OLED Device architectures


Bottom or top emission
Bottom emission devices use a transparent or semi-transparent bottom electrode to get the light through a transparent substrate. Top emission devices[45][46] use a transparent or semi-transparent top electrode emitting light directly. Top-emitting OLEDs are better suited for active-matrix applications as they can be more easily integrated with a non-transparent transistor backplane.
Transparent OLEDs
Transparent OLEDs use transparent or semi-transparent contacts on both sides of the device to create displays that can be made to be both top and bottom emitting (transparent). TOLEDs can greatly improve contrast, making it much easier to view displays in bright sunlight.[47] This technology can be used in Head-up displays, smart windows or augmented realityapplications.
Graded Heterojunction
Graded heterojunction OLEDs gradually decrease the ratio of electron holes to electron transporting chemicals.[48] This results in almost double the quantum efficiency of existing OLEDs.
Stacked OLEDs
Stacked OLEDs use a pixel architecture that stacks the red, green, and blue subpixels on top of one another instead of next to one another, leading to substantial increase in gamut and color depth, and greatly reducing pixel gap. Currently, other display technologies have the RGB (and RGBW) pixels mapped next to each other decreasing potential resolution.
Inverted OLED
In contrast to a conventional OLED, in which the anode is placed on the substrate, an Inverted OLED uses a bottom cathode that can be connected to the drain end of an n-channel TFT especially for the low cost amorphous silicon TFT backplane useful in the manufacturing of AMOLED displays.[49]

[edit]Patterning technologies

Patternable organic light-emitting devices use a light or heat activated electroactive layer. A latent material (PEDOT-TMA) is included in this layer that, upon activation, becomes highly efficient as a hole injection layer. Using this process, light-emitting devices with arbitrary patterns can be prepared.[50]

Colour patterning can be accomplished by means of laser, such as radiation-induced sublimation transfer (RIST).[51]

Organic vapour jet printing (OVJP) uses an inert carrier gas, such as argon or nitrogen, to transport evaporated organic molecules (as in Organic Vapor Phase Deposition). The gas is expelled through a micron sized nozzle or nozzle array close to the substrate as it is being translated. This allows printing arbitrary multilayer patterns without the use of solvents.

Conventional OLED displays are formed by vapor thermal evaporation (VTE) and are patterned by shadow-mask. A mechanical mask has openings allowing the vapor to pass only on the desired location.

Backplane technologies

For a high resolution display like a TV, a TFT backplane is necessary to drive the pixels correctly. Currently, Low Temperature Polycrystalline silicon LTPS-TFT is used for commercial AMOLEDdisplays. LTPS-TFT has variation of the performance in a display, so various compensation circuits have been reported.[45] Due to the size limitation of the excimer laser used for LTPS, theAMOLED size was limited. To cope with the hurdle related to the panel size, amorphous-silicon/microcrystalline-silicon backplanes have been reported with large display prototype demonstrations

OLED material

Material technologies

Small molecules

Alq3,[18] commonly used in small molecule OLEDs

Efficient OLEDs using small molecules were first developed by Dr. Ching W. Tang et al.[18] at Eastman Kodak. The term OLED traditionally refers specifically to this type of device, though the term SM-OLED is also in use.

Molecules commonly used in OLEDs include organometallic chelates (for example Alq3, used in the organic light-emitting device reported by Tang et al.), fluorescent and phosphorescent dyes and conjugated dendrimers. A number of materials are used for their charge transport properties, for exampletriphenylamine and derivatives are commonly used as materials for hole transport layers.[29] Fluorescent dyes can be chosen to obtain light emission at different wavelengths, and compounds such as perylene, rubrene and quinacridone derivatives are often used.[30] Alq3 has been used as a green emitter, electron transport material and as a host for yellow and red emitting dyes.

The production of small molecule devices and displays usually involves thermal evaporation in a vacuum. This makes the production process more expensive and of limited use for large-area devices than other processing techniques. However, contrary to polymer-based devices, the vacuum deposition process enables the formation of well controlled, homogeneous films, and the construction of very complex multi-layer structures. This high flexibility in layer design, enabling distinct charge transport and charge blocking layers to be formed, is the main reason for the high efficiencies of the small molecule OLEDs.

Coherent emission from a laser dye-doped tandem SM-OLED device, excited in the pulsed regime, has been demonstrated.[31] The emission is nearly diffraction limited with a spectral width similar to that of broadband dye lasers.[32]

[edit]Polymer light-emitting diodes

poly(p-phenylene vinylene), used in the first PLED[19]

Polymer light-emitting diodes (PLED), also light-emitting polymers (LEP), involve an electroluminescent conductive polymer that emits light when connected to an external voltage. They are used as a thin film for full-spectrum colour displays. Polymer OLEDs are quite efficient and require a relatively small amount of power for the amount of light produced.

Vacuum deposition is not a suitable method for forming thin films of polymers. However, polymers can be processed in solution, and spin coating is a common method of depositing thin polymer films. This method is more suited to forming large-area films than thermal evaporation. No vacuum is required, and the emissive materials can also be applied on the substrate by a technique derived from commercial inkjet printing.[33][34] However, as the application of subsequent layers tends to dissolve those already present, formation of multilayer structures is difficult with these methods. The metal cathode may still need to be deposited by thermal evaporation in vacuum. An alternative method to vacuum deposition is to deposit a Langmuir-Blodgett film.

Typical polymers used in PLED displays include derivatives of poly(p-phenylene vinylene) and polyfluorene. Substitution of side chains onto the polymer backbone may determine the colour of emitted light[35] or the stability and solubility of the polymer for performance and ease of processing.[36]

While unsubstituted poly(p-phenylene vinylene) (PPV) is typically insoluble, a number of PPVs and related poly(naphthalene vinylene)s (PNVs) that are soluble in organic solvents or water have been prepared via ring opening metathesis polymerization.[37][38][39]

[edit]Phosphorescent materials

Ir(mppy)3, a phosphorescent dopant which emits green light.[40]

Main article: Phosphorescent organic light-emitting diode

Phosphorescent organic light emitting diodes use the principle of electrophosphorescence to convert electrical energy in an OLED into light in a highly efficient manner,[41][42] with the internal quantum efficiencies of such devices approaching 100%.[43]

Typically, a polymer such as poly(n-vinylcarbazole) is used as a host material to which an organometallic complex is added as a dopant. Iridium complexes[42] such as Ir(mppy)3[40] are currently the focus of research, although complexes based on other heavy metals such as platinum[41] have also been used.

The heavy metal atom at the centre of these complexes exhibits strong spin-orbit coupling, facilitating intersystem crossing between singlet and triplet states. By using these phosphorescent materials, both singlet and triplet excitons will be able to decay radiatively, hence improving the internal quantum efficiency of the device compared to a standard PLED where only the singlet states will contribute to emission of light.

Applications of OLEDs in solid state lighting require the achievement of high brightness with good CIE coordinates (for white emission). The use of macromolecular species like polyhedral oligomeric silsesquioxanes (POSS) in conjunction with the use of phosphorescent species such as Ir for printed OLEDs have exhibited brightnesses as high as 10,000 cd/m2.[44]

OLED’s Working principle

A typical OLED is composed of a layer of organic materials situated between two electrodes, the anode and cathode, all deposited on a substrate. The organic molecules are electrically conductive as a result of delocalization of pi electrons caused by conjugation over all or part of the molecule. These materials have conductivity levels ranging from insulators to conductors, and therefore are considered organic semiconductors. The highest occupied and lowest unoccupied molecular orbitals (HOMO and LUMO) of organic semiconductors are analogous to the valence andconduction bands of inorganic semiconductors.

Schematic of a bilayer OLED: 1. Cathode (−), 2. Emissive Layer, 3. Emission of radiation, 4. Conductive Layer, 5. Anode (+)

Originally, the most basic polymer OLEDs consisted of a single organic layer. One example was the first light-emitting device synthesised by J. H. Burroughes et al., which involved a single layer of poly(p-phenylene vinylene). However multilayer OLEDs can be fabricated with two or more layers in order to improve device efficiency. As well as conductive properties, different materials may be chosen to aid charge injection at electrodes by providing a more gradual electronic profile,[20] or block a charge from reaching the opposite electrode and being wasted.[21] Many modern OLEDs incorporate a simple bilayer structure, consisting of a conductive layer and an emissive layer. More recent developments in OLED architecture improves quantum efficiency (up to 19%) by using a graded heterojunction.[22] In the graded heterojunction architecture, the composition of hole and electron-transport materials varies continuously within the emissive layer with a dopant emitter. The graded heterojunction architecture combines the benefits of both conventional architectures by improving charge injection while simultaneously balancing charge transport within the emissive region.[23]

During operation, a voltage is applied across the OLED such that the anode is positive with respect to the cathode. A current of electrons flows through the device from cathode to anode, as electrons are injected into the LUMO of the organic layer at the cathode and withdrawn from the HOMO at the anode. This latter process may also be described as the injection of electron holes into the HOMO. Electrostatic forces bring the electrons and the holes towards each other and they recombine forming an exciton, a bound state of the electron and hole. This happens closer to the emissive layer, because in organic semiconductors holes are generally more mobile than electrons. The decay of this excited state results in a relaxation of the energy levels of the electron, accompanied by emission of radiation whose frequency is in the visible region. The frequency of this radiation depends on the band gap of the material, in this case the difference in energy between the HOMO and LUMO.

As electrons and holes are fermions with half integer spin, an exciton may either be in a singlet state or a triplet state depending on how the spins of the electron and hole have been combined. Statistically three triplet excitons will be formed for each singlet exciton. Decay from triplet states (phosphorescence) is spin forbidden, increasing the timescale of the transition and limiting the internal efficiency of fluorescent devices. Phosphorescent organic light-emitting diodes make use of spin–orbit interactions to facilitate intersystem crossing between singlet and triplet states, thus obtaining emission from both singlet and triplet states and improving the internal efficiency.

Indium tin oxide (ITO) is commonly used as the anode material. It is transparent to visible light and has a high work function which promotes injection of holes into the HOMO level of the organic layer. A typical conductive layer may consist of PEDOT:PSS[24] as the HOMO level of this material generally lies between the workfunction of ITO and the HOMO of other commonly used polymers, reducing the energy barriers for hole injection. Metals such as barium and calcium are often used for the cathode as they have low work functions which promote injection of electrons into the LUMO of the organic layer.[25] Such metals are reactive, so they require a capping layer of aluminium to avoid degradation.

Single carrier devices are typically used to study the kinetics and charge transport mechanisms of an organic material and can be useful when trying to study energy transfer processes. As current through the device is composed of only one type of charge carrier, either electrons or holes, recombination does not occur and no light is emitted. For example, electron only devices can be obtained by replacing ITO with a lower work function metal which increases the energy barrier of hole injection. Similarly, hole only devices can be made by using a cathode comprised solely of aluminium, resulting in an energy barrier too large for efficient electron injection


An OLED (organic light-emitting diode) is a light-emitting diode (LED) in which the emissive electroluminescent layer is a film of organic compoundwhich emits light in response to an electric current. This layer of organic semiconductor material is situated between two electrodes. Generally, at least one of these electrodes is transparent. OLEDs are used to create digital displays in devices such as television screens, computer monitors, portable systems such as mobile phones, handheld games consoles and PDAs.

There are two main families of OLEDs: those based on small molecules and those employing polymers. Adding mobile ions to an OLED creates a light-emitting electrochemical cell or LEC, which has a slightly different mode of operation. OLED displays can use either passive-matrix (PMOLED) or active-matrix addressing schemes. Active-matrix OLEDs (AMOLED) require a thin-film transistor backplane to switch each individual pixel on or off, but allow for higher resolution and larger display sizes.

An OLED display works without a backlight. Thus, it can display deep black levels and can be thinner and lighter than a liquid crystal display (LCD). In low ambient light conditions such as a dark room an OLED screen can achieve a higher contrast ratio than an LCD, whether the LCD uses cold cathode fluorescent lamps or LED backlight. Due to its low thermal conductivity, an OLED typically emits less light per area than an inorganic LED.

2,3,4,5-TETRAMETHYLPYRROLE 1003-90-3

CAS No. 1003-90-3
Chemical Name: 2,3,4,5-TETRAMETHYLPYRROLE
Synonyms: 2,3,4,5-TETRAMETHYLPYRROLE;2,3,4,5-tetramethyl-1H-pyrrole;1H-Pyrrole, 2,3,4,5-tetraMethyl-;2,3,4,5-TETRAMETHYLPYRROLE: TECH., 85%
CBNumber: CB3215360
Molecular Formula: C8H13N
Formula Weight: 123.2
MOL File: 1003-90-3.mol
mp : 107-110°C
Sensitive : Air & Light Sensitive
BRN : 107096
Safety Statements : 22-24/25









Benzenamine, N-(2-aminoethyl)-
Ethylenediamine, N-phenyl-



【Molecular Formula】


【MDL Number】


【Molecular Weight】


【MOL File】


Chemical Properties Back Directory


【bp 】

262-264 °C(lit.)

【density 】

1.041 g/mL at 25 °C(lit.)

【refractive index 】

n20/D 1.587(lit.)

【Fp 】

>230 °F

【Sensitive 】

Air Sensitive

【BRN 】


【CAS DataBase Reference】

1664-40-0(CAS DataBase Reference)

Safety Data Back Directory
【Hazard Codes 】


【Risk Statements 】

R34:Causes burns.
R37:Irritating to the respiratory system.

【Safety Statements 】

S26:In case of contact with eyes, rinse immediately with plenty of water and seek medical advice .
S36/37/39:Wear suitable protective clothing, gloves and eye/face protection .
S45:In case of accident or if you feel unwell, seek medical advice immediately (show label where possible) .



【WGK Germany 】


【HazardClass 】


【PackingGroup 】

what ‘s MSDS (Material safety data sheet)

material safety data sheet (MSDS), safety data sheet (SDS),[1] or product safety data sheet (PSDS) is an important component of product stewardship and occupational safety and health. It is intended to provide workers and emergency personnel with procedures for handling or working with that substance in a safe manner, and includes information such as physical data (melting point, boiling point, flash point, etc.),toxicity, health effects, first aid, reactivity, storage, disposal, protective equipment, and spill-handling procedures. MSDS formats can vary from source to source within a country depending on national requirements.

SDSs are a widely used system for cataloging information on chemicals, chemical compounds, and chemical mixtures. SDS information may include instructions for the safe use and potential hazards associated with a particular material or product. These data sheets can be found anywhere where chemicals are being used.

There is also a duty to properly label substances on the basis of physico-chemical, health and/or environmental risk. Labels can include hazard symbols such as the European Union standard black diagonal cross on an orange background, used to denote a harmful substance.

An SDS for a substance is not primarily intended for use by the general consumer, focusing instead on the hazards of working with the material in an occupational setting.

In some jurisdictions, the SDS is required to state the chemical’s risks, safety, and effect on the environment.

It is important to use an SDS specific to both country and supplier, as the same product (e.g. paints sold under identical brand names by the same company) can have different formulations in different countries. The formulation and hazard of a product using a generic name (e.g. sugar soap) may vary between manufacturers in the same country.

National and international requirements


In Canada, the program known as the Workplace Hazardous Materials Information System (WHMIS) establishes the requirements for MSDS’s in workplaces and is administered federally byHealth Canada under the Hazardous Products Act, Part II, and the Controlled Products Regulations. WHMIS and MSDS requirements are also enforced by provincial Ministries or Departments of Labour.

European Union

Safety data sheets have been made an integral part of the system of Regulation (EC) No 1907/2006 (REACH).[2] The original requirements of REACH for SDSs have been further adapted to take into account the rules for safety data sheets of the Global Harmonised System (GHS)[3] and the implementation of other elements of the GHS into EU legislation that were introduced by Regulation (EC) No 1272/2008 (CLP)[4] via an update to Annex II of REACH.[5]

The SDS follows a 16 section format which is internationally agreed and for substances especially, the SDS should be followed with an Annex which contains the exposure scenarios of this particular substance.[6] The SDS must be supplied in an official language of the Member State(s) where the substance or mixture is placed on the market, unless the Member State(s) concerned provide(s) otherwise (Article 31(5) of REACH).

The European Chemicals Agency (ECHA) has published a guidance document on the compilation of safety data sheets.


The German Federal Water Management Act requires that substances be evaluated for negative influence on the physical, chemical or biological characteristics of water. These are classified into numeric water hazard classes (WGK or WHC depending whether you use the German or English abbreviation).

  • WGK nwg: Non-water polluting substance
  • WGK 1: Slightly water polluting substance
  • WGK 2: Water polluting substance
  • WGK 3: Highly water polluting substance

[edit]The Netherlands

Dutch Safety Data Sheets are well known as veiligheidsinformatieblad nl:Veiligheidsinformatieblad or Chemiekaarten. This is a collection of Safety Data Sheets of the most widely used chemicals. The Chemiekaarten boek is commercially available, but also made available through educational institutes, such as the web site offered by the university of Groningen[7]

United Kingdom

In the U.K., the Chemicals (Hazard Information and Packaging for Supply) Regulations 2002 – known as CHIP Regulations – impose duties upon suppliers, and importers into the EU, of hazardous materials.[8] The Control of Substances Hazardous to Health (COSHH) Regulations govern the use of hazardous substances in the workplace in the UK and specifically require an assessment of the use of a substance.[9] Regulation 12 requires that an employer provides employees with information, instruction and training for people exposed to hazardous substances. This duty would be very nearly impossible without the data sheet as a starting point. It is important for employers therefore to insist on receiving a data sheet from a supplier of a substance.

The duty to supply information is not confined to informing only business users of products. MSDSs for retail products sold by large DIY shops are usually obtainable on those companies’ web sites.

Web sites of manufacturers and large suppliers do not always include them even if the information is obtainable from retailers but written or telephone requests for paper copies will usually be responded to favourably.

United Nations

The United Nations (UN) defines certain details used in SDSs such as the UN numbers used to identify some hazardous materials in a standard form while in international transit.

United States

In the U.S., the Occupational Safety and Health Administration requires that MSDSs be available to employees for potentially harmful substances handled in the workplace under the Hazard Communication regulation. The MSDS is also required to be made available to local fire departments and local and state emergency planning officials under Section 311 of the Emergency Planning and Community Right-to-Know Act. The American Chemical Society defines Chemical Abstracts Service Registry Numbers (CAS numbers) which provide a unique number for each chemical and are also used internationally in MSDSs.

SDS authoring

Many companies offer the service of collecting, or writing and revising, data sheets to ensure they are up to date and available for their subscribers or users.[10] Some jurisdictions impose an explicit duty of care that each SDS be regularly updated (usually every three to five years).

Ethanimidamide,hydrochloride 124-42-5

identification of 124-42-5

  • Name:Ethanimidamide,hydrochloride (1:1) (Related Reference)
  • EINECS:204-700-9
  • Molecular Formula:C2H6N2.HCl
  • CAS Registry Number:124-42-5
  • Synonyms:Acetamidine,hydrochloride (6CI,7CI);Acetamidine, monohydrochloride (8CI);Ethanimidamide,monohydrochloride (9CI);Acetamidinium chloride;Acetimidinium chloride;Ethanamidine hydrochloride;Ethanimidamide,hydrochloride;Methylamidine hydrochloride;SN 4455;a-Amino-a-iminoethanehydrochloride;Ethanimidamide, Monohydrochloride;
  • InChI:InChI=1/C2H6N2.ClH/c1-2(3)4;/h1H3,(H3,3,4);1H
  • HS Code:29252000
  • Molecular Structure:Ethanimidamide,hydrochloride (1:1) C2H6N2.HCl (cas 124-42-5) Molecular Structure
  • This structure is also available as a2d Mol file.

Chemical Properties

  • Molecular Weight:94.54
  • Density:g/cm3
  • Water solubility:1 g/mL
  • Boiling Point:62.8°Cat760mmHg
  • Melting Point:165-170℃
  • Flash Point:26.1°C
  • Storage Temperature:Store in a tightly closed container. Store in a cool, dry, well-ventilated area away from incompatible substances.
  • Refractive index:1.458
  • Solubility:1 g/mL
  • Appearance:Colorless to white solid.
  • Stability:Stable at room temperature in closed containers under normal storage and handling conditions.

Safety Data of 124-42-5

  • Risk Codes:R36/38
  • Safety Statements :S26;S37/39
  • Hazard Symbols:

Material Safety Data Sheet(MSDS)

  • 【msds infomation】:Ethanimidamide,hydrochloride (1:1) (124-42-5).msds




Since cholesterol is essential for all animal life, each cell synthesizes it from simpler molecules, a complex 37-step process which starts with the intracellular protein enzyme HMG-CoA reductase. However, normal and especially high levels of fats (including cholesterol) within the blood circulation, depending on how it is transported within lipoproteins, are strongly associated with progression of atherosclerosis.

For a man of about 68 kg (150 pounds), typical total body-cholesterol synthesis is about 1 g (1,000 mg) per day, and total body content is about 35 g, primarily located within all the membranes of all the cells of the body. Typical daily dietary intake of additional cholesterol, in the United States, is 200–300 mg.[6]

However, most ingested cholesterol is esterified and esterified cholesterol is poorly absorbed. The body also compensates for any absorption of additional cholesterol by reducing cholesterol synthesis.[7] For these reasons, cholesterol intake in food has little, if any, effect on total body cholesterol content or concentrations of cholesterol in the blood.

Cholesterol is recycled. The liver excretes it in a non-esterified form (via bile) into the digestive tract. Typically about 50% of the excreted cholesterol is reabsorbed by the small bowel back into the bloodstream.

Some plants make cholesterol in very small amounts.[8] Plants manufacture phytosterols (substances chemically similar to cholesterol produced within plants), which can compete with cholesterol for reabsorption in the intestinal tract, thus potentially reducing cholesterol reabsorption.[9] However, phytosterols are foreign to animal cells and, if absorbed, accelerate the progression ofatherosclerosis.[citation needed] When intestinal lining cells absorb phytosterols, in place of cholesterol, they usually excrete the phytosterol molecules back into the GI tract, an important protective mechanism.


Cholesterol is required to build and maintain membranes; it modulates membrane fluidity over the range of physiological temperatures. The hydroxyl group on cholesterol interacts with the polar head groups of the membrane phospholipids and sphingolipids, while the bulkysteroid and the hydrocarbon chain are embedded in the membrane, alongside the nonpolar fatty-acid chain of the other lipids. Through the interaction with the phospholipid fatty-acid chains, cholesterol increases membrane packing, which reduces membrane fluidity.[10]The structure of the tetracyclic ring of cholesterol contributes to the decreased fluidity of the cell membrane as the molecule is in a trans conformation making all but the side chain of cholesterol rigid and planar.[11] In this structural role, cholesterol reduces the permeability of the plasma membrane to neutral solutes,[12] protons, (positive hydrogen ions) and sodium ions.[13]

Within the cell membrane, cholesterol also functions in intracellular transport, cell signaling and nerve conduction. Cholesterol is essential for the structure and function of invaginated caveolae and clathrin-coated pits, including caveola-dependent and clathrin-dependentendocytosis. The role of cholesterol in such endocytosis can be investigated by using methyl beta cyclodextrin (MβCD) to remove cholesterol from the plasma membrane. Recently, cholesterol has also been implicated in cell signaling processes, assisting in the formation of lipid rafts in the plasma membrane. Lipid raft formation brings receptor proteins in close proximity with high concentrations of second messenger molecules.[14] In many neurons, a myelin sheath, rich in cholesterol, since it is derived from compacted layers of Schwann cell membrane, provides insulation for more efficient conduction of impulses.[15]

Within cells, cholesterol is the precursor molecule in several biochemical pathways. In the liver, cholesterol is converted to bile, which is then stored in thegallbladder. Bile contains bile salts, which solubilize fats in the digestive tract and aid in the intestinal absorption of fat molecules as well as the fat-soluble vitamins, A, D, E, and K. Cholesterol is an important precursor molecule for the synthesis of vitamin D and the steroid hormones, including the adrenal gland hormones cortisol and aldosterone, as well as the sex hormones progesterone, estrogens, and testosterone, and their derivatives.[3]

Some research indicates cholesterol may act as an antioxidant.[16]

[edit]Dietary sources

Animal fats are complex mixtures of triglycerides, with lesser amounts of phospholipids and cholesterol. As a consequence, all foods containing animal fat contain cholesterol to varying extents.[17] Major dietary sources of cholesterol include cheese, egg yolks, beef, pork, poultry, fish, and shrimp.[18]Human breast milk also contains significant quantities of cholesterol.[19]

From a dietary perspective, cholesterol is not found in significant amounts in plant sources.[18][20] In addition, plant products such as flax seeds and peanuts contain cholesterol-like compounds called phytosterols, which are believed to compete with cholesterol for absorption in the intestines.[21] Phytosterols can be supplemented through the use of phytosterol-containing functional foods or nutraceuticals that are widely recognized as having a proven LDL cholesterol-lowering efficacy.[22] Current supplemental guidelines recommend doses of phytosterols in the 1.6-3.0 grams per day range (Health Canada, EFSA, ATP III,FDA) with a recent meta-analysis demonstrating an 8.8% reduction in LDL-cholesterol at a mean dose of 2.15 gram per day.[23] However, the benefits of a diet supplemented with phytosterol has been questioned.[24][25]

Fat-intake also plays a role in blood-cholesterol levels. This effect is thought[by whom?] to come about by changes in the quantity of cholesterol and lipoproteins that are synthesized by the body. Isocalorically replacing dietary carbohydrates with monounsaturated and polyunsaturated fats has been shown to lower serum LDL and total cholesterol levels and increase serumHDL levels, while replacing carbohydrates with saturated fat was shown to increase total, HDL, and LDL cholesterol levels.[26] Trans fats have been shown to reduce levels of HDL whilst increasing levels of LDL.[27] Based on such evidence and evidence implicating low HDL and high LDL levels in cardiovascular disease (see Hypercholesterolemia), many health authorities advocate reducing LDL cholesterol through changes in diet in addition to other lifestyle modifications.[4] The USDA for example recommends that those wishing to reduce their cholesterol through a change in diet should aim to consume less than 7% of their daily energy needs from saturated fat and fewer than 200 mg of cholesterol per day.[28] An alternative view is that any reduction to dietary cholesterol intake could be counteracted by the organs compensating to try to keep blood cholesterol levels constant.[29]

However, the The China Study uses epidemiological evidence to claim that casein raises blood cholesterol even more than the ingested saturated fat or cholesterol.[30]


All animal cells manufacture cholesterol with relative production rates varying by cell type and organ function. About 20–25% of total daily cholesterol production occurs in the liver; other sites of higher synthesis rates include the intestines, adrenal glands, and reproductive organs. Synthesis within the body starts with one molecule of acetyl CoA and one molecule ofacetoacetyl-CoA, which are hydrated to form 3-hydroxy-3-methylglutaryl CoA (HMG-CoA). This molecule is then reduced to mevalonate by the enzyme HMG-CoA reductase. This step is the regulated, rate-limiting and irreversible step in cholesterol synthesis and is the site of action for the statin drugs (HMG-CoA reductase competitive inhibitors).

Mevalonate is then converted to 3-isopentenyl pyrophosphate in three reactions that require ATP. Mevalonate is decarboxylated to isopentenyl pyrophosphate, which is a key metabolite for various biological reactions. Three molecules of isopentenyl pyrophosphate condense to form farnesyl pyrophosphate through the action of geranyl transferase. Two molecules of farnesyl pyrophosphate then condense to form squalene by the action of squalene synthase in the endoplasmic reticulum. Oxidosqualene cyclase then cyclizes squalene to form lanosterol. Finally, lanosterol is then converted to cholesterol through a 19 step complex process.[31][32]

Konrad Bloch and Feodor Lynen shared the Nobel Prize in Physiology or Medicine in 1964 for their discoveries concerning the mechanism and regulation of cholesterol and fatty acid metabolism.

[edit]Regulation of cholesterol synthesis

Biosynthesis of cholesterol is directly regulated by the cholesterol levels present, though the homeostatic mechanisms involved are only partly understood. A higher intake from food leads to a net decrease in endogenous production, whereas lower intake from food has the opposite effect. The main regulatory mechanism is the sensing of intracellular cholesterol in theendoplasmic reticulum by the protein SREBP (sterol regulatory element-binding protein 1 and 2).[33] In the presence of cholesterol, SREBP is bound to two other proteins: SCAP (SREBP-cleavage-activating protein) and Insig1. When cholesterol levels fall, Insig-1 dissociates from the SREBP-SCAP complex, allowing the complex to migrate to the Golgi apparatus, where SREBP is cleaved by S1P and S2P (site-1 and -2 protease), two enzymes that are activated by SCAP when cholesterol levels are low. The cleaved SREBP then migrates to the nucleus and acts as atranscription factor to bind to the sterol regulatory element (SRE), which stimulates the transcription of many genes. Among these are the low-density lipoprotein (LDL) receptor and HMG-CoA reductase. The former scavenges circulating LDL from the bloodstream, whereas HMG-CoA reductase leads to an increase of endogenous production of cholesterol.[34] A large part of this signaling pathway was clarified by Dr. Michael S. Brown and Dr. Joseph L. Goldstein in the 1970s. In 1985, they received the Nobel Prize in Physiology or Medicine for their work. Their subsequent work shows how the SREBP pathway regulates expression of many genes that control lipid formation and metabolism and body fuel allocation.

Cholesterol synthesis can be turned off when cholesterol levels are high, as well. HMG CoA reductase contains both a cytosolic domain (responsible for its catalytic function) and a membrane domain. The membrane domain functions to sense signals for its degradation. Increasing concentrations of cholesterol (and other sterols) cause a change in this domain’s oligomerization state, which makes it more susceptible to destruction by the proteosome. This enzyme’s activity can also be reduced by phosphorylation by an AMP-activated protein kinase. Because this kinase is activated by AMP, which is produced when ATP is hydrolyzed, it follows that cholesterol synthesis is halted when ATP levels are low.[35]

[edit]Plasma transport and regulation of absorption

See also: Blood lipids

Cholesterol is only slightly soluble in water; it can dissolve and travel in the water-based bloodstream at exceedingly small concentrations. Since cholesterol is insoluble in blood, it is transported in the circulatory system within lipoproteins, complex discoidal particles that have an exterior composed of amphiphilic proteins and lipids whose outward-facing surfaces are water-soluble and inward-facing surfaces are lipid-soluble; triglycerides and cholesterol esters are carried internally. Phospholipids and cholesterol, being amphipathic, are transported in the surface monolayer of the lipoprotein particle.

In addition to providing a soluble means for transporting cholesterol through the blood, lipoproteins have cell-targeting signals that direct the lipids they carry to certain tissues. For this reason, there are several types of lipoproteins within blood called, in order of increasing density, chylomicrons, very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL), and high-density lipoprotein (HDL). The more lipid and less protein a lipoprotein has the less dense it is. The cholesterol within all the various lipoproteins is identical, although some cholesterol is carried as the “free” alcohol and some is carried as fatty acyl esters referred to as cholesterol esters. However, the different lipoproteins contain apolipoproteins, which serve as ligands for specific receptors on cell membranes. In this way, the lipoprotein particles are molecular addresses that determine the start- and endpoints for cholesterol transport.

Chylomicrons, the least dense type of cholesterol transport molecules, contain apolipoprotein B-48, apolipoprotein C, and apolipoprotein E in their shells. Chylomicrons are the transporters that carry fats from the intestine to muscle and other tissues that need fatty acids for energy or fat production. Cholesterol that is not used by muscles remains in more cholesterol-rich chylomicron remnants, which are taken up from here to the bloodstream by the liver.

VLDL molecules are produced by the liver and contain excess triacylglycerol and cholesterol that is not required by the liver for synthesis of bile acids. These molecules contain apolipoprotein B100 and apolipoprotein E in their shells. During transport in the bloodstream, the blood vessels cleave and absorb more triacylglycerol from IDL molecules, which contain an even higher percentage of cholesterol. The IDL molecules have two possible fates: Half are into metabolism by HTGL, taken up by the LDL receptor on the liver cell surfaces, and the other half continue to lose triacylglycerols in the bloodstream until they form LDL molecules, which have the highest percentage of cholesterol within them.

LDL molecules, therefore, are the major carriers of cholesterol in the blood, and each one contains approximately 1,500 molecules of cholesterol ester. The shell of the LDL molecule contains just one molecule of apolipoprotein B100, which is recognized by the LDL receptor in peripheral tissues. Upon binding of apolipoprotein B100, many LDL receptors become localized inclathrin-coated pits. Both the LDL and its receptor are internalized by endocytosis to form a vesicle within the cell. The vesicle then fuses with a lysosome, which has an enzyme calledlysosomal acid lipase that hydrolyzes the cholesterol esters. Now within the cell, the cholesterol can be used for membrane biosynthesis or esterified and stored within the cell, so as to not interfere with cell membranes.

Synthesis of the LDL receptor is regulated by SREBP, the same regulatory protein as was used to control synthesis of cholesterol de novo in response to cholesterol presence in the cell. When the cell has abundant cholesterol, LDL receptor synthesis is blocked so new cholesterol in the form of LDL molecules cannot be taken up. On the converse, more LDL receptors are made when the cell is deficient in cholesterol. When this system is deregulated, many LDL molecules appear in the blood without receptors on the peripheral tissues. These LDL molecules are oxidized and taken up by macrophages, which become engorged and form foam cells. These cells often become trapped in the walls of blood vessels and contribute to atherosclerotic plaqueformation. Differences in cholesterol homeostasis affect the development of early atherosclerosis (carotid intima-media thickness).[36] These plaques are the main causes of heart attacks, strokes, and other serious medical problems, leading to the association of so-called LDL cholesterol (actually a lipoprotein) with “bad” cholesterol.[35]

Also, HDL particles are thought to transport cholesterol back to the liver for excretion or to other tissues that use cholesterol to synthesize hormones in a process known as reverse cholesterol transport (RCT).[37] Having large numbers of large HDL particles correlates with better health outcomes.[38] In contrast, having small numbers of large HDL particles is independently associated with atheromatous disease progression within the arteries.

[edit]Metabolism, recycling and excretion

Cholesterol is susceptible to oxidation and easily forms oxygenated derivatives known as oxysterols. Three different mechanisms can form these; autoxidation, secondary oxidation to lipid peroxidation, and cholesterol-metabolizing enzyme oxidation. A great interest in oxysterols arose when they were shown to exert inhibitory actions on cholesterol biosynthesis.[39] This finding became known as the “oxysterol hypothesis”. Additional roles for oxysterols in human physiology include their: participation in bile acid biosynthesis, function as transport forms of cholesterol, and regulation of gene transcription.[40]

In biochemical experiments radiolabelled forms of cholesterol, such as tritiated-cholesterol are used. These derivatives undergo degradation upon storage and it is essential to purify cholesterol prior to use. Cholesterol can be purified using small Sephadex LH-20 columns.[41]

Cholesterol is oxidized by the liver into a variety of bile acids.[42] These, in turn, are conjugated with glycine, taurine, glucuronic acid, or sulfate. A mixture of conjugated and nonconjugated bile acids, along with cholesterol itself, is excreted from the liver into the bile. Approximately 95% of the bile acids are reabsorbed from the intestines, and the remainder are lost in the feces.[43] The excretion and reabsorption of bile acids forms the basis of the enterohepatic circulation, which is essential for the digestion and absorption of dietary fats. Under certain circumstances, when more concentrated, as in the gallbladder, cholesterol crystallises and is the major constituent of most gallstones. Although, lecithin and bilirubin gallstones also occur, but less frequently.[44] Every day, up to 1 g of cholesterol enters the colon. This cholesterol originates from the diet, bile, and desquamated intestinal cells, and can be metabolized by the colonic bacteria. Cholesterol is converted mainly into coprostanol, a nonabsorbable sterol that is excreted in the feces. A cholesterol-reducing bacterium origin has been isolated from human feces.[45][non-primary source needed]

[edit]Clinical significance


Main articles: hypercholesterolemia and lipid hypothesis

According to the lipid hypothesis, abnormal cholesterol levels (hypercholesterolemia) — that is, higher concentrations of LDL and lower concentrations of functional HDL — are strongly associated with cardiovascular disease because these promote atheroma development in arteries (atherosclerosis). This disease process leads to myocardial infarction (heart attack), stroke, and peripheral vascular disease. Since higher blood LDL, especially higher LDL particle concentrations and smaller LDL particle size, contribute to this process more than the cholesterol content of the HDL particles,[46] LDL particles are often termed “bad cholesterol” because they have been linked to atheroma formation. On the other hand, high concentrations of functional HDL, which can remove cholesterol from cells and atheroma, offer protection and are sometimes referred to as “good cholesterol”. These balances are mostly genetically determined, but can be changed by body build, medications, food choices, and other factors.[47] Resistin, a protein secreted by fat tissue, has been shown to increase the production of LDL in human liver cells and also degrades LDL receptors in the liver. As a result, the liver is less able to clear cholesterol from the bloodstream. Resistin accelerates the accumulation of LDL in arteries, increasing the risk of heart disease. Resistin also adversely impacts the effects of statins, the main cholesterol-reducing drug used in the treatment and prevention of cardiovascular disease.[48]

Conditions with elevated concentrations of oxidized LDL particles, especially “small dense LDL” (sdLDL) particles, are associated with atheroma formation in the walls of arteries, a condition known as atherosclerosis, which is the principal cause of coronary heart disease and other forms of cardiovascular disease. In contrast, HDL particles (especially large HDL) have been identified as a mechanism by which cholesterol and inflammatory mediators can be removed from atheroma. Increased concentrations of HDL correlate with lower rates of atheroma progressions and even regression. A 2007 study pooling data on almost 900,000 subjects in 61 cohorts demonstrated that blood total cholesterol levels have an exponential effect on cardiovascular and total mortality, with the association more pronounced in younger subjects. Still, because cardiovascular disease is relatively rare in the younger population, the impact of high cholesterol on health is still larger in older people.[49]

Elevated levels of the lipoprotein fractions, LDL, IDL and VLDL are regarded as atherogenic (prone to cause atherosclerosis).[50] Levels of these fractions, rather than the total cholesterol level, correlate with the extent and progress of atherosclerosis. Conversely, the total cholesterol can be within normal limits, yet be made up primarily of small LDL and small HDL particles, under which conditions atheroma growth rates would still be high. In contrast, however, if LDL particle number is low (mostly large particles) and a large percentage of the HDL particles are large, then atheroma growth rates are usually low, even negative, for any given total cholesterol concentration.[citation needed] Recently, a post hoc analysis of the IDEAL and the EPIC prospective studies found an association between high levels of HDL cholesterol (adjusted for apolipoprotein A-I and apolipoprotein B) and increased risk of cardiovascular disease, casting doubt on the cardioprotective role of “good cholesterol”.[51]

Elevated cholesterol levels are treated with a strict diet consisting of low saturated fat, trans fat-free, low cholesterol foods,[52][53] often followed by one of various hypolipidemic agents, such as statins, fibrates, cholesterol absorption inhibitors, nicotinic acid derivatives or bile acid sequestrants.[54] Extreme cases have previously been treated with partial ileal bypass surgery, which has now been superseded by medication. Apheresis-based treatments are still used for very severe hyperlipidemias that are either unresponsive to treatment or require rapid lowering of blood lipids.[citation needed]

Multiple human trials using HMG-CoA reductase inhibitors, known as statins, have repeatedly confirmed that changing lipoprotein transport patterns from unhealthy to healthier patterns significantly lowers cardiovascular disease event rates, even for people with cholesterol values currently considered low for adults.[citation needed] Studies have also found that statins reduce atheroma progression.[55] As a result, people with a history of cardiovascular disease may derive benefit from statins irrespective of their cholesterol levels,[56] and in men without cardiovascular disease, there is benefit from lowering abnormally high cholesterol levels (“primary prevention”).[57] Primary prevention in women is practiced only by extension of the findings in studies on men,[58] since in women, none of the large statin trials has shown a reduction in overall mortality or in cardiovascular endpoints.[59]

Level mg/dL Level mmol/L Interpretation
< 200 < 5.2 Desirable level corresponding to lower risk for heart disease
200–240 5.2–6.2 Borderline high risk
> 240 > 6.2 High risk

The 1987 report of National Cholesterol Education Program, Adult Treatment Panels suggests the total blood cholesterol level should be: < 200 mg/dL normal blood cholesterol, 200–239 mg/dL borderline-high, > 240 mg/dL high cholesterol.[60] The American Heart Association provides a similar set of guidelines for total (fasting) blood cholesterol levels and risk for heart disease:[61]

However, as today’s testing methods determine LDL (“bad”) and HDL (“good”) cholesterol separately, this simplistic view has become somewhat outdated. The desirable LDL level is considered to be less than 100 mg/dL (2.6 mmol/L),[62] although a newer upper limit of 70 mg/dL (1.8 mmol/L) can be considered in higher-risk individuals based on some of the above-mentioned trials. A ratio of total cholesterol to HDL—another useful measure—of far less than 5:1 is thought to be healthier. Of note, typical LDL values for children before fatty streaks begin to develop is 35 mg/dL.

Cholesterol, from the Greek chole- (bile) and stereos (solid) followed by the chemical suffix -ol for an alcohol, is an organic chemical substance classified as a waxy steroid of fat. It is an essential structural component of mammalian cell membranes and is required to establish proper membrane permeability and fluidity.

In addition to its importance within cells, cholesterol also serves as a precursor for the biosynthesis of steroid hormones, bile acids, andvitamin D.[3] Cholesterol is the principal sterol synthesized by animals; in vertebrates it is formed predominantly in the liver. Small quantities are synthesized in other cellular organisms (eukaryotes) such as plants and fungi. It is almost completely absent among prokaryotes (i.e., bacteria).

Although cholesterol is important and necessary for human health, high levels of cholesterol in the blood have been linked to damage to arteries and cardiovascular disease.[4]

François Poulletier de la Salle first identified cholesterol in solid form in gallstones, in 1769. However, it was only in 1815 that chemist Eugène Chevreul named the compound “cholesterine

CAS number 57-88-5 Yes
PubChem 5997
ChemSpider 5775 Yes
KEGG D00040 Yes
ChEBI CHEBI:16113 Yes
Jmol-3D images Image 1
Molecular formula C27H46O
Molar mass 386.65 g/mol
Appearance white crystalline powder[2]
Density 1.052 g/cm3
Melting point 148–150 °C[2]
Boiling point 360 °C (decomposes)
Solubility inwater 0.095 mg/L (30 °C)
Solubility soluble in acetone, benzene,chloroform, ethanol, ether, hexane,isopropyl myristate, methanol
Flash point 209.3 ±12.4°C [1]
 Yes (verify) (what is: Yes/?)
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Infobox references

Hydrogen peroxide


Hydrogen peroxide (H2O2) is the simplest peroxide (a compound with an oxygen-oxygen single bond). It is also a strong oxidizer. Hydrogen peroxide is a clear liquid, slightly more viscous than water. In dilute solution, it appears colorless. Due to its oxidizing properties, hydrogen peroxide is often used as a bleach or cleaning agent. The oxidizing capacity of hydrogen peroxide is so strong that it is considered a highlyreactive oxygen species. Hydrogen peroxide is therefore used as a propellant in rocketry.[1] Organisms also naturally produce hydrogen peroxide as a by-product of oxidative metabolism. Consequently, nearly all living things (specifically, all obligate and facultative aerobes) possess enzymes known as catalase peroxidases, which harmlessly and catalytically decompose low concentrations of hydrogen peroxide to water and oxygen.

Hydrogen peroxide
CAS number 7722-84-1 Yes
PubChem 784
ChemSpider 763 Yes
EC number 231-765-0
UN number 2015 (>60% soln.)
2014 (20–60% soln.)
2984 (8–20% soln.)
KEGG D00008 Yes
ChEBI CHEBI:16240 Yes
IUPHAR ligand 2448
RTECS number MX0900000 (>90% soln.)
MX0887000 (>30% soln.)
ATC code A01AB02,D08AX01,S02AA06
Jmol-3D images Image 1
Molecular formula 2(HO)
Molar mass 34.0147 g/mol
Appearance Very light blue color; colorless in solution
Odor slightly sharp
Density 1.135 g/cm3 (20 °C, 30-percent)
1.450 g/cm3 (20 °C, pure)
Melting point -0.43 °C, 273 K, 31 °F
Boiling point 150.2 °C, 423 K, 302 °F
Solubility in water Miscible
Solubility soluble in ether, alcohol
insoluble in petroleum ether
Acidity (pKa) 11.75
Refractive index(nD) 1.4061
Viscosity 1.245 cP (20 °C)
Dipole moment 2.26 D
Std enthalpy of
formation ΔfHo298
-135.77 kJ/mol
Specific heat capacity, C 1.267 J/g K (gas)
2.619 J/g K (liquid)
MSDS ICSC 0164 (>60% soln.)
EU Index 008-003-00-9
EU classification Hazard O.svgOxidant (O)
Hazard C.svgCorrosive (C)
Hazard X.svgHarmful (Xn)
R-phrases R5R8R20/22R35
S-phrases (S1/2)S17S26S28,S36/37/39S45
NFPA 704
NFPA 704.svg
Flash point Non-flammable
LD50 1518 mg/kg
Related compounds
Related compounds Water
Hydrogen disulfide
Dioxygen difluoride


Structure and properties

O-O bond length = 147.4 pm O-H bond length = 95.0 pm
Structure and dimensions of the H2O2 molecule in the gas phase…
O-O bond length = 145.8 pm O-H bond length = 98.8 pm
… and in the solid (crystalline) phase.
Phase diagram hydrogen peroxide water.svg

H2O2 adopts a nonplanar structure of C2 symmetry. Although chiral, the molecule undergoes rapidracemization. The flat shape of the anti conformer would minimize steric repulsions, the 90° torsion angle of the syn conformer would optimize mixing between the filled p-type orbital of the oxygen (one of the lone pairs) and the LUMO of the vicinal O-H bond.[2] The observed anticlinal ”skewed” shape is a compromise between the two conformers.

Although the O−O bond is a single bond, the molecule has a relatively high barrier to rotation, of 29.45kJ/mol; the rotational barrier is 12.5 kJ/mol for the bulkier molecule ethane. The increased barrier is ascribed to repulsion between nonbonding electrons (lone pairs) on the adjacent oxygen centres. The bond anglesare affected by hydrogen bonding, which is relevant to the difference between the structure of gaseous andcrystalline forms; indeed a wide range of values is seen in crystals containing H2O2.

[edit]Comparison with analogues

Analogues of hydrogen peroxide include the chemically identical deuterium peroxide, and hydrogen disulfide.[3] Hydrogen disulfide has a boiling point of only 70.7 °C despite having a higher molecular weight, indicating that hydrogen bonding increases the boiling point of hydrogen peroxide.

[edit]Physical properties of hydrogen peroxide solutions

In aqueous solutions hydrogen peroxide differs from the pure material. This demonstrates the effects of hydrogen bonding between water and hydrogen peroxide molecules. Hydrogen peroxide and water form a eutectic mixture, exhibiting freezing-point depression. Pure water melts and freezes at approximately 273 K, and pure hydrogen peroxide just 0.4 K below that, but a 50% (by volume) solution melts and freezes at 221 K. The boiling point of the same mixture is less than the average (398 K) of the boiling points of pure water (373 K) and hydrogen peroxide (423 K) at 387 K.[4]

[edit]pH of H2O2

Pure hydrogen peroxide has a pH of 6.2; thus it is considered to be a weak acid. The pH can be as low as 4.5 when diluted at approximately 60%.[5]


Louis Jacques Thénard first described hydrogen peroxide in 1818. He produced it by reacting barium peroxide with nitric acid.[6] An improved version of this process used hydrochloric acid, followed by addition of sulfuric acid to precipitate the barium sulfate byproduct. Thénard’s process was used from the end of the 19th century until the middle of the 20th century.[7] Modern production methods are discussed below.

Pure hydrogen peroxide was long believed to be unstable. This was because of failed attempts to separate the hydrogen peroxide from the water, which is present during synthesis. However, this instability was due to traces of impurities (transition metals salts) that catalyze the decomposition of the hydrogen peroxide. One hundred percent pure hydrogen peroxide was first obtained through vacuum distillation byRichard Wolffenstein in 1894.[8] At the end of the 19th century, Petre Melikishvili and his pupil L. Pizarjevski showed that of the many proposed formulas of hydrogen peroxide, the correct one was H−O−O−H.

The use of H2O2 sterilization in biological safety cabinets and barrier isolators is a popular alternative to ethylene oxide (EtO) as a safer, more efficient decontamination method. H2O2 has long been widely used in the pharmaceutical industry. In aerospace research, H2O2 is used to sterilize artificial satellites and space probes.

The U.S. FDA has granted 510(k) clearance to use H2O2 in individual medical device manufacturing applications. EtO criteria outlined in ANSI/AAMI/ISO 14937 may be used as a validation guideline. Sanyo was the first manufacturer to use the H2O2 process in situ in a cell culture incubator, which is a faster and more efficient cell culture sterilization process.[citation needed]


Formerly, hydrogen peroxide was prepared by the electrolysis of an aqueous solution of sulfuric acid or acidic ammonium bisulfate (NH4HSO4), followed by hydrolysis of the peroxodisulfate S2O82− that is formed.

Today, hydrogen peroxide is manufactured almost exclusively by the Riedl-Pfleiderer or anthraquinone process which was formalized in 1936 and patented in 1939, and involves theautoxidation of a 2-alkyl anthrahydroquinone (or 2-alkyl-9,10-dihydroxyanthracene) to the corresponding 2-alkyl anthraquinone. Major producers commonly use either the 2-ethyl or the 2-amyl derivative. The cyclic reaction depicted below shows the 2-ethyl derivative, where 2-ethyl-9,10-dihydroxyanthracene (C16H12(OH)2) is oxidized to the corresponding 2-ethylanthraquinone (C16H12O2) and hydrogen peroxide. Most commercial processes achieve this by bubbling compressed air through a solution of the derivatized anthracene, whereby the oxygen present in the air reacts with the labile hydrogen atoms (of the hydroxy group), giving hydrogen peroxide and regenerating the anthraquinone. Hydrogen peroxide is thenextracted and the anthraquinone derivative is reduced back to the dihydroxy (anthracene) compound using hydrogen gas in the presence of a metal catalyst. The cycle then repeats itself.[9][10]

Hydrogen peroxide production with the Riedl-Pfleiderer process process

The simplified overall equation for the process is deceptively simple:[9]

H2 + O2 → H2O2

The economics of the process depend heavily on effective recycling of the quinone (which is expensive) and extraction solvents, and of the hydrogenation catalyst.

In 1994, world production of H2O2 was around 1.9 million tonnes and grew to 2.2 million in 2006,[11] most of which was at a concentration of 70% or less.[citation needed] In that year bulk 30%H2O2 sold for around US $0.54 per kg, equivalent to US $1.50 per kg (US $0.68 per lb) on a “100% basis”.[citation needed]

[edit]New developments

A new, so-called “high-productivity/high-yield” process, based on an optimized distribution of isomers of 2-amyl anthraquinone, has been developed by Solvay. In July 2008, this process allowed the construction of a “mega-scale” single-train plant in Zandvliet (Belgium). The plant has an annual production capacity more than twice that of the world’s next-largest single-train plant. An even larger plant was commissioned in October, 2011 by a joint venture of Solvay and Dow in Map Ta Phut (Thailand). This plant has a projected production capacity of 330,000 tons of hydrogen peroxide per year at 100% concentration.[12] It is likely that this will lead to a reduction in the cost of production due to economies of scale.[13]

A process to produce hydrogen peroxide directly from the elements has been of interest for many years. The problem with the direct synthesis process is that, in terms of thermodynamics, the reaction of hydrogen with oxygen favors production of water. It had been recognized for some time that a finely dispersed catalyst is beneficial in promoting selectivity to hydrogen peroxide, but, while selectivity was improved, it was still not sufficiently high to permit commercial development of the process. However, an apparent breakthrough was made in the early 2000s by researchers at Headwaters Technology. The breakthrough revolves around development of a minute (nanometer-size) phase-controlled noble metal crystal particles on carbon support. This advance led, in a joint venture with Evonik Industries, to the construction of a pilot plant in Germany in late 2005. It is claimed that there are reductions in investment cost because the process is simpler and involves less equipment; however, the process is also more corrosive and unproven. This process results in low concentrations of hydrogen peroxide (about 5–10 wt% versus about 40 wt% through the anthraquinone process).[13]

In 2009, another catalyst development was announced by researchers at Cardiff University.[14] This development also relates to the direct synthesis, but, in this case, using gold–palladiumnanoparticles. Under normal circumstances, the direct synthesis must be carried out in an acid medium to prevent immediate decomposition of the hydrogen peroxide once it is formed. Whereas hydrogen peroxide tends to decompose on its own (which is why, even after production, it is often necessary to add stabilisers to the commercial product when it is to be transported or stored for long periods), the nature of the catalyst can cause this decomposition to accelerate rapidly. It is claimed that the use of this gold-palladium catalyst reduces this decomposition and, as a consequence, little to no acid is required. The process is in a very early stage of development and currently results in very low concentrations of hydrogen peroxide being formed (less than about 1–2 wt%). Nonetheless, it is envisaged by the inventors that the process will lead to an inexpensive, efficient, and environmentally friendly process.[13][14][15][16]

A novel electrochemical process for the production of alkaline hydrogen peroxide has been developed by Dow. The process employs a monopolar cell to achieve an electrolytic reduction of oxygen in a dilute sodium hydroxide solution.[13]


Hydrogen peroxide is most commonly available as a solution in water. For consumers, it is usually available from pharmacies at 3 and 6 wt% concentrations. The concentrations are sometimes described in terms of the volume of oxygen gas generated; one milliliter of a 20-volume solution generates twenty milliliters of oxygen gas when completely decomposed. For laboratory use, 30 wt% solutions are most common. Commercial grades from 70% to 98% are also available, but due to the potential of solutions of >68% hydrogen peroxide to be converted entirely to steam and oxygen (with the temperature of the steam increasing as the concentration increases above 68%) these grades are potentially far more hazardous, and require special care in dedicated storage areas. Buyers must typically allow inspection by commercial manufacturers.



Manganese dioxide decomposing a very dilute solution of hydrogen peroxide

Hydrogen peroxide decomposes (disproportionates) exothermically into water and oxygen gas spontaneously:

2 H2O2 → 2 H2O + O2

This process is thermodynamically favorable. It has a ΔHo of −98.2 kJ·mol−1 and a ΔS of 70.5 J·mol−1·K−1. The rate of decomposition is dependent on the temperature (cool environment slows down decomposition, therefore hydrogen peroxide is often stored in refrigerator) and concentration of the peroxide, as well as the pH and the presence of impurities and stabilizers. Hydrogen peroxide is incompatible with many substances that catalyse its decomposition, including most of the transition metals and their compounds. Common catalysts include manganese dioxide, silver, and platinum.[17] The same reaction is catalysed by the enzyme catalase, found in the liver, whose main function in the body is the removal of toxic byproducts of metabolism and the reduction of oxidative stress. The decomposition occurs more rapidly in alkali, so acid is often added as a stabilizer.

The liberation of oxygen and energy in the decomposition has dangerous side-effects. Spilling high concentrations of hydrogen peroxide on a flammable substance can cause an immediate fire, which is further fueled by the oxygen released by the decomposing hydrogen peroxide. High test peroxide, or HTP (also called high-strength peroxide) must be stored in a suitable,[citation needed] vented container to prevent the buildup of oxygen gas, which would otherwise lead to the eventual rupture of the container.

In the presence of certain catalysts, such as Fe2+ or Ti3+, the decomposition may take a different path, with free radicals such as HO· (hydroxyl) and HOO· (hydroperoxyl) being formed. A combination of H2O2 and Fe2+ is known as Fenton’s reagent.

A common concentration for hydrogen peroxide is 20-volume, which means that, when 1 volume of hydrogen peroxide is decomposed, it produces 20 volumes of oxygen. A 20-volumeconcentration of hydrogen peroxide is equivalent to 1.667 mol/dm3 (Molar solution) or about 6%.

[edit]Redox reactions

In acidic solutions, H2O2 is one of the most powerful oxidizers known—stronger than chlorine, chlorine dioxide, and potassium permanganate. Also, through catalysis, H2O2 can be converted into hydroxyl radicals (OH), which are highly reactive.

Oxidant/Reduced product Oxidation potential, V
Fluorine/Hydrogen fluoride 3.0
Ozone/Oxygen 2.1
Hydrogen peroxide/Water 1.8
Potassium permanganate/Manganese dioxide 1.7
Chlorine dioxide/HClO 1.5
Chlorine/Chloride 1.4

In aqueous solutions, hydrogen peroxide can oxidize or reduce a variety of inorganic ions. When it acts as a reducing agent, oxygen gas is also produced.

In acidic solutions Fe2+ is oxidized to Fe3+ (hydrogen peroxide acting as an oxidizing agent),

2 Fe2+(aq) + H2O2 + 2 H+(aq) → 2 Fe3+(aq) + 2H2O(l)

and sulfite (SO2−
3) is oxidized to sulfate (SO2−
4). However, potassium permanganate is reduced to Mn2+ by acidic H2O2. Under alkaline conditions, however, some of these reactions reverse; for example, Mn2+ is oxidized to Mn4+ (as MnO2).

Other examples of hydrogen peroxide’s action as a reducing agent are reaction with sodium hypochlorite or potassium permanganate, which is a convenient method for preparing oxygenin the laboratory.

NaOCl + H2O2 → O2 + NaCl + H2O
2 KMnO4 + 3 H2O2 → 2 MnO2 + 2 KOH + 2 H2O + 3 O2

Hydrogen peroxide is frequently used as an oxidizing agent in organic chemistry. One application is for the oxidation of thioethers to sulfoxides.[citation needed] For example, methyl phenyl sulfide can be readily oxidized in high yield to methyl phenyl sulfoxide:[18]

Ph−S−CH3 + H2O2 → Ph−S(O)−CH3 + H2O

Alkaline hydrogen peroxide is used for epoxidation of electron-deficient alkenes such as acrylic acids, and also for oxidation of alkylboranes to alcohols, the second step of hydroboration-oxidation.

[edit]Formation of peroxide compounds

Hydrogen peroxide is a weak acid, and it can form hydroperoxide or peroxide salts or derivatives of many metals.

For example, on addition to an aqueous solution of chromic acid (CrO3) or acidic solutions of dichromate salts, it will form an unstable blue peroxide CrO(O2)2. In aqueous solution it rapidly decomposes to form oxygen gas and chromium salts.

It can also produce peroxoanions by reaction with anions; for example, reaction with borax leads to sodium perborate, a bleach used in laundry detergents:

Na2B4O7 + 4 H2O2 + 2 NaOH → 2 Na2B2O4(OH)4 + H2O

H2O2 converts carboxylic acids (RCOOH) into peroxy acids (RCOOOH), which are themselves used as oxidizing agents. Hydrogen peroxide reacts with acetone to form acetone peroxide, and it interacts with ozone to form hydrogen trioxide, also known as trioxidane. Reaction with urea produces carbamide peroxide, used for whitening teeth. An acid-base adduct withtriphenylphosphine oxide is a useful “carrier” for H2O2 in some reactions.


Hydrogen peroxide can still form adducts with very strong acids. The superacid HF/SbF5 forms unstable compounds containing the [H3O2]+ ion.


[edit]Municipal wastewater applications

Hydrogen peroxide is replacing prechlorination as a way to deal with odors entering wastewater treatment plants.[19] The processing of wastewater sludge (or biosolids) can cause the generation of hydrogen sulfide (H2S), a poisonous and odoriferous gas. Hydrogen sulfide can also damage equipment and concrete structures. Hydrogen peroxide has been utilized to minimize hydrogen sulfide formation.[20]

[edit]Industrial applications

ISO tank container for hydrogen peroxide transportation

About 50% of the world’s production of hydrogen peroxide in 1994 was used for pulp- and paper-bleaching.[11] Other bleaching applications are becoming more important as hydrogen peroxide is seen as an environmentally benign alternative to chlorine-based bleaches.[citation needed]

[edit]Sulfide oxidation

Sulfide is found throughout the environment as a result of both natural and industrial processes. Most sulfide found in nature was produced biologically (under anaerobic conditions) and occurs as free hydrogen sulfide (H2S) – characterized by its rotten egg odor. Biogenic H2S is encountered in sour groundwaters, swamps and marshes, natural gas deposits, and sewage collection/treatment systems. Manmade sources of H2S typically occur as a result of natural materials containing sulfur (e.g., coal, gas and oil) being refined into industrial products. For a variety of reasons – aesthetics (odor control), health (toxicity), ecological (oxygen depletion in receiving waters), and economic (corrosion of equipment and infrastructure) – sulfide laden wastewaters must be handled carefully and remediated before they can be released to the environment. Typical discharge limits for sulfide are < 1 mg/L.[21]

[edit]BOD and COD removal from wastewater

Hydrogen peroxide has been used to reduce the BOD and COD of industrial wastewaters for many years. While the cost of removing BOD/COD through chemical oxidation is typically greater than that through physical or biological means, there are nonetheless specific situations which justify its use. These include:

  • Predigestion of wastewaters which contain moderate to high levels of compounds that are toxic, inhibitory, or recalcitrant to biological treatment (e.g., pesticides, plasticizers, resins, coolants, and dyestuffs);
  • Pretreatment of high strength / low flow wastewaters – where biotreatment may not be practical – prior to discharge to a Publicly Owned Treatment Works (POTW);
  • Enhanced separation of entrained organics by flotation and settling processes; and

Supply of supplemental Dissolved Oxygen (DO) when biological treatment systems experience temporary overloads or equipment failure.

As indicated by these examples, hydrogen peroxide can be used as a stand-alone treatment or as an enhancement to existing physical or biological treatment processes, depending on the situation.[22]

[edit]High strength wastewater pretreatment

Hydrogen peroxide is one of the most versatile, dependable and environmentally compatible oxidizing agents. The relative safety and simplicity of its use as an oxidizing agent has led to the development of a number of applications in refinery wastewater systems.

Uncatalyzed hydrogen peroxide

The strong oxidizing power of hydrogen peroxide makes it suitable for the destruction of a variety of pollutants. Optimization of conditions using hydrogen peroxide to destroy these pollutants can involve control of pH, temperature and reaction time. No additional additives are required.

Catalyzed hydrogen peroxide

Pollutants that are more difficult to oxidize require hydrogen peroxide to be activated with catalysts such as iron. Catalyzed oxidation can also be used to destroy easily oxidized pollutants more rapidly.

Under acid pH conditions, the addition of iron salts to a wastewater solution activates hydrogen peroxide to generate free radicals, which can attack a variety of organic compounds. Other metal salts and conditions can apply (e.g. in cyanide destruction, a copper catalyst can be used at a pH of 8.5 – 11.5).[23]

[edit]Nitrogen oxide (NOx) abatement

Nitrogen oxides are major pollutants in the atmosphere, being a precursor to acid rain, photochemical smog, and ozone accumulation. The oxides are mainly nitric oxide (NO) and nitrogen dioxide (NO2) both of which are corrosive and hazardous to health. With the use of catalytic converters on automobiles, the initial regulatory focus of controlling of mobile NOx emissions has reached the point where further restriction has become economically impractical. Consequently, the stationary sources of NOx emissions are now being subjected to more stringent standards in many areas of the U.S. Stationary sources include nitric acid manufacturing plants, manufacturers of nitrated materials such as fertilizer and explosives, and industrial manufacturers (metallurgical processors, glass manufacturers, cement kilns, power generators, etc.) where high processing temperatures are used. Because of the environmental concerns posed by air pollution, a great deal of research time and money has been expended to develop methods for controlling NOx emissions.[24]

Other major industrial applications for hydrogen peroxide include the manufacture of sodium percarbonate and sodium perborate, used as mild bleaches in laundry detergents. It is used in the production of certain organic peroxides, such as dibenzoyl peroxide, used in polymerisations and other chemical processes. Hydrogen peroxide is also used in the production ofepoxides, such as propylene oxide. Reaction with carboxylic acids produces a corresponding peroxy acid. Peracetic acid and meta-chloroperoxybenzoic acid (commonly abbreviated mCPBA) are prepared from acetic acid and meta-chlorobenzoic acid, respectively. The latter is commonly reacted with alkenes to give the corresponding epoxide.

In the PCB manufacturing process, hydrogen peroxide mixed with sulfuric acid was used as the microetch chemical for copper surface roughening preparation.

A combination of a powdered precious metal-based catalyst, hydrogen peroxide, methanol and water can produce superheated steam in one to two seconds, releasing only CO2 and high-temperature steam for a variety of purposes.[25]

Recently, there has been increased use of vaporized hydrogen peroxide in the validation and bio-decontamination of half-suit and glove-port isolators in pharmaceutical production.

Nuclear pressurized water reactors (PWRs) use hydrogen peroxide during the plant shutdown to force the oxidation and dissolution of activated corrosion products deposited on the fuel. The corrosion products are then removed with the cleanup systems before the reactor is disassembled.

Hydrogen peroxide is also used in the oil and gas exploration industry to oxidize rock matrix in preparation for micro-fossil analysis.

[edit]Chemical applications

A method of producing propylene oxide from hydrogen peroxide has been developed. The process is claimed to be environmentally friendly, since the only significant byproduct is water. Two of these “HPPO” (hydrogen peroxide to propylene oxide) plants came onstream in 2008: One of them located in Belgium is a Solvay, Dow-BASF joint venture, and the other in Korea is an EvonikHeadwaters, SK Chemicals joint venture. A caprolactam application for hydrogen peroxide has been commercialized. Potential routes to phenol and epichlorohydrin utilizing hydrogen peroxide have been postulated.[13]

[edit]Biological function

Hydrogen peroxide is also one of the two chief chemicals in the defense system of the bombardier beetle, reacting with hydroquinone to discourage predators.

A study published in Nature found that hydrogen peroxide plays a role in the immune system. Scientists found that hydrogen peroxide inside of cells increased after tissues are damaged inzebra fish, which is thought to act as a signal to white blood cells to converge on the site and initiate the healing process. When the genes required to produce hydrogen peroxide were disabled, white blood cells did not accumulate at the site of damage. The experiments were conducted on fish; however, because fish are genetically similar to humans, the same process is speculated to occur in humans. The study in Nature suggested asthma sufferers have higher levels of hydrogen peroxide in their lungs than healthy people, which could explain why asthma sufferers have inappropriate levels of white blood cells in their lungs.[26][27]

Hydrogen peroxide has important roles as a signaling molecule in the regulation of a variety of biological processes.[28] Hydrogen peroxide also plays an important role in aging[29] and cancer.[30]

The amount of hydrogen peroxide in biological systems can be assayed using a fluorimetric assay.[31]

[edit]Domestic uses


Skin immediately after exposure to 30% H2O2

  • Diluted H2O2 (between 3% and 8%) is used to bleach human hair when mixed with ammonium hydroxide, hence the phrase “peroxide blonde”.
  • It is absorbed by skin upon contact and creates a local skin capillary embolism that appears as a temporary whitening of the skin.
  • It is used to whiten bones that are to be put on display.
  • 3% H2O2 is effective at treating fresh (red) blood-stains in clothing and on other items. It must be applied to clothing before blood stains can be accidentally “set” with heated water. Cold water and soap are then used to remove the peroxide treated blood.
  • Some horticulturalists and users of hydroponics advocate the use of weak hydrogen peroxide solution in watering solutions. Its spontaneous decomposition releases oxygen that enhances a plant’s root development and helps to treat root rot (cellular root death due to lack of oxygen) and a variety of other pests.[32][33][34]
  • Laboratory tests conducted by fish culturists in recent years have demonstrated that common household hydrogen peroxide can be used safely to provide oxygen for small fish.[35][36] Hydrogen peroxide releases oxygen by decomposition when it is exposed to catalysts such as manganese dioxide.
  • Hydrogen peroxide is a strong oxidizer effective in controlling sulfide and organic-related odors in wastewater collection and treatment systems. It is typically applied to a wastewater system where there is a retention time of 30 minutes to 5 hours before hydrogen sulfide is released. Hydrogen peroxide oxidizes the hydrogen sulfide and promotes bio-oxidation of organic odors. Hydrogen peroxide decomposes to oxygen and water, adding dissolved oxygen to the system, thereby negating some Biochemical Oxygen Demand (BOD).
  • Mixed with baking soda and a small amount of hand soap, hydrogen peroxide is effective at removing skunk odor.[37]
  • Hydrogen peroxide is used with phenyl oxalate ester and an appropriate dye in glow sticks as an oxidizing agent. It reacts with the ester to form an unstable CO2 dimer, which excites the dye to an excited state; the dye emits a photon (light) when it spontaneously relaxes back to the ground state.
  • Hydrogen peroxide can be combined with vinegar and table salt to form a substitute for industrial chemicals such as ferric chloride, ammonium persulfate, or hydrochloric acid as a hobbyist’s printed circuit board etchant.[38]
  • Hydrogen peroxide can be used to clean tile and grout on floors. Sometimes it is recommended to clean with baking soda together with the hydrogen peroxide.[39]


For more details on this topic, see High test peroxide.

Rocket Belt hydrogen peroxide propulsion system used in a jet pack

High concentration H2O2 is referred to as High Test Peroxide (HTP). It can be used either as a monopropellant (not mixed with fuel) or as the oxidizer component of a bipropellant rocket. Use as a monopropellant takes advantage of the decomposition of 70–98+% concentration hydrogen peroxide into steam and oxygen. The propellant is pumped into a reaction chamber where a catalyst, usually a silver or platinum screen, triggers decomposition, producing steam at over 600 °C (1,112 °F), which is expelled through a nozzle, generating thrust. H2O2 monopropellant produces a maximum specific impulse (Isp) of 161 s (1.6 kN·s/kg), which makes it a low-performance monopropellant. Peroxide generates much less thrust than hydrazine. The Bell Rocket Belt used hydrogen peroxide monopropellant.

As a bipropellant H2O2 is decomposed to burn a fuel as an oxidizer. Specific impulses as high as 350 s (3.5 kN·s/kg) can be achieved, depending on the fuel. Peroxide used as an oxidizer gives a somewhat lower Isp than liquid oxygen, but is dense, storable, noncryogenic and can be more easily used to drive gas turbines to give high pressures using an efficient closed cycle. It can also be used for regenerative cooling of rocket engines. Peroxide was used very successfully as an oxidizer in World-War-II German rockets (e.g. T-Stoff, containing oxyquinoline stabilizer, for the Me-163), and for the low-cost BritishBlack Knight and Black Arrow launchers.

In the 1940s and 1950s, the Walter turbine used hydrogen peroxide for use in submarines while submerged; it was found to be too noisy and require too much maintenance compared to diesel-electric power systems. Some torpedoes used hydrogen peroxide as oxidizer or propellant, but this was dangerous and has been discontinued by most navies. Hydrogen peroxide leaks were blamed for the sinkings of HMS Sidon and the Russian submarineKursk. It was discovered, for example, by the Japanese Navy in torpedo trials, that the concentration of H2O2 in right-angle bends in HTP pipework can often lead to explosions in submarines and torpedoes. SAAB Underwater Systems is manufacturing the Torpedo 2000. This torpedo, used by the Swedish navy, is powered by a piston engine propelled by HTP as an oxidizer and kerosene as a fuel in a bipropellant system.[40]

While rarely used now as a monopropellant for large engines, small hydrogen peroxide attitude control thrusters are still in use on some satellites.They are easy to throttle, and safer to fuel and handle before launch than hydrazine thrusters. However, hydrazine is more often used in spacecraft because of its higher specific impulse and lower rate of decomposition.

[edit]Therapeutic use

Hydrogen peroxide is generally recognized as safe (GRAS) as an antimicrobial agent, an oxidizing agent and for other purposes by the U.S. FDA.[41] For example, 35% hydrogen peroxide is used to prevent infection transmission in the hospital environment, and hydrogen peroxide vapor is registered with the US EPA as a sporicidal sterilant.
While dilute solutions of hydrogen peroxide were long used for cleaning small surface wounds, studies suggest that hydrogen peroxide is ineffective in treating these wounds, and may increase healing time.[42][43] While it is an effective cleaning agent, hydrogen peroxide may not actually improve the rate of wound healing. High enough concentrations to provide antiseptic effect may also increase the time of wound healing by damaging human cells.[44] Further, hydrogen peroxide applied to wounds can impede healing and lead to scarringbecause it destroys newly formed skin cells.[45]

  • Hydrogen peroxide is used, in sufficient concentrations, to disinfect inanimate objects[46]
  • Hydrogen peroxide can be used as a toothpaste, or oral debriding agent, when mixed with correct quantities of baking soda and salt. This use is no more effective than toothpaste alone, however.[47]
  • Hydrogen peroxide and benzoyl peroxide are sometimes used to treat acne.[48]
  • Hydrogen peroxide is used as an emetic in veterinary practice.[49][50]

[edit]Alternative uses

See also: Liquid Oxygen (supplement)
  • Following the call by alternative medicine advisors for drinking diluted hydrogen peroxide, and using it in various ways such as in shampoo and as an additive to toothpaste, as a treatment to illness in general and cancer in particular, the American Cancer Society states that “there is no scientific evidence that hydrogen peroxide is a safe, effective or useful cancer treatment”, and advises cancer patients to “remain in the care of qualified doctors who use proven methods of treatment and approved clinical trials of promising new treatments.”[51]
  • Another controversial alternative medical procedure is inhalation of hydrogen peroxide at a concentration of about 1%. Intravenous usage of hydrogen peroxide has been linked to several deaths.[52][53]

[edit]Improvised explosive device / home-made bomb precursor

Hydrogen peroxide was the main ingredient in the 7 July 2005 London bombings that killed 52 London Underground and bus passengers. The bomb-making ingredients are reported to be easier to buy than large numbers of aspirin pills.[54]


Regulations vary, but low concentrations, such as 3%, are widely available and legal to buy for medical use. Most over-the-counter peroxide solutions are not suitable for ingestion. Higher concentrations may be considered hazardous and are typically accompanied by a Material Safety Data Sheet (MSDS). In high concentrations, hydrogen peroxide is an aggressive oxidizer and will corrode many materials, including human skin. In the presence of a reducing agent, high concentrations of H2O2 will react violently.

High-concentration hydrogen peroxide streams, typically above 40%, should be considered a D001 hazardous waste, due to concentrated hydrogen peroxide’s meeting the definition of aDOT oxidizer according to U.S. regulations, if released into the environment. The EPA Reportable Quantity (RQ) for D001 hazardous wastes is 100 pounds (45 kg), or approximately 10 US gallons (38 L), of concentrated hydrogen peroxide.

Hydrogen peroxide should be stored in a cool, dry, well-ventilated area and away from any flammable or combustible substances.[55] It should be stored in a container composed of non-reactive materials such as stainless steel or glass (other materials including some plastics and aluminium alloys may also be suitable).[56] Because it breaks down quickly when exposed to light, it should be stored in an opaque container, and pharmaceutical formulations typically come in brown bottles that filter out light.[57]

Hydrogen peroxide, either in pure or diluted form, can pose several risks:

  • Explosive vapors. Above roughly 70% concentrations, hydrogen peroxide can give off vapor that can detonate above 70 °C (158 °F) at normal atmospheric pressure.[citation needed]This can then cause a boiling liquid expanding vapor explosion (BLEVE) of the remaining liquid. Distillation of hydrogen peroxide at normal pressures is thus highly dangerous.
  • Hazardous reactions. Hydrogen peroxide vapors can form sensitive contact explosives with hydrocarbons such as greases. Hazardous reactions ranging from ignition to explosion have been reported with alcohols, ketones, carboxylic acids (particularly acetic acid), amines and phosphorus.[citation needed]
  • Corrosive. Concentrated hydrogen peroxide (>50%) is corrosive, and even domestic-strength solutions can cause irritation to the eyes, mucous membranes and skin.[58] Swallowing hydrogen peroxide solutions is particularly dangerous, as decomposition in the stomach releases large quantities of gas (10 times the volume of a 3% solution) leading to internal bleeding. Inhaling over 10% can cause severe pulmonary irritation.[citation needed]
  • Bleach agent. Low concentrations of hydrogen peroxide, on the order of 3% or less, will chemically bleach many types of clothing to a pinkish hue. Caution should be exercised when using common products that may contain hydrogen peroxide, such as facial cleaner or contact lens solution, which easily splatter upon other surfaces.
  • Internal ailments. Large oral doses of hydrogen peroxide at a 3% concentration may cause “irritation and blistering to the mouth (which is known as Black hairy tongue), throat, and abdomen”, as well as “abdominal pain, vomiting, and diarrhea”.[59]
  • Vapor pressure. Hydrogen peroxide has a significant vapor pressure (1.2 kPa at 50 °C[CRC Handbook of Chemistry and Physics, 76th Ed, 1995-1996]) and exposure to the vapor is potentially hazardous. Hydrogen peroxide vapor is a primary irritant, primarily affecting the eyes and respiratory system and the NIOSH Immediately dangerous to life and health limit (IDLH) is only 75 ppm.[60] Long term exposure to low ppm concentrations is also hazardous and can result in permanent lung damage and Occupational Safety and Health Administration (OSHA) has established a permissible exposure limit of 1.0 ppm calculated as an eight hour time weighted average (29 CFR 1910.1000, Table Z-1) and hydrogen peroxide has also been classified by the American Conference of Governmental Industrial Hygienists (ACGIH) as a “known animal carcinogen, with unknown relevance on humans.[2008 Threshold Limit Values for Chemical Substances and Physical Agents & Biological Exposure Indices, ACGIH] In applications where high concentrations of hydrogen peroxide are used, suitable personal protective equipment should be worn and it is prudent in situations where the vapor is likely to be generated, such as hydrogen peroxide gas or vapor sterilization, to ensure that there is adequate ventilation and the vapor concentration monitored with a continuous gas monitor for hydrogen peroxide. Continuous gas monitors for hydrogen peroxide are available from several suppliers. Further information on the hazards of hydrogen peroxide is available from OSHA[61] and from the ATSDR.[62]
  • Skin disorders. Vitiligo is an acquired skin disorder with the loss of native skin pigment, which affects about 0.5-1% of the world population. Recent studies have discovered increased H2O2levels in the epidermis and in blood are one of many hallmarks of this disease.[63]

[edit]Historical incidents

  • On July 16, 1934, in Kummersdorf, Germany, a rocket engine using hydrogen peroxide exploded, killing three people. As a result of this incident, Wernher von Braun decided not to use hydrogen peroxide as an oxidizer in the rockets he developed afterward.
  • Several people received minor injuries after a hydrogen peroxide spill on board Northwest Airlines flight 957 from Orlando to Memphis on October 28, 1998 and subsequent fire on Northwest Airlines flight 7.[64]
  • During the Second World War, doctors in German concentration camps experimented with the use of hydrogen peroxide injections in the killing of human subjects.[65]
  • Hydrogen peroxide was said to be one of the ingredients in the bombs that failed to explode in the July 21, 2005 London bombings.[66]
  • The Russian submarine K-141 Kursk sailed out to sea to perform an exercise of firing dummy torpedoes at the Pyotr Velikiy, a Kirov class battlecruiser. On August 12, 2000 at 11:28 local time (07:28 UTC), there was an explosion while preparing to fire the torpedoes. The only credible report to date is that this was due to the failure and explosion of one of the Kursk’s hydrogen peroxide-fueled torpedoes. It is believed that HTP, a form of highly concentrated hydrogen peroxide used as propellant for the torpedo, seeped through rust in the torpedo casing. A similar incident was responsible for the loss of HMS Sidon in 1955
  • On August 15, 2010 a spill of about 30 US gallons (110 L) of cleaning fluid occurred on the 54th floor of 1515 Broadway, in Times Square, New York City. The spill, which a spokesperson for the New York City fire department said was of hydrogen peroxide, shut down Broadway between West 42nd and West 48th streets as a number of fire engines responded to the hazmatsituation. There were no reported injuries.[67]