Hydrogen sulfide
Hydrogen sulfide, H2S, is a colorless chalcogen hydride gas with the characteristic foul odor of rotten eggs.
It is poisonous, corrosive, and flammable gas.
It is often produced from the microbial breakdown of organic matter in the absence of oxygen gas, such as in swamps and sewers: anaerobic digestion which is done by sulfate-reducing microorganisms.
H2S also occurs in volcanic gases, natural gas, and in some sources of well water.
The body produces small amounts of H
2S.
A mixture of H2S and air can be explosive.
Hydrogen sulfide burns in oxygen with a blue flame to form sulfur dioxide and water.
Hydrogen sulfide acts as a reducing agent, especially in the presence of base: forms SH−.
Sulfur dioxide reacts with hydrogen sulfide to form elemental sulfur and water, important industrially to dispose of hydrogen sulfide.
It is slightly soluble in water and acts as a weak acid, giving the hydrosulfide ion HS−(SH-).
Hydrogen sulfide is colorless.
When exposed to air, it slowly oxidizes to form elemental sulfur.
It reacts with metal ions to form metal sulfides, which are insoluble.
Lead acetate paper is used to detect hydrogen sulfide because it readily converts to lead sulfide, which is black.
Hydrogen sulfide can become a metallic conductor of electricity at varying temperatures.
Hydrogen sulfide is most commonly obtained from sour gas, which is natural gas with a high content of H
2S.
Sulfate-reducing bacteria use sulfates to oxidize organic compounds or hydrogen; producing hydrogen sulfide as a waste product.
Many metal and nonmetal sulfides: aluminium sulfide, phosphorus pentasulfide, silicon disulfide liberate hydrogen sulfide upon exposure to water:
Water heaters aid in the conversion of sulfate in water to hydrogen sulfide gas.
Hydrogen sulfide can be generated in cells via enzymatic or non enzymatic pathway.
H2S in the body acts as a gaseous signaling molecule which inhibits the mitochondrial electron transport chain which effectively reduces ATP generation and biochemical activity within cells.
Three enzymes are known to synthesize H2S: cystathionine γ-lyase (CSE), cystathionine β-synthetase (CBS) and 3-mercaptopyruvate sulfurtransferase (3-MST), have been identified in biological cells and tissues.
These enzyme’s activity has been observed to be induced by a number of disease states, and they transfer of a sulfur atom from methionine to serine to form a cysteine molecule.
H2S is an important mediator of a wide range of cell functions in health and in disease.
3-MST also contributes to hydrogen sulfide production by way of the cysteine catabolic pathway.
Amino acids, such as methionine and cysteine in the diet are substrates for the transulfuration pathways and in the production of hydrogen sulfide.
Hydrogen Sulfide increases the levels of glutathione which acts to reduce or disrupt ROS levels in cells.
Pathophysiological states with H2S overproduction include: cancer, and Down Syndrome
Pathophysiological states with H2S deficit include vascular disease.
Its use of hydrogen sulfide is as a precursor to elemental sulfur.
Many metal ions react with hydrogen sulfide to give the corresponding metal sulfides.
Small amounts of hydrogen sulfide occur in crude petroleum, but natural gas can contain up to 30%.
Volcanoes and some hot springs, as well as cold springs, emit some H2S.
H2S can be present naturally in well water, often as a result of the action of sulfate-reducing bacteria.
It is created by the human body in small doses through bacterial breakdown of proteins containing sulfur in the intestinal tract, contributing to the characteristic odor of flatulence.
H2S is also produced in the mouth as halitosis.
The largest industrial source of H2S is petroleum refineries
Other anthropogenic sources of hydrogen sulfide include coke ovens, paper mills. tanneries and sewerage.
H2S arises where elemental sulfur comes in contact with organic material, especially at high temperatures.
H2S is responsible for deterioration of material through the action of sulfur oxidizing microorganisms, biogenic sulfide corrosion.
People are exposed to hydrogen sulfide living near a gas and oil drilling operations, near waste water treatment facilities, landfills and farms with manure storage.
Exposure of H2S occurs through breathing contaminated air or drinking contaminated water.
In waste landfills the burial of organic material rapidly leads to the production of anaerobic digestion within the waste mass and biogas is produced as soon as the air within the waste mass has been reduced.
In the presence of a sulfur containing material such as plasterboard or natural gypsum under anaerobic conditions, sulfate reducing bacteria converts this to hydrogen sulfide.
In industrial anaerobic digestion processes, such as waste water treatment, digestion of organic waste from agriculture, hydrogen sulfide can be formed from the reduction of sulfate and the degradation of amino acids and proteins within organic compounds.
Sulfates can be reduced to H2S by sulfate reducing bacteria.
Processes to remove hydrogen sulfide from drinking water by continuous chlorination yields insoluble solid sulfur:
Aeration, Oxygenation, and nitrate addition are other techniques.
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.
Hydrogen sulfide is a highly toxic and flammable gas
Eva use H2S is heavier than air, it accumulates at the bottom of poorly ventilated spaces.
Although very pungent like a rotten egg smell, it quickly deadens the sense of smell, putting victims at risk.
Hydrogen sulfide can poison several different systems in the body.
The nervous system is most affected.
H2S toxicity is comparable with that of carbon monoxide: Binds with iron in the mitochondrial cytochrome enzymes, thus preventing cellular respiration.
H2S occurs naturally in the body, the environment, and the gut, and enzymes exist to detoxify it.
At a threshold level, around 300–350 ppm, the oxidative enzymes become overwhelmed.
Detoxification is effected by oxidation to sulfate, which is harmless.[47] Hence, low levels of hydrogen sulfide may be tolerated indefinitely.
Poisoning by H2S causes them discolouration of copper coins.
H2S poisoning is treated by 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.
Lower H2S concentrations can result in eye irritation, a sore throat and cough, nausea, shortness of breath, and pulmonary edema.
H2S toxic 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 to H2S may result in fatigue, loss of appetite, headaches, irritability, poor memory, and dizziness.
Chronic exposure to low level H2S, around 2 ppm, has been linked to increased miscarriage and reproductive health issues.
High-level exposure can induce immediate collapse, with loss of breathing and a high probability of death,and survivors can have cortical pseudolaminar necrosis, degeneration of the basal ganglia and cerebral edema.
0.00047 ppm 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.
20 ppm is the OSHA permissible exposure limit in an 8 hour time-weighted average.
10 ppm is the recommended exposure limit set by NIOSH, the US National Institute for Occupational Safety and Health.
10–20 ppm is the borderline concentration for eye irritation.
20 ppm is the acceptable ceiling concentration established by OSHA.
50–100 ppm leads to eye damage.
At 100–150 ppm the olfactory nerve becomes paralyzed after a few inhalations: 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 of H2S exposure causes stimulation of the central nervous system and rapid breathing.
800 ppm is the lethal concentration for 50% of humans after 5 minutes’ exposure (LC50).
Concentrations over 1000 ppm of H2S cause immediate collapse with loss of breathing, even after inhalation of a single breath.
Sludge from a pond, creates the black color due to metal sulfides.
Hydrogen sulfide is a central participant in the sulfur cycle.
H2S is the biogeochemical cycle of sulfur on Earth.
In the absence of oxygen, sulfur/sulfate reducing bacteria derive energy from oxidizing hydrogen or organic molecules by reducing elemental sulfur or sulfate to hydrogen sulfide.
Some bacteria liberate hydrogen sulfide from sulfur-containing amino acids; giving rise to the odor of rotten eggs and contributes to the odor of flatulence.
Organic matter decays under hypoxic conditions: swamps, 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 reacts with metal ions in the water to produce non-soluble metal sulfides, such as ferrous sulfide FeS, which are often black or brown, leading to the dark color of sludge.
Groups of bacteria can use hydrogen sulfide as fuel, oxidizing it to elemental sulfur or to sulfate by using dissolved oxygen, metal oxides or nitrate as electron acceptors.
Cutting back on meat forces the tissues to make hydrogen sulphide (H2S), a gas that’s poisonous if inhaled and smells like rotten eggs, but promotes health inside the body.
The body naturally produces small amounts of H2S as a signalling molecule to act as a chemical messenger.
Restricting the intake of two sulphur amino acids – cysteine and methionine, causes ramped up production of H2S in tissues, which triggers a cascade of beneficial effects.
These beneficial effects of H2S include:
new blood vessel generation, which promotes cardiovascular health, and better resistance to oxidative stress in the liver, which is linked to liver disease.
The NHANES III study of 11,576 adults in the US national nutrition survey found that reduced dietary intake of these sulphur amino acids, cysteine and methionine, is linked to lower cardiometabolic risk factors, including lower levels of cholesterol and glucose in the blood.
Limiting intake of foods containing high levels of sulphur amino acids can reduce the risk of chronic diseases, such as diabetes and heart disease, and promote healthy aging.
Sulphur amino acids are abundant in meat, dairy and eggs,
eating on average 2.5 times our daily requirement of them.
Red meat is high in sulphur amino acids.
Fish and poultry white meat also contain a lot of sulfur amino acids, and the dark meat has less.
Beans, lentils and legumes are good sources of protein that are also low in sulphur amino acids.
Soy protein, which is the basis of foods like tofu, is surprisingly high in sulphur amino acids.
Vegetables like broccoli contain lots of sulphur but not in amino acid form.
Sulphur amino acids play vital roles in growth, so children should not adopt diets that are low in them.