 24-hour average of 0-8.8 ppm H2S. Mercaptans, carbon-oxide-sulfide and total reduced sulfur were also detected. Neurobehavioural functions and a profile of mood states were examined and compared to 32 matched controls. Statistically significant differences were noted with simple reaction time, balance, colour discrimination, and psychomotor speed. Significantly elevated mood state scores included anger, confusion, depression, tension/anxiety and fatigue.(50) It is difficult to draw specific conclusions from this study regarding the potential effects of H2S because of limitations such as the relatively small number of people studied, the possibility of self-reporting biases, and concurrent exposures to other potentially harmful chemicals.
In another study, two groups of workers were compared. Group 1 (459 men) were exposed to H2S in their daily work - often at concentrations exceeding 20 ppm (cited as 0.002%). Group 2 (384 men) were generally not exposed. Group 1 more frequently reported symptoms such as fatigue, loss of appetite, headache, irritability, poor memory, dizziness and itching.(32) Limitations of this study include the lack of statistical analysis, possible self-reporting biases and lack of control over potential confounding factors.
Four workers who had experienced a severe short-term exposure (without losing consciousness), as well as long-term ("months"), low-level exposure to H2S developed impaired ability to smell. Medical evaluation confirmed a reduced sensitivity to odour in all 4 employees.(21) Further study of these workers included a series of physical, neurologic, psychiatric and chemosensory tests. All 4 had abnormal brain waves and met diagnostic criteria for 3-8 H2S-induced neuropsychiatric disorders.(87) These studies are limited by factors such as the small number of employees evaluated, lack of control over other potential causal factors (e.g. alcohol consumption), and lack of exposure information.
Nineteen people with short- and long-term exposures to H2S were compared with 202 unexposed people. Exposure was long-term (7 months-9 years) in 10 people and these people were studied 4 months-10 years after exposures. Overall, there were significant differences in reaction times, balance, visual performance, colour discrimination, cognitive performance, and significantly elevated mood state scores for tension, depression, anger, fatigue and confusion. The duration of exposure was not associated with the results.(88) It is difficult to draw conclusions from this study because of the relatively small numbers of people evaluated, the combination of short- and long-term exposures and the lack of exposure information.
In animal studies, subtle evidence of mild brain dysfunction was observed in male rats exposed to a relatively high concentration of H2S (125 ppm) for 11 weeks. Loss of sensory neurons in the nasal cavity was observed in male rats exposed to 30 or 80 ppm for 10 weeks.

Lungs/Respiratory System:
Firm conclusions cannot be drawn from limited studies that indicate respiratory effects in workers from long-term exposure to H2S.
A limited study suggests that long-term, low-level exposure to H2S may be associated with reduced lung function. The respiratory function of 68 sewer workers (who were assumed to be exposed to H2S) was measured and compared with results for 60 water workers (who were assumed not to be exposed to H2S). Significantly poorer lung function was noted in the sewer workers, particularly those assumed to have "high" H2S exposure.(18) A large number of workers were excluded from the study due to the poor quality of their lung function test results. Other study limitations include the lack of exposure monitoring, and the potential for exposure to other chemicals (e.g. chlorine).
No significant changes in lung function were observed in 26 male pulp mill workers with daily exposure to H2S usually below 10 ppm (duration of exposure not provided).(34)
The respiratory function of 69 male workers exposed to sour gas plant emissions (most likely H2S) for an average of 4.5 years, were compared with 34 unexposed controls. There was no significant difference in the measured pulmonary function between the 2 groups. However, there was an increase in self-reported respiratory symptoms in the exposed group (37.7% vs 23.3%, significance not reported).(89) This study is limited by lack of information on H2S exposure, by self-reporting bias and lack of statistical evaluation for respiratory symptoms.
In animals, increased bronchial responsiveness was observed in individual rats exposed to 1-100 ppm for 5 weeks.

Skin Sensitization:
H2S is not an occupational skin sensitizer. Only one non-occupational case report of sensitization was located.
A woman with several pre-existing health problems developed a severe skin reaction (a red, scaling rash on her eyelids, neck, arms and chest) following non-occupational exposure to airborne H2S. The woman had a pre-existing allergy to sulfur.(14)

Heart/Blood Vessels:
It is not possible to draw any conclusions from the one limited study available. A slight increase in the number of deaths, especially cardiovascular deaths, was observed in sulfate mill workers exposed to H2S and organic sulfide compounds. In general, the excess risk of cardiovascular death was small and in most subgroups the effect was not statistically significant. The workers had been employed for at least one year between 1945-1961. Death rates were compared to national rates and were followed until 1981. Exposure monitoring conducted in the early 1980s showed exposures to 0-20 ppm H2S, 0-15 ppm methyl mercaptan, 0-12 ppm dimethyl sulfide and 0-1.5 ppm dimethyl disulfide.(57) This study is limited by factors such as the lack of control over other potential causes of cardiovascular disease.

Eyes/Vision:
Evaluation of 123 male viscose rayon workers exposed to H2S and/or carbon disulfide for at least one year showed a significantly higher incidence of eye pain, burning and sensitivity to light compared to unexposed workers. Exposures varied from 1.3-36 ppm for carbon disulfide and 0.14-6 ppm for H2S. Some workers had only carbon disulfide exposure, while no one had only H2S exposure. It is not possible to determine if H2S, carbon disulfide or the combined exposure resulted in the reported eye effects.(9) Although, based on information available for short-term exposures, it is likely that the combined exposure resulted in the observed effects. This study is limited by factors such as the combined exposure, the relatively small number of workers studied and the possibility of self-reporting biases.

Carcinogenicity:

Hydrogen sulfide is not known to cause cancer. No human or animal information was located.

The International Agency for Research on Cancer (IARC) has not evaluated the carcinogenicity of this chemical.

The American Conference of Governmental Industrial Hygienists (ACGIH) has not assigned a carcinogenicity designation to this chemical.

The US National Toxicology Program (NTP) has not listed this chemical in its report on carcinogens.

Teratogenicity and Embryotoxicity:
There is insufficient information available to conclude that H2S is a developmental toxin. No conclusions can be drawn from 2 studies in humans, which have limitations such as mixed exposures, lack of exposure information and possible self-reporting bias. No significant developmental effects were observed in rat studies with inhalation exposures of up to 100 ppm. Studies designed to evaluate subtle changes in blood or brain biochemistry have shown some effects in the pups. The clinical significance of some of the changes is not known. Sometimes the pup effects were observed in the presence of biochemical changes in the mothers. In other cases, maternal toxicity was not evaluated. No conclusions can be drawn based on the other limited studies available.
In a large human population study, with 2,853 female petrochemical workers studied, an increased risk of miscarriages (8.8%) was associated with exposure to petrochemicals. Frequent exposure chemicals were identified from information on a job history questionnaire, including benzene, gasoline, and H2S. Of 106 women exposed to H2S, 13 reported a miscarriage (Odds Ratio: 2.3, 95% CI 1.2-4.4).(51,90) No specific conclusions can be drawn from this study regarding H2S because of limitations such as possible self-reporting bias, concurrent exposure to other potentially harmful chemicals and lack of specific exposure information.
In an industrial community in Finland, the miscarriage rate was examined in relation to the mothers or fathers occupation and assumed levels of residential environmental pollution. It was found that women employed in viscose rayon textile and paper products jobs had an increased rate of miscarriages (10.3 and 16.7%), as did women whose husbands worked in viscose rayon textile and chemical processing jobs. There was no specific information available on possible chemical exposures in these industries. Possible environmental chemical exposures were to sulfur dioxide, hydrogen sulfide and carbon disulfide. There was no clear evidence that environmental exposure to these chemicals was associated with an increased risk of miscarriage.(52) It is not possible to draw firm conclusions from this study due to factors such as the lack of specific exposure information and the possible concurrent to other potentially harmful chemicals.

Reproductive Toxicity:
There is insufficient information available to conclude that H2S is a reproductive toxin. No conclusions can be drawn based on the limited human information available. In animals, no significant reproductive effects were observed in one study with rats exposed by inhalation to up to 80 ppm.
No conclusion can be drawn from a study of limited quality which suggested that long-term exposure to H2S might affect the menstrual function of female workers.(11) The validity of this report is questionable because of limitations such as concurrent exposure to carbon disulfide, poor reporting of study methods and lack of control over confounding factors.
No conclusions can be drawn from a single report which suggested that retarded development and listlessness of breast-fed infants of mothers working in rayon factories was due to H2S.(24, unconfirmed) The original report is not available in English.

Mutagenicity:
The limited information available does not suggest that H2S is mutagenic. There is no human information available. Negative results were obtained in one study using live animals and one bacteria test.

Toxicologically Synergistic Materials:
No information was located.

Potential for Accumulation:
H2S is readily absorbed following inhalation. Absorption through the skin appears to be minimal. H2S is rapidly eliminated from the body and does not accumulate.(2,24)

Health Comments:
In the past, it has been reported that persons with perforated eardrums may be exposed to H2S leaking through the eardrum, even if appropriate respiratory protection is worn. A thorough review on this subject has concluded that the presence of an eardrum defect does NOT significantly reduce the effectiveness of respiratory protection against H2S. Furthermore, no medical literature or personal reports documenting H2S toxicity due to exposure via an eardrum perforation were located.(54)
H2S inhibits the enzyme cytochrome oxidase, which prevents body cells from using oxygen. Thus, H2S impairs the body's ability to use oxygen and the primary target organs for acute toxicity are the central nervous system and the heart. It also has direct toxicity by disrupting macromolecules.(90)


SECTION 4. FIRST AID MEASURES

Inhalation:
This is chemical is extremely flammable and very toxic. Take proper precautions to ensure your own safety before attempting rescue (e.g. remove any sources of ignition, wear appropriate protective equipment, use the buddy system). Remove source of contamination or move victim to fresh air. If breathing is difficult, trained personnel should administer emergency oxygen. DO NOT allow victim to move about unnecessarily. Symptoms of pulmonary edema can be delayed up to 48 hours after exposure. If breathing has stopped, trained personnel should begin artificial respiration (AR) or, if the heart has stopped, cardiopulmonary resuscitation (CPR) or automated external defibrillation (AED) immediately. Avoid mouth-to-mouth contact by using mouth guards or shields. Quickly transport victim to an emergency care facility. NOTE: Victims who have been exposed to 500 ppm or higher may pose a threat to responders due to H2S released from their clothing, skin and exhaled air.(81)

Skin Contact:
GAS: Remove, double bag, seal, label and leave contaminated clothing, shoes and leather goods at the scene for safe disposal. Any skin contact will involve significant inhalation exposure. See "Inhalation" above. LIQUEFIED GAS: Quickly remove victim from source of contamination and briefly flush with lukewarm, gently flowing water. DO NOT attempt to rewarm the affected area on site. DO NOT rub area or apply dry heat. Gently remove clothing or jewelry that may restrict circulation. Carefully cut around clothing that sticks to the skin and remove the rest of the garment. Loosely cover the affected area with a sterile dressing. DO NOT allow the victim to drink alcohol or smoke. Quickly transport victim to an emergency care facility. Double bag, seal, label and leave contaminated clothing, shoes and leather goods at the scene for safe disposal.

Eye Contact:
GAS: If irritation occurs, immediately flush the contaminated eye(s) with lukewarm, gently flowing water for 15-20 minutes, while holding the eyelid(s) open. Immediately obtain medical attention. Any eye contact will also involve significant inhalation exposure. See "Inhalation" above. LIQUEFIED GAS: Quickly remove victim from source of contamination. Immediately and briefly flush eye(s) with lukewarm, gently flowing water until the chemical is removed. DO NOT attempt to rewarm. Cover both eyes with a sterile dressing. DO NOT allow victim to drink alcohol or smoke. Quickly transport victim to an emergency care facility.

Ingestion:
Ingestion is not an applicable route of exposure for gases.

First Aid Comments:
Provide general supportive measures (comfort, warmth, rest).
Consult a doctor and/or the nearest Poison Control Centre for all exposures.
Some first aid procedures recommended above require advanced first aid training. Protocols for undertaking advanced procedures must be developed in consultation with a doctor and routinely reviewed.
All first aid procedures should be periodically reviewed by a doctor familiar with the material and its conditions of use in the workplace.

Note to Physicians:
NOTE: Amyl nitrite has been recommended as an antidote to hydrogen sulfide toxicity. However, its use is controversial, as researchers have concluded that it can only be effective within the first few minutes following exposure and may actually slow sulfide removal thereafter.(12) A recent review concludes that nitrite therapy, although not entirely free of controversy, should be considered if the level of medical preparedness and supervision is sufficient to carry out this procedure safely and efficiently.(13)



SECTION 5. FIRE FIGHTING MEASURES

Flash Point:
Flammable gas.

Lower Flammable (Explosive) Limit (LFL/LEL):
4.0 % (20,62)

Upper Flammable (Explosive) Limit (UFL/UEL):
46% (1,62)

Autoignition (Ignition) Temperature:
260 deg C (500 deg F) (1,60); also reported as 290 deg C (554 deg F) (62)

Sensitivity to Mechanical Impact:
Probably not sensitive. Stable material.

Sensitivity to Static Charge:
Liquid H2S will not accumulate static charge since it has medium to high electrical conductivity.(64) The gas can be ignited by a static discharge of sufficient energy.

Electrical Conductivity:
1000 pS/m (liquid in cylinder at boiling point) (65,66)

Minimum Ignition Energy:
0.068 millijoules.(63,66,67)

Combustion and Thermal Decomposition Products:
Sulfur oxides (mainly sulfur dioxide), water, and deposits of sulfur.(2) H2S can dissociate at very high temperatures (above 850 deg C) into hydrogen and sulfur.(1)

Fire Hazard Summary:
FLAMMABLE GAS. Burns with a pale blue flame. Form explosive mixtures with air over a wide range. Very low ignition energy. Ignites spontaneously at 260 deg C (500 deg F). Leaking gas will be initially colder and heavier than air, and may hug the ground and travel a considerable distance to a source of ignition and flash back to a leak. During a fire, irritating/toxic sulfur oxides (mainly sulfur dioxide) may be generated. Can accumulate in confined spaces, especially in low-lying, poorly ventilated areas, producing a fire/toxicity/explosion hazard. Compressed gas. Heat from fire can cause a rapid build-up of pressure inside cylinders, which may cause explosive rupture and a sudden release of large amounts of flammable gas or may cause cylinder to rocket.

Extinguishing Media:
Carbon dioxide, dry chemical powder, water spray or fog.(62,63)

Fire Fighting Instructions:
Extreme caution is required in a fire situation. Evacuate area and fight fire from a safe distance or a protected location. Approach fire from upwind to avoid extremely hazardous gas and toxic decomposition products.
For fires involving flammable gases, the best procedure is to stop the flow of gas before attempting to extinguish the fire. It is extremely dangerous to extinguish the fire while allowing continued flow of the gas. The gas could form an explosive mixture with air and reignite, which may cause far more damage than if the original fire had been allowed to burn. In some cases, extinguishing the fire with carbon dioxide or dry chemical powder may be necessary to permit immediate access to valves to shut off the flow of gas. However, this must be done carefully. If it is not possible to stop the flow of gas and if there is no risk to the surrounding area, allow the fire to continue burning while protecting exposed materials with water spray, to prevent ignition of other combustible materials. Gas clouds may be controlled by water spray or fog.
Isolate containers exposed to heat, but not directly involved in the fire and protect personnel. Move cylinders/containers from fire area, if this can be done without risk. Handle damaged cylinders with extreme care. Otherwise, fire-exposed containers, cylinders, tanks or pipelines should be cooled by application of hose streams and this should begin as soon as possible (within the first several minutes) and should concentrate on any unwetted portions. No part of a cylinder should be subjected to a temperature higher than 52 deg C (approximately 125 deg F). If this is not possible, use unmanned monitor nozzles and immediately evacuate the area.
DO NOT direct water at open or leaking containers or cylinders and take precautions not to get water inside a container or cylinder. Reverse flow into cylinder may cause rupture. Take care not to block pressure relief valves.
If possible, avoid spraying cold areas of equipment to avoid rapid freezing of water, which can result in heavy icing and possible blockage of pressure release valves. May cause dense fog, reducing visibility.
For a massive fire in a large area, use unmanned hose holder or monitor nozzles; if this is not possible withdraw from fire area and allow fire to burn. Stay away from ends of tanks, but be aware that flying material from ruptured tanks may travel in any direction. Withdraw immediately in case of rising sound from venting safety device or any discolouration of tank due to fire. After the fire has been extinguished, explosive, toxic atmospheres may linger. Before entering such an area, especially confined areas, check the atmosphere with an appropriate monitoring device.

Protection of Fire Fighters:
Hydrogen sulfide is an extremely toxic, flammable gas. The combustion products of hydrogen sulfide (e.g., sulfur dioxide) are skin contact and inhalation hazards. Do not enter without wearing specialized equipment suitable for the situation. Firefighter's normal protective clothing (Bunker Gear) will not provide adequate protection. Chemical protective clothing (e.g. chemical splash suit) and positive pressure self-contained breathing apparatus (NIOSH approved or equivalent) may be necessary.



NATIONAL FIRE PROTECTION ASSOCIATION (NFPA) HAZARD IDENTIFICATION

NFPA - Health: 4 - Very short exposure could cause death or major residual injury.
NFPA - Flammability: 4 - Will rapidly or completely vaporize at atmospheric pressure and normal ambient temperature, or readily disperse in air and burn readily.
NFPA - Instability: 0 - Normally stable, even under fire conditions, and not reactive with water.

SECTION 9. PHYSICAL AND CHEMICAL PROPERTIES

Molecular Weight: 34.08

Conversion Factor:
1 ppm = 1.4 mg/m3; 1 mg/m3 = 0.717 ppm at 25 deg C (calculated)

Physical State: Gas
Melting Point: -85.5 deg C (-122 deg F) (1,65)
Boiling Point: -60.3 deg C (-76.6 deg F) (1,65)
Relative Density (Specific Gravity): Not applicable (gas)
Solubility in Water: Slightly soluble (398 mg/100 g at 20 deg C (1); 290 mL/100 mL at 20 deg C(2))
Solubility in Other Liquids: Very soluble in alkanolamines; soluble in ethanol, methanol, acetone, diethyl ether, glycerol, glycol ethers, N-methylpyrrolidone, propylene carbonate, gasoline, kerosene, carbon disulfide and crude oil; moderately soluble in hexane and benzene.(1,2)
Coefficient of Oil/Water Distribution (Partition Coefficient): Log P(oct) = -1.38 (experimental) (70)
pH Value: Not applicable (gas); 4.1 (0.1N aqueous solution) (61)
Acidity: Anhydrous hydrogen sulfide gas is practically non-acidic. Water solutions are weakly acidic.(1,20)
Viscosity-Dynamic: Not applicable
Surface Tension: Not applicable
Vapour Density: 1.177 at 21.1 deg C and 101.3 kPa (air = 1) (58)
Vapour Pressure: Absolute vapour pressure in cylinder: 1823.3 kPa, abs (18 atm) at 21.1 deg C (60); also reported as 1814 kPa (17.9 atm) at 20 deg C (1)
Vapour Pressure at 50 deg C: 3553.3 kPa (35.1 atm) at 50 deg C (from experimentally-derived coefficients) (65)
Saturation Vapour Concentration: Not applicable (gas)
Evaporation Rate: Not applicable (gas)
Henry's Law Constant: 8.67 X 10(2) Pa.m3/mol (cited as 8.56 X 10(-3) atm.m3/mol) at 20 deg C (71); log H = -0.45 (dimensionless constant; calculated)
Critical Temperature: 100.4 deg C (212.7 deg F) (1,65)
Critical Pressure: 9006-9008 kPa (88.9 atm) (1,60)

Other Physical Properties:
TRIPLE POINT: -85.5 deg C (-122 deg F) at 23.2 kPa (20)


SECTION 10. STABILITY AND REACTIVITY

Stability:
Normally stable.

Hazardous Polymerization:
Will not occur.

Incompatibility - Materials to Avoid:

NOTE: Chemical reactions that could result in a hazardous situation (e.g. generation of flammable or toxic chemicals, fire or detonation) are listed here. Many of these reactions can be done safely if specific control measures (e.g. cooling of the reaction) are in place. Although not intended to be complete, an overview of important reactions involving common chemicals is provided to assist in the development of safe work practices.


Hydrogen sulfide (H2S) is a strong reducing agent and is highly reactive.(1,20,60)
METAL OXIDES (e.g. barium peroxide, chromium trioxide, copper oxide, lead dioxide, manganese dioxide, nickel oxide, silver oxides and sodium peroxide) - may ignite on contact.(63,72,73)
RUST - H2S may ignite if passed through rusty iron pipes.(72,73)
OXIDANTS (e.g. bromine pentafluoride, copper chromate, fluorine, lead hypochlorite, fuming nitric acid and sodium peroxide) - ignite on contact. Chlorine trifluoride and dichlorine oxide explode on contact.(63,72,73)
OXYGEN - mixtures are explosive between 280 and 360 deg C; extensive self-heating occurs.(72,73)
SODIUM - melts and ignites in the presence of moist H2S.(73)
COPPER POWDER - may ignite and explode.(63,72,73)
TUNGSTEN - finely divided tungsten glows red hot in a stream of H2S.(72,73)
SODA-LIME, or SODIUM AND POTASSIUM HYDROXIDES - exothermic reaction, accompanied by incandescence in the presence of air; may result in a violent explosion.(63,72,73)
ACETALDEHYDE - reaction can be violent.(63)
SILVER FULMINATE - explodes violently at room temperature.(72,73)
4-BROMOBENZENEDIAZONIUM CHLORIDE - forms an explosive compound.(63,72,73)

Hazardous Decomposition Products:
None reported

Conditions to Avoid:
Flames, sparks, static discharge, heat and other ignition sources.

Corrosivity to Metals:
H2S is corrosive to some metals under some conditions (e.g. moisture and temperature). Wet or moist H2S is corrosive to copper, brass, bronze, cast iron, types 1010 and 1020 carbon steel (100% concentration at temperatures of 21-65.5 deg C (70-150 deg F), lead, Monel and 400 series stainless steels.(61,74- 76) It has been reported that wet H2S can corrode carbon steel at corrosion rates that can exceed 2.5 mm/year, depending on temperature and concentration (sulfide stress cracking and hydrogen embrittlement may occur).(1,20,61,75) Wet H2S is not corrosive to types 3003 and Cast B-365 aluminum, high nickel cast iron (Ni-Resist), high silicon cast iron, 300 series stainless steels, nickel-based alloys (like Inconel and Incoloy) at room temperature.(61,74,75,76) It is not corrosive at high temperatures (up to 150 deg C) to Incoloy, tantalum and titanium.(75) Anhydrous (dry) H2S is corrosive to ductile cast iron, copper, silicon-copper, aluminum bronze and silicon bronze.(61,74,75) Dry H2S can severely attack carbon steel at temperatures greater than 260 deg C.(1) Dry H2S is not corrosive to types 1075 and 1095 carbon steel, stainless steel (types 305, 446 and Carpenter-20 Cb-3), types 3003 and 6061-T6 aluminum, nickel and nickel-based alloys at room temperature.(60,61,74,75) It is not corrosive at high temperatures (up to 315 deg C) to types 316 and 317 stainless steels, chromium-molybdenum alloy steels, high nickel cast iron (Ni-Resist), Monel, and tantalum.(1,75)

Corrosivity to Non-Metals:
Dry H2S can attack plastics, like nylon and polyurethane, and elastomers, like Viton A, chlorinated polyethylene, hard rubber, polyacrylate and silicone VMQ.(68,74,77) Wet H2S can attack plastics, like acetal, nylon and polyurethane, and elastomers, like Viton A, chlorinated polyethylene, natural rubber, soft rubber, isoprene, Nitrile Buna-N (NBR), styrene-butadiene (SBR), polyacrylate, polyurethane and silicone VMQ.(68,74,77) Dry and wet H2S do not attack plastics, like chlorinated polyvinyl chloride (CPVC), Teflon and other fluorocarbons, like Kynar (PVDF), polyethylene, polypropylene, polystyrene, polyvinyl chloride (PVC), and elastomers, like ethylene propylene, ethylene propylene diene, chloroprene, Butyl rubber (isobutylene-isoprene), Hypalon (chloro-sulfonyl-polyethylene (CSM)), neoprene, and ethylene vinyl acetate.(68,74,77)


SECTION 11. TOXICOLOGICAL INFORMATION

LC50 (rat): 444 ppm (4-hour exposure) (10)
LC50 (mouse): 335 ppm (4-hour exposure); cited as 673 ppm (1-hour exposure) (3)
LC50 (rat): 415 ppm (4-hour exposure); cited as 587 ppm (2-hour exposure) (40)*
LC50 (rat): 501 ppm (4-hour exposure) (40)*
LC50 (rat): 410 ppm (4-hour exposure); cited as 335 ppm (6-hour exposure) (40)*
*All rats that died had fluid build-up in the lungs (pulmonary edema). (40)

Eye Irritation:

Hydrogen sulfide (H2S) gas is irritating to the eyes.

Eye irritation was reported in rats exposed to 35-65 ppm for 4-8 hours and to 310 ppm for 2-3 minutes. Dogs exposed to 103 ppm for 4-8 hours or to 350 ppm for 2-30 minutes had tearing (lachrymation).(86) Exposure of dogs, cats, rabbits and guinea pigs to 50-100 ppm for several hours or days caused tearing, and reversible damage to the cells on the outer layer of the eye.(17, unconfirmed) Rats exposed to approximately 1300 ppm for 10 minutes or approximately 54 ppm for 3 hours developed lesions of the cornea.(2, unconfirmed)

Effects of Short-Term (Acute) Exposure:

Inhalation:
In LC50 studies, the range of concentrations causing death is very small, indicating that H2S has a very steep dose-response curve. For example, a 4-hour exposure to 400 ppm killed 3/10 rats, 500 ppm killed 8/10 rats and 600 ppm killed 10/10 rats.(10) Exposure of rats to 35-65 ppm continuously for 100 hours produced eye and nose irritation. Rats exposed to 100-140 ppm showed respiratory distress from 8 hours onwards and some died at 18-48 hours. With concentrations of 310-350 ppm or 190-240 ppm, respiratory distress was observed in rats within 30-60 minutes. Some animals exposed to 310-350 died from one hours onwards, while animals exposed to 190-240 ppm died at 8-18 hours. Exposure of two monkeys to 500 ppm produced unconsciousness and death in one animal within 35 minutes. The other monkey became unconscious and was removed from exposure after 22 minutes. It regained consciousness approximately 2.5 hours later, but showed incoordination, reduced activity, and loss of appetite for the following ten days, when the study was terminated. Exposure of rabbits to 470 ppm and 750 ppm caused fluid build up in the lungs, bleeding of internal organs, convulsions, collapse and death between 4.5 and 6.5 hours. Exposure to 750-1000 ppm has produced unconsciousness and death in several animal species within a few minutes. In general, sensitivity to the effects of H2S is similar in most animal species.(26, unconfirmed) Male rats were exposed to 0, 10, 30 or 80 ppm (whole-body); 0, 30 and 80 ppm (nose-only) or 0, 30, 80, 200 or 400 ppm (nose-only) for 3 hours/day for 5 days. Learning and memory were not impaired with exposures up to 80 ppm. Exposure to 400 ppm did impair acquisition and retention. This may have been due to decreased motor activity and body temperature also observed in animals exposed to greater than 80 ppm.(23) Male rats were exposed to 0, 30, 80, 200 or 400 ppm (nose-only) for 1 or 5 days (3 hr/d). A dose-related increase in cell death (necrosis) in the olfactory epithelium was seen for single or multiple exposures to 80 ppm and higher. The olfactory epithelium was completely regenerated 6 weeks after treatment, although some abnormalities (e.g. small cysts) were still noted.(91)

Skin Contact:
Two studies indicate limited potential for H2S gas to be absorbed very slowly through the skin. Exposure of approximately one-half of the body area to pure H2S was lethal to two guinea pigs within 45 minutes, but was without effect in a dog. Precautions were taken to prevent inhalation exposure.(42) In rabbits, whole-body exposure (excluding head) of moist skin to H2S gas resulted in the detection of sulfides in expired air. Two of three exposed rabbits died.(41)

Effects of Long-Term (Chronic) Exposure:

Inhalation exposure to 30 ppm or above has produced signs of irritation of the nasal passages, including sensory neuron loss in male rats, in rats and mice for 10-13 weeks. Increased bronchial responsiveness was observed in individual rats exposed to 1-100 ppm for 5 weeks. Subtle evidence of mild brain dysfunction was observed in male rats exposed to 125 ppm for 11 weeks.

Inhalation:
Male rats exposed to 0, 10, 30 or 80 ppm for 10 weeks showed lesions in the olfactory mucosa at 30 and 80 ppm. The lesions consisted of sensory neuron loss and increased cell growth in the olfactory region of the nasal cavity.(37,49) A subsequent study indicates that H2S exposure damages most cell types in the olfactory epithelium, but there is probably a slower rate of replacement of the olfactory neurons.(91) Studies exposing rats to up 0, 10.1, 30.5 or 80 ppm for 90 days showed significant reductions in weight gain in males and females exposed to 80 ppm and reduced brain weight in males exposed to 80 ppm. No other abnormalities were noted. Mice exposed in a similar experiment showed inflammation of the nasal passages at 80 ppm.(5,15,33) Rats exposed to 0, 1, 10 or 100 ppm for 5 weeks showed no significant respiratory effects, except individual animals in all exposure groups showed a significant increase in bronchial responsiveness.(24,25-unconfirmed) Male rats were repeatedly exposed to 125 ppm for up to 11 weeks to evaluate potential effects on learning and memory. Exposure to H2S did not produce any obvious signs of eye irritation, respiratory distress, behavioural dysfunction or impaired consciousness. There was, however, subtle evidence of a mild brain dysfunction.(27) Rats exposed to 14-28 ppm for 4 months developed dose-dependent lesions of the thyroid gland. However, no hormonal assays were done, so it cannot be concluded that there were functional changes.(2, unconfirmed) This study is not available in English, therefore cannot be evaluated.

Teratogenicity, Embryotoxicity and/or Fetotoxicity:
No significant developmental effects were observed in rat studies with inhalation exposures of up to 100 ppm. Studies designed to evaluate subtle changes in blood or brain biochemistry have shown some effects in the pups. The clinical significance of some of the changes is not known. Sometimes the pup effects were observed in the presence of biochemical changes in the mothers. In other cases, maternal toxicity was not evaluated.(36,45,46,47,56) No conclusions can be drawn based on the other limited studies available.(4,38)
Rats were exposed to 0, 20, 50, 75 ppm from day 6 of pregnancy to postnatal day 21. Maternal food intake was reduced during the first 4 days of exposure to 50 ppm and for the first 8 days of exposure to 75 ppm. The cholesterol content of maternal livers and brains was elevated at 75 ppm. There were no significant differences in length of gestation, litter size, pup birth weight, male to female pup ratio or viability.(44) In a preliminary study, rats (8-9/group) were exposed to 0, 50, 100 or 150 ppm during days 6-20 of pregnancy. Maternal weight gain was significantly reduced at 150 ppm. Pup body weight was reduced slightly, but significantly, in all exposure groups. In a follow-up experiment, 23 females were exposed to 100 ppm on days 6-20 of pregnancy. Neither maternal toxicity nor any adverse effects on the developing fetuses were observed.(43) Rats were exposed to 0, 10, 30 or 80 ppm for 2 weeks prior to breeding. Exposures continued during a 2-week mating period and then from days 0-19 of pregnancy. Exposure of dams and their pups resumed from postnatal day 5-18. Adult male rats were exposed for 70 consecutive days. There were no significant signs of developmental toxicity (e.g. pup mortality, litter size, length of gestation, malformations or altered weight gain) or neurotoxicity (neuropathology. motor activity, passive avoidance, functional observation battery or acoustic startle response) in exposed pups. There was no maternal toxicity.(48) This study is somewhat limited by the relatively small number of animals exposed (12/sex/group).

Reproductive Toxicity:
No significant reproductive effects were observed in one study with rats exposed by inhalation to up to 80 ppm. No conclusions can be drawn from the other limited studies available.
Rats were exposed to 0, 10, 30 or 80 ppm for 2 weeks prior to breeding. Exposures continued during a 2-week mating period and then from days 0-19 of pregnancy. Exposure of dams and their pups resumed from postnatal day 5-18. Adult male rats were exposed for 70 consecutive days. No significant reproductive effects (e.g. mating index, fertility index, post-implantation loss/litter) were observed.(48) This study is somewhat limited by the small number of animals (12/sex/group). Rats were exposed to 0, 20, 50, 75 ppm from day 6 of pregnancy to postnatal day 21. Maternal food intake was reduced during the first 4 days of exposure to 50 ppm and for the first 8 days of exposure to 75 ppm. There were no other significant signs of maternal toxicity. A dose-dependent increase in parturition (delivery) time and difficult delivery was noted in the exposed animals (10, 20 and 42% longer than controls).(44) There was no statistical analysis of the data conducted. A few older studies.(2,4,11) cannot be taken as evidence that H2S causes reproductive problems, because of limitations such as non-standard experimental designs, poorly reported methodology, flawed analysis of results, inadequate controls and/or concurrent exposure to other potentially harmful chemicals (e.g. carbon disulfide).

Mutagenicity:
The limited information available does not suggest that H2S is mutagenic. Negative results were obtained in a study in live rats and in an unconfirmed study in bacteria.
Negative results were obtained in a dominant lethal study where male rats were exposed to 220 ppm for 1 week and then mated over a 10-week period.(38)
Negative results (point mutations) were obtained in bacteria, both with and without metabolic activation. The concentration of H2S gas was limited by its solubility in ethanol (the test solvent). The highest dose obtainable was 1750 microg/plate.(33, unconfirmed)

Toxicological Synergisms:
A limited study suggests that ethanol may increase susceptibility to H2S toxicity. Injection with 330 or 660 mg/kg ethanol, with inhalation exposure to 800 ppm H2S, shortened the mean time-to-unconsciousness in male rats.(55) Statistical evaluation of the results was not conducted.


SECTION 16. OTHER INFORMATION

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Information on chemicals reviewed in the CHEMINFO database is drawn from a number of publicly available sources. A list of general references used to compile CHEMINFO records is available in the database Help.


Review/Preparation Date: 2005-10-03



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