|Systematic IUPAC name
3D model (Jmol)
|Molar mass||34.08 g·mol−1|
|Density||1.363 g dm−3|
|Melting point||−82 °C (−116 °F; 191 K)|
|Boiling point||−60 °C (−76 °F; 213 K)|
|4 g dm−3 (at 20 °C)|
|Vapor pressure||1740 kPa (at 21 °C)|
Refractive index (nD)
|1.000644 (0 °C)|
|1.003 J K−1 g−1|
|206 J mol−1 K−1|
Std enthalpy of
|−21 kJ mol−1|
|Safety data sheet||External MSDS|
EU classification (DSD)
|F+ T+ N|
|R-phrases||R12, R26, R50|
|S-phrases||(S1/2), S9, S16, S36, S38, S45, S61|
|Flash point||−82.4 °C (−116.3 °F; 190.8 K) |
|232 °C (450 °F; 505 K)|
|Lethal dose or concentration (LD, LC):|
LC50 (median concentration)
LCLo (lowest published)
|US health exposure limits (NIOSH):|
|C 20 ppm; 50 ppm [10-minute maximum peak]|
|C 10 ppm (15 mg/m3) [10-minute]|
IDLH (Immediate danger)
Related hydrogen chalcogenides
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
|what is ?)(|
Hydrogen sulfide often results from the microbial breakdown of organic matter in the absence of oxygen gas, such as in swamps and sewers; this process is commonly known as anaerobic digestion. H
2S also occurs in volcanic gases, natural gas, and in some sources of well water. The human body produces small amounts of H
2S and uses it as a signaling molecule.
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 Removal from water
- 7 Safety
- 8 Function in the body
- 9 Involvement in diseases
- 10 Induced hypothermia and suspended animation
- 11 Participant in the sulfur cycle
- 12 Mass extinctions
- 13 Life adapted to hydrogen sulfide
- 14 See also
- 15 References
- 16 Additional resources
- 17 External links
Hydrogen sulfide is slightly heavier than air; a mixture of H
2S and air can be 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, especially in the presence of base, which forms SH−.
At high temperatures or in the presence of catalysts, sulfur dioxide reacts with hydrogen sulfide to form elemental sulfur and water. This reaction is exploited in the Claus process, an important industrial method to dispose of hydrogen sulfide.
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). Hydrogen sulfide and its solutions are colorless. When exposed to air, it slowly oxidizes elemental sulfur, which is not soluble in water. 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 are insoluble, often dark colored solids. Lead(II) acetate paper was once used to detect hydrogen sulfide because it readily converts to lead(II) sulfide, which is black. Treating metal sulfides with strong acid often liberates hydrogen sulfide.
At pressures above 90 GPa (Gigapascal), hydrogen sulfide becomes a metallic conductor of electricity. When cooled below a critical temperature this high-pressure phase exhibits superconductivity. The critical temperature increases with pressure, ranging from 23 K at 100 GPa to 150 K at 200 GPa. If hydrogen sulfide is pressurized at higher temperatures, then cooled, the critical temperature reaches 203 K (−70 °C), the highest accepted superconducting critical temperature as of 2015. By substituting a small part of sulfur with phosphorus and using even higher pressures, it has been predicted that it may be possible to raise the critical temperature to above 0 °C (273 K) and achieve room-temperature superconductivity.
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 treating hydrogen with molten elemental sulfur at about 450 °C. Hydrocarbons can serve as a source of 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
- CH3C(S)NH2 + H2O → CH3C(O)NH2 + 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.
Water heaters can aid the conversion of sulfate in water to hydrogen sulfide gas. This is due to providing a warm environment sustainable for sulfur bacteria and maintaining the reaction which interacts between sulfate in the water and the water heater anode, which is usually made from magnesium metal.
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. Hydrogen sulfide is created by the human body in small doses through bacterial breakdown of proteins containing sulfur in the intestinal tract. It is also produced in the mouth (halitosis).
A portion of global H
2S emissions are due to human activity. By far the largest industrial source of H
2S is 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 Kraft process), tanneries and sewerage. H
2S arises from virtually anywhere where elemental sulfur comes in contact with organic material, especially at high temperatures. Depending on environmental conditions, it is responsible for deterioration of material through the action of some sulfur oxidizing microorganisms. It is called biogenic sulfide corrosion.
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".
Besides living near a gas and oil drilling operations, ordinary citizens can be exposed to hydrogen sulfide by being near waste water treatment facilities, landfills and farms with manure storage. Exposure occurs through breathing contaminated air or drinking contaminated water.
Production of sulfur, thioorganic compounds, and alkali metal sulfides
The main use of hydrogen sulfide is as a precursor to elemental sulfur. Several organosulfur compounds are produced using hydrogen sulfide. These include methanethiol, ethanethiol, and thioglycolic acid.
- H2S + NaOH → NaSH + H2O
- NaHS + NaOH → Na2S + H2O
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, and are thus identified.
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.
Scientists from the University of Exeter discovered that cell exposure to small amounts of hydrogen sulfide gas can prevent mitochondrial damage. When the cell is stressed with disease, enzymes are drawn into the cell to produce small amounts of hydrogen sulfide. This study could have further implications on preventing strokes, heart disease and arthritis.
Removal from fuel gases
Hydrogen sulfide is commonly found in raw natural gas and biogas. It is typically removed by amine gas treating technologies. In such processes, the hydrogen sulfide is first converted to an ammonium salt, whereas the natural gas is unaffected.
- RNH2 + H2S RNH+
3 + SH−
The bisulfide anion is subsequently regenerated by heating of the amine sulfide solution. Hydrogen sulfide generated in this process is typically converted to elemental sulfur using the Claus Process.
Removal from water
- Continuous chlorination
- Nitrate addition
- Calcium nitrate can be used to prevent hydrogen sulfide formation in wastewater streams.
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 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 carbon monoxide. It binds 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 to detoxify it. 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. Detoxification is effected by oxidation to sulfate, which is harmless. Hence, low levels of hydrogen sulfide may be tolerated indefinitely.
Diagnostic of extreme poisoning by H
2S is the discolouration 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 loss of breathing and a high probability of death. If death does not occur, high exposure to hydrogen sulfide can lead to cortical pseudolaminar necrosis, degeneration of the basal ganglia and cerebral edema. Although respiratory paralysis may be immediate, it can also be delayed up to 72 hours.
- 0.00047 ppm or 0.47 ppb is the odor threshold, the point at which 50% of a human panel can detect the presence of an odor without being able to identify it.
- 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.
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.
In 2014, Levels of Hydrogen Sulfide as high as 83 ppm have been detected at a recently built mall in Thailand called Siam Square One at the Siam Square area. Shop tenants at the mall reported health complications such as sinus inflammation, breathing difficulties and eye irritation. After investigation it was determined that the large amount of gas originated from imperfect treatment and disposal of waste water in the building.
In November 2014, a substantial amount of hydrogen sulfide gas shrouded the central, eastern and southeastern parts of Moscow. Residents living in the area were urged to stay indoors by the emergencies ministry. Although the exact source of the gas was not known, blame had been placed on a Moscow oil refinery.
In June 2016, a mother and her daughter were found deceased in their Porsche SUV. The medical examiner determined the cause to be hydrogen sulfide intoxication from the vehicles battery located under the driver seat.
In January 2017, three utility workers in Key Largo, Florida, died one by one within seconds of descending into a narrow space beneath a manhole to check a section of paved street.
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 in mammals and has a number of biological signaling functions. Two other gases function as signaling molecules, nitric oxide (NO) and carbon monoxide (CO).
The gas is derived from cysteine by the enzymes cystathionine beta-synthase, cystathionine gamma-lyase, and 3-mercaptopyruvate sulfurtransferase. Hydrogen sulfide serves as an endothelium-derived relaxing factor (EDRF) and as an endothelium-derived hyperpolarizing factor (EDHF). 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.
Its effects are similar to those of nitric oxide, hydrogen sulfide potentially protects 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.
Although both nitric oxide and hydrogen sulfide relax blood vessels, their mechanisms of action differ: whereas 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.
Recent findings suggest strong cellular crosstalk of NO and H
2S, demonstrating that the vasodilatatory effects of these two gases are mutually dependent. Additionally, H
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.
Hydrogen sulfide, similar to carbon monoxide (see carbon monoxide#Normal human physiology) and nitric oxide (see nitric oxide#Biological functions), possesses Specialized pro-resolving mediators activity. That is, it blunts, reverses, and promotes the healing of diverse inflammatory reactions. In whole animal, animal tissue, and human tissue studies, hydrogen sulfide: a) suppresses the expression of ICAM-1 and P-selectin adhesion molecules on vascular endothelial cells and LFA-1 adhesion molecules on leukocytes thereby inhibiting pro-inflammatory leukocytes from moving out of the circulation into tissue sites of inflammation; b) acts as a scavenger to neutralizes toxic substances (e.g. superoxide anion, peroxynitrite, hypochlorous acid, and hydrogen peroxide) released by leukocytes in inflamed tissues; c) renders pro-inflammatory tissue macrophages hypo-responsive to inflammatory stimuli; d) inhibits inflammatory cells from expressing pro-inflammatory cytokines such as TNFα, Interleukin 2, Interleukin 23 while stimulating their expression of the anti-inflammatory cytokine, Interleukin 10; and e) stimulates leukocyte apoptosis thereby promoting the removal of these potentially toxic cells from inflamed tissues. In animal models, hydrogen sulfide also promotes, and appears to be a natural mediator responsible for, repairing damaged tissues such as those due to Hypoxia and stomach ulcers.
Involvement in diseases
Hydrogen sulfide deficiency after heart attack
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.
H2S therapy uses a H2S donor, such as diallyl trisulfide (from garlic), 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.
In animal disease models caused and/or promoted by pathological inflammation, e.g. chronic inflammatory diseases (see Inflammation), drugs causing the release of hydrogen sulfide (e.g. ATB-429 and hydrogen sulfide-releasing NSAID) have shown clinically significant effects and are in development for use in humans.
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.)
The biochemistry of hydrogen sulfide is an important part of the chemistry of the iron-sulfur world. In this model of the origin of life on Earth, geologically produced hydrogen sulfide is postulated as an electron donor driving the reduction of carbon dioxide.
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.
Life adapted to hydrogen sulfide
Freshwater springs rich in hydrogen sulfide are mainly home to invertebrates, but also include a small number of fish: Cyprinodon bobmilleri (a pupfish from Mexico), Limia sulphurophila (a poeciliid from the Dominican Republic), Gambusia eurystoma (a poeciliid from Mexico), and a few Poecilia (poeciliids from Mexico). Invertebrates and microorganisms in some cave systems, such as Movile Cave, are adapted to high levels of hydrogen sulfide.
In the deep sea, hydrothermal vents and cold seeps with high levels of hydrogen sulfide are home to a number of extremely specialized lifeforms, ranging from bacteria to fish.[which?] Because of the absence of light at these depths, these ecosystems rely on chemosynthesis rather than photosynthesis.
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