|Jmol-3D images||Image 1|
|Molar mass||34.08 g mol−1|
|Odor||faint rotten egg|
|Density||1.363 g dm−3|
|Melting point||−82 °C (−116 °F; 191 K)|
|Boiling point||−60 °C (−76 °F; 213 K)|
|Solubility in water||4 g dm−3 (at 20 °C)|
|Vapor pressure||1740 kPa (at 21 °C)|
|Refractive index (nD)||1.000644 (0 °C)|
|Dipole moment||0.97 D|
heat capacity C
|1.003 J K−1 g−1|
|Std enthalpy of
|EU classification||F+ T+ N|
|R-phrases||R12, R26, R50|
|S-phrases||(S1/2), S9, S16, S36, S38, S45, S61|
|Flash point||-82.4 °C|
|Related hydrogen chalcogenides||Water
|Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa)|
|(what is: / ?)|
Hydrogen sulfide (British English: hydrogen sulphide, but this spelling is not recommended by the International Union of Pure and Applied Chemistry nor the Royal Society of Chemistry) is the chemical compound with the formula H
2S. It is a colorless gas with the characteristic foul odor of rotten eggs; it is heavier than air, very poisonous, corrosive, flammable, and explosive.
Hydrogen sulfide often results from the bacterial breakdown of organic matter in the absence of oxygen, such as in swamps and sewers; this process is commonly known as anaerobic digestion. H
2S also occurs in volcanic gases, natural gas, and some well waters. The human body produces small amounts of H
2S and uses it as a signaling molecule.
Dissolved in water, hydrogen sulfide is known as hydrosulfuric acid or sulfhydric acid, a weak acid.
Swedish chemist Carl Wilhelm Scheele is credited with having discovered hydrogen sulfide in 1777.
- 1 Properties
- 2 Production
- 3 Occurrence
- 4 Uses
- 5 Removal from fuel gases
- 6 Safety
- 7 Function in the body
- 8 Induced hypothermia and suspended animation
- 9 Participant in the sulfur cycle
- 10 Mass extinctions
- 11 See also
- 12 References
- 13 Additional resources
- 14 External links
|This section needs additional citations for verification. (December 2012)|
Hydrogen sulfide is slightly heavier than air; a mixture of H
2S and air is explosive. Hydrogen sulfide and oxygen burn with a blue flame to form sulfur dioxide (SO
2) and water. In general, hydrogen sulfide acts as a reducing agent.
At high temperature or in the presence of catalysts, sulfur dioxide can be made to react with hydrogen sulfide to form elemental sulfur and water. This is exploited in the Claus process, the main way to convert hydrogen sulfide into elemental sulfur.
Hydrogen sulfide  is slightly soluble in water and acts as a weak acid, giving the hydrosulfide ion HS− (pKa = 6.9 in 0.01-0.1 mol/litre solutions at 18 °C). A solution of hydrogen sulfide in water, known as sulfhydric acid or hydrosulfuric acid, is initially clear but over time turns cloudy. This is due to the slow reaction of hydrogen sulfide with the oxygen dissolved in water, yielding elemental sulfur, which precipitates out. The sulfide dianion S2− exists only in strongly alkaline aqueous solutions; it is exceptionally basic with a pKa > 14.
Hydrogen sulfide reacts with metal ions to form metal sulfides, which may be considered the salts of hydrogen sulfide. Some ores are sulfides. Metal sulfides often have a dark color. Lead(II) acetate paper is used to detect hydrogen sulfide because it turns grey in the presence of the gas as lead(II) sulfide is produced. Reacting metal sulfides with strong acid liberates hydrogen sulfide.
If gaseous hydrogen sulfide is put into contact with concentrated nitric acid, it explodes.
Hydrogen sulfide is most commonly obtained by its separation from sour gas, which is natural gas with high content of H
2S. It can also be produced by reacting hydrogen gas with molten elemental sulfur at about 450 °C. Hydrocarbons can replace hydrogen in this process.
Sulfate-reducing (resp. sulfur-reducing) bacteria generate usable energy under low-oxygen conditions by using sulfates (resp. elemental sulfur) to oxidize organic compounds or hydrogen; this produces hydrogen sulfide as a waste product.
- FeS + 2 HCl → FeCl2 + H2S
- 6 H2O + Al2S3 → 3 H2S + 2 Al(OH)3
This gas is also produced by heating sulfur with solid organic compounds and by reducing sulfurated organic compounds with hydrogen.
Hydrogen sulfide production can be costly because of the dangers involved in production.
Small amounts of hydrogen sulfide occur in crude petroleum, but natural gas can contain up to 90%. Volcanoes and some hot springs (as well as cold springs) emit some H
2S, where it probably arises via the hydrolysis of sulfide minerals, i.e. MS + H
2O → MO + H
2S. Hydrogen sulfide can be present naturally in well water, often as a result of the action of sulfate-reducing bacteria.
A portion of global H
2S emissions are due to human activity. By far the largest industrial route to H
2S occurs in petroleum refineries: The hydrodesulfurization process liberates sulfur from petroleum by the action of hydrogen. The resulting H
2S is converted to elemental sulfur by partial combustion via the Claus process, which is a major source of elemental sulfur. Other anthropogenic sources of hydrogen sulfide include coke ovens, paper mills (using the sulfate method), and tanneries. H
2S arises from virtually anywhere where elemental sulfur comes in contact with organic material, especially at high temperatures.
In 2011 it was reported that increased concentration of H
2S, possibly due to oil field practices, was observed in the Bakken formation crude and presented challenges such as "health and environmental risks, corrosion of wellbore, added expense with regard to materials handling and pipeline equipment, and additional refinement requirements".
Production of thioorganic compounds
Alkali metal sulfides
Upon combining with alkali metal bases, hydrogen sulfide converts to alkali hydrosulfides such as sodium hydrosulfide and sodium sulfide, which are used in the degradation of biopolymers. The depilation of hides and the delignification of pulp by the Kraft process both are effected by alkali sulfides.
For well over a century, hydrogen sulfide was important in analytical chemistry, in the qualitative inorganic analysis of metal ions. In these analyses, heavy metal (and nonmetal) ions (e.g., Pb(II), Cu(II), Hg(II), As(III)) are precipitated from solution upon exposure to H
2S. The components of the resulting precipitate redissolve with some selectivity.
For small-scale laboratory use in analytic chemistry, the use of thioacetamide has superseded H
2S as a source of sulfide ions.
Precursor to metal sulfides
As indicated above, many metal ions react with hydrogen sulfide to give the corresponding metal sulfides. This conversion is widely exploited. For example, gases or waters contaminated by hydrogen sulfide can be cleaned with metal sulfides. In the purification of metal ores by flotation, mineral powders are often treated with hydrogen sulfide to enhance the separation. Metal parts are sometimes passivated with hydrogen sulfide. Catalysts used in hydrodesulfurization are routinely activated with hydrogen sulfide, and the behavior of metallic catalysts used in other parts of a refinery is also modified using hydrogen sulfide.
Removal from fuel gases
- Reaction with iron oxide
- Gas is pumped through a container of hydrated iron(III) oxide, which combines with hydrogen sulfide.
3(s) + H
2O(l) + 3 H
2S(g) → Fe
3(s) + 4 H
- In order to regenerate iron(III) oxide, the container must be taken out of service, flooded with water and aerated.
- 2 Fe
3(s) + 3 O
2(g) + 2 H
2O(l) → 2 Fe
3(s) + 2 H
2O(l) + 6 S(s)
- 2 Fe
- On completion of the regeneration reaction the container is drained of water and can be returned to service. The advantage of this system is that it is completely passive during the extraction phase.
- Hydrodesulfurization is a more complex method of removing sulfur from fuels.
- Filtration through impregnated activated carbon
- A gas stream containing hydrogen sulfide can be purified by passing it through a suitably designed filter containing an impregnated activated carbon. This method is typically used for odor abatement at municipal sewage works and for the purification of landfill biogas, prior to its use in combined heat and power (CHP) engines, or injection into the gas grid.
- Treatment by plasma
- Plasma dissociation of hydrogen sulfide is a new method of treatment which utilizes plasma to dissociate hydrogen sulfide into hydrogen gas and elemental sulfur.
Hydrogen sulfide is a highly toxic and flammable gas (flammable range: 4.3–46%). Being heavier than air, it tends to accumulate at the bottom of poorly ventilated spaces. Although very pungent at first, it quickly deadens the sense of smell, so victims may be unaware of its presence until it is too late. For safe handling procedures, a hydrogen sulfide material safety data sheet (MSDS) should be consulted.
Hydrogen sulfide is considered a broad-spectrum poison, meaning that it can poison several different systems in the body, although the nervous system is most affected. The toxicity of H
2S is comparable with that of hydrogen cyanide or carbon monoxide. It forms a complex bond with iron in the mitochondrial cytochrome enzymes, thus preventing cellular respiration.
Since hydrogen sulfide occurs naturally in the body, the environment and the gut, enzymes exist in the body capable of detoxifying it by oxidation to (harmless) sulfate. Hence, low levels of hydrogen sulfide may be tolerated indefinitely.
At some threshold level, believed to average around 300–350 ppm, the oxidative enzymes become overwhelmed. Many personal safety gas detectors, such as those used by utility, sewage and petrochemical workers, are set to alarm at as low as 5 to 10 ppm and to go into high alarm at 15 ppm.
A diagnostic clue of extreme poisoning by H
2S is the discoloration of copper coins in the pockets of the victim. Treatment involves immediate inhalation of amyl nitrite, injections of sodium nitrite or administration of 4-dimethylaminophenol in combination with inhalation of pure oxygen, administration of bronchodilators to overcome eventual bronchospasm, and in some cases hyperbaric oxygen therapy (HBOT). HBOT has clinical and anecdotal support.
Exposure to lower concentrations can result in eye irritation, a sore throat and cough, nausea, shortness of breath, and fluid in the lungs (pulmonary edema). These effects are believed to be due to the fact that hydrogen sulfide combines with alkali present in moist surface tissues to form sodium sulfide, a caustic. These symptoms usually go away in a few weeks.
Long-term, low-level exposure may result in fatigue, loss of appetite, headaches, irritability, poor memory, and dizziness. Chronic exposure to low level H
2S (around 2 ppm) has been implicated in increased miscarriage and reproductive health issues among Russian and Finnish wood pulp workers, but the reports have not (as of circa 1995) been replicated.
Short-term, high-level exposure can induce immediate collapse, with a high probability of death. If death does not occur, studies have shown that, in humans, high exposure to hydrogen sulfide can lead to cortical pseudolaminar necrosis and degeneration of the basal ganglia. It has also been shown that Cerebral edema has been the cause of death in some fatal exposures with hydrogen sulfide.
- 0.00047 ppm or 0.47 ppb is the odor threshold, also known as the recognition threshold, the point at which 50% of a human panel can detect the presence of the compound by its smell. Its characteristic odor is normally described as resembling a rotten egg.
- 10 ppm is the OSHA permissible exposure limit (PEL) (8 hour time-weighted average).
- 10–20 ppm is the borderline concentration for eye irritation.
- 20 ppm is the acceptable ceiling concentration established by OSHA.
- 50 ppm is the acceptable maximum peak above the ceiling concentration for an 8 hour shift, with a maximum duration of 10 minutes.
- 50–100 ppm leads to eye damage.
- At 100–150 ppm the olfactory nerve is paralyzed after a few inhalations, and the sense of smell disappears, often together with awareness of danger.
- 320–530 ppm leads to pulmonary edema with the possibility of death.
- 530–1000 ppm causes strong stimulation of the central nervous system and rapid breathing, leading to loss of breathing.
- 800 ppm is the lethal concentration for 50% of humans for 5 minutes exposure (LC50).
- Concentrations over 1000 ppm cause immediate collapse with loss of breathing, even after inhalation of a single breath. Cortical pseudolaminar necrosis, degeneration of the basal ganglia and cerebral edema have also been shown.
Although respiratory paralysis may be immediate, it can also be delayed up to 72 hours.
Hydrogen sulfide was used by the British Army as a chemical weapon during World War I. It was not considered to be an ideal war gas, but, while other gases were in short supply, it was used on two occasions in 1916.
In 1975, a hydrogen sulfide release from an oil drilling operation in Denver City, Texas, killed nine people and caused the state legislature to focus on the deadly hazards of the gas. State Representative E L Short took the lead in endorsing an investigation by the Texas Railroad Commission and urged that residents be warned "by knocking on doors if necessary" of the imminent danger stemming from the gas. One may die from the second inhalation of the gas, and a warning itself may be too late.
The gas, produced by mixing certain household ingredients, was used in a suicide wave in 2008 in Japan. The wave prompted staff at Tokyo's suicide prevention center to set up a special hot line during "Golden Week", as they received an increase in calls from people wanting to kill themselves during the annual May holiday.
As of 2010, this phenomenon has occurred in a number of US cities, prompting warnings to those arriving at the site of the suicide. These first responders, such as emergency services workers or family members are at risk of death from inhaling lethal quantities of the gas, or by fire. Local governments have also initiated campaigns to prevent such suicides.
Function in the body
Hydrogen sulfide is produced in small amounts by some cells of the mammalian body and has a number of biological signaling functions. (Only two other such gases are currently known: nitric oxide (NO) and carbon monoxide (CO).)
The gas is produced from cysteine by the enzymes cystathionine beta-synthase and cystathionine gamma-lyase. It acts as a relaxant of smooth muscle and as a vasodilator and is also active in the brain, where it increases the response of the NMDA receptor and facilitates long term potentiation, which is involved in the formation of memory.
Eventually the gas is converted to sulfite in the mitochondria by thiosulfate reductase, and the sulfite is further oxidized to thiosulfate and sulfate by sulfite oxidase. The sulfates are excreted in the urine.
Due to its effects similar to nitric oxide (without its potential to form peroxides by interacting with superoxide), hydrogen sulfide is now recognized as potentially protecting against cardiovascular disease. The cardioprotective role effect of garlic is caused by catabolism of the polysulfide group in allicin to H
2S, a reaction that could depend on reduction mediated by glutathione.
Though both nitric oxide (NO) and hydrogen sulfide have been shown to relax blood vessels, their mechanisms of action are different: while NO activates the enzyme guanylyl cyclase, H
2S activates ATP-sensitive potassium channels in smooth muscle cells. Researchers are not clear how the vessel-relaxing responsibilities are shared between nitric oxide and hydrogen sulfide. However there exists some evidence to suggest that nitric oxide does most of the vessel-relaxing work in large vessels and hydrogen sulfide is responsible for similar action in smaller blood vessels.
2S reacts with intracellular S-nitrosothiols to form the smallest S-nitrosothiol (HSNO), and a role of hydrogen sulfide in controlling the intracellular S-nitrosothiol pool has been suggested.
Interdependence of Hydrogen Sulfide and Nitric Oxide
Recent findings suggest strong cellular crosstalk of NO and H
2S, demonstrating that the vasodilatatory effects of these two gases are mutually dependent.
Hydrogen Sulfide Deficiency
A hydrogen sulfide (H2S) deficiency can be detrimental to the vascular function after an acute myocardial infarction (AMI). AMIs can lead to cardiac dysfunction through two distinct changes; increased oxidative stress via free radical accumulation and decreased NO bioavailability. Free radical accumulation occurs due to increased electron transport uncoupling at the active site of endothelial nitric oxide synthase (eNOS), an enzyme involved in converting L-arginine to NO. During an AMI, oxidative degradation of tetrahydrobiopterin (BH4), a cofactor in NO production, limits BH4 availability and limits NO productionby eNOS. Instead, eNOS reacts with oxygen, another cosubstrates involved in NO production. The products of eNOS are reduced to superoxides, increasing free radical production and oxidative stress within the cells. A H2S deficiency impairs eNOS activity by limiting Akt activation and inhibiting Akt phosphorylation of the eNOSS1177 activation site. Instead, Akt activity is increased to phosphorylate the eNOST495 inhibition site, downregulating eNOS production of NO.
Hydrogen Sulfide Therapy in Acute Myocardial Infarction
H2S therapy uses a H2S donor, such as diallyl trisulfide (DATS), to increase the supply of H2S to an AMI patient. H2S donors reduce myocardial injury and reperfusion complications. Increased H2S levels within the body will react with oxygen to produce sulfane sulfur, a storage intermediate for H2S. H2S pools in the body attracts oxygen to react with excess H2S and eNOS to increase NO production. With increased use of oxygen to produce more NO, less oxygen is available to react with eNOS to produce superoxides during an AMI, ultimately lowering the accumulation of reactive oxygen species (ROS). Furthermore, decreased accumulation of ROS lowers oxidative stress in vascular smooth muscle cells, decreasing oxidative degeneration of BH4. Increased BH4 cofactor contributes to increased production of NO within the body. Higher concentrations of H2S directly increase eNOS activity through Akt activation to increase phosphorylation of the eNOSS1177 activation site, and decrease phosphorylation of the eNOST495 inhibition site. This phosphorylation process upregulates eNOS activity, catalyzing more conversion of L-arginine to NO. Increased NO production enables soluble guanylyl cyclase (sGC) activity, leading to an increased conversion of guanosine triphosphate (GTP) to 3’,5’-cyclic guanosine monophosphate (cGMP). In H2S therapy immediately following an AMI, increased cGMP triggers an increase in protein kinase G (PKG) activity. PKG reduces intracellular Ca2+ in vascular smooth muscle to increase smooth muscle relaxation and promote blood flow. PKG also limits smooth muscle cell proliferation, reducing intima thickening following AMI injury, ultimately decreasing myocardial infarct size.
In Alzheimer's disease the brain's hydrogen sulfide concentration is severely decreased. In a certain rat model of Parkinson's disease, the brain's hydrogen sulfide concentration was found to be reduced, and administering hydrogen sulfide alleviated the condition. In trisomy 21 (Down syndrome) the body produces an excess of hydrogen sulfide. Hydrogen sulfide is also involved in the disease process of type 1 diabetes. The beta cells of the pancreas in type 1 diabetes produce an excess of the gas, leading to the death of these cells and to a reduced production of insulin by those that remain.
Induced hypothermia and suspended animation
In 2005, it was shown that mice can be put into a state of suspended animation-like hypothermia by applying a low dosage of hydrogen sulfide (81 ppm H
2S) in the air. The breathing rate of the animals sank from 120 to 10 breaths per minute and their temperature fell from 37 °C to just 2 °C above ambient temperature (in effect, they had become cold-blooded). The mice survived this procedure for 6 hours and afterwards showed no negative health consequences. In 2006 it was shown that the blood pressure of mice treated in this fashion with hydrogen sulfide did not significantly decrease.
A similar process known as hibernation occurs naturally in many mammals and also in toads, but not in mice. (Mice can fall into a state called clinical torpor when food shortage occurs). If the H
2S-induced hibernation can be made to work in humans, it could be useful in the emergency management of severely injured patients, and in the conservation of donated organs. In 2008, hypothermia induced by hydrogen sulfide for 48 hours was shown to reduce the extent of brain damage caused by experimental stroke in rats.
As mentioned above, hydrogen sulfide binds to cytochrome oxidase and thereby prevents oxygen from binding, which leads to the dramatic slowdown of metabolism. Animals and humans naturally produce some hydrogen sulfide in their body; researchers have proposed that the gas is used to regulate metabolic activity and body temperature, which would explain the above findings.
Two recent studies cast doubt that the effect can be achieved in larger mammals. A 2008 study failed to reproduce the effect in pigs, concluding that the effects seen in mice were not present in larger mammals. Likewise a paper by Haouzi et al. noted that there is no induction of hypometabolism in sheep, either.
At the February 2010 TED conference, Mark Roth announced that hydrogen sulfide induced hypothermia in humans had completed Phase I clinical trials. The clinical trials commissioned by the company he helped found, Ikaria, were however withdrawn or terminated by August 2011.
Participant in the sulfur cycle
In the absence of oxygen, sulfur-reducing and sulfate-reducing bacteria derive energy from oxidizing hydrogen or organic molecules by reducing elemental sulfur or sulfate to hydrogen sulfide. Other bacteria liberate hydrogen sulfide from sulfur-containing amino acids; this gives rise to the odor of rotten eggs and contributes to the odor of flatulence.
As organic matter decays under low-oxygen (or hypoxic) conditions (such as in swamps, eutrophic lakes or dead zones of oceans), sulfate-reducing bacteria will use the sulfates present in the water to oxidize the organic matter, producing hydrogen sulfide as waste. Some of the hydrogen sulfide will react with metal ions in the water to produce metal sulfides, which are not water soluble. These metal sulfides, such as ferrous sulfide FeS, are often black or brown, leading to the dark color of sludge.
Several groups of bacteria can use hydrogen sulfide as fuel, oxidizing it to elemental sulfur or to sulfate by using dissolved oxygen, metal oxides (e.g., Fe oxyhydroxides and Mn oxides) or nitrate as oxidant.
The purple sulfur bacteria and the green sulfur bacteria use hydrogen sulfide as electron donor in photosynthesis, thereby producing elemental sulfur. (In fact, this mode of photosynthesis is older than the mode of cyanobacteria, algae, and plants, which uses water as electron donor and liberates oxygen.)
Hydrogen sulfide has been implicated in several mass extinctions that have occurred in the Earth's past. In particular, a buildup of hydrogen sulfide in the atmosphere may have caused the Permian-Triassic extinction event 252 million years ago.
Organic residues from these extinction boundaries indicate that the oceans were anoxic (oxygen-depleted) and had species of shallow plankton that metabolized H
2S. The formation of H
2S may have been initiated by massive volcanic eruptions, which emitted carbon dioxide and methane into the atmosphere, which warmed the oceans, lowering their capacity to absorb oxygen that would otherwise oxidize H
2S. The increased levels of hydrogen sulfide could have killed oxygen-generating plants as well as depleted the ozone layer, causing further stress. Small H
2S blooms have been detected in modern times in the Dead Sea and in the Atlantic ocean off the coast of Namibia.
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