Type II cells, macrophages and the alveolar lining play a major role in surfactant turnover. Cyclical changes in the alveolar surface appear to promote conversion of newly secreted, apoprotein-rich, active surfactant aggregates into protein-poor, inactive forms that are ready for clearance [ 3 ]. Surfactant components are removed from air spaces through uptake by Type II cells and alveolar macrophages, with the bulk done by the Type II cells. The phospholipids are taken up by endocytosis into the Type II cells where they are recycled and re-secreted, whereas the SPs are recycled back into the lamellar bodies for re-secretion with surfactant. Surfactant is also transformed during the cyclic compression and expansion of alveoli from large, highly surface active aggregates into smaller, less active subtypes [ 42 ].
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Surfactant secretion can be stimulated by a number of mechanisms. Type II cells have beta-adrenergic receptors and respond to beta-agonists with increased surfactant secretion [ 40 ]. Purines, such as adenosine triphosphate are potent stimulators of surfactant secretion and may be important for its secretion at birth. Mechanical stretch such as lung distension and hyperventilation, have also been found to be involved in stimulating surfactant secretion. Stretch-mediated enhancement of surfactant secretion during exercise prevents a loss of alveolar surfactant [ 41 ]. Hormones also play a role in surfactant secretion. Thyroxine accelerates Type II cell differentiation while acting synergistically with glucocorticoids to enhance the distensibility of the lung and DPPC synthesis. However, glucocorticoids alone are used in clinical practice to induce lung maturity because studies have not shown that the synergistic effect with thyroxine is greater than the effect achieved by glucocorticoids alone [ 3 ].
The rate of synthesis and the half-life of surfactant are influenced by many factors. Surfactant synthesis and turnover in preterm infants using stable isotopes of glucose, acetate and palmitic acid demonstrates that synthesis from glucose to surfactant phosphatidylcholine (PC) takes approximately 19 hours and reaches a peak at 70 hours after labeling. The absolute production rate of PC is 4.2 mg/kg/day while the half-life is 113 (± 25) hours [ 38 ]. The fractional synthesis rate of surfactant PC from plasma palmitate was significantly higher than that from palmitate synthesized de novo from acetate or glucose, but only accounted for half of the total surfactant production in preterm infants [ 39 ].
Pulmonary surfactant is synthesized, assembled, transported and secreted into the alveolus where it is degraded. It is then recycled in a highly complex and regulated mechanism. This process is slower in newborns (especially those born prematurely) than in adults or those with lung injury.
Defective surfactant metabolism leads to both morbidity and mortality in preterm and term neonates. In general, defects in surfactant metabolism occur due to accelerated breakdown of the surfactant complex by oxidation, proteolytic degradation, and inhibition [43, 44]. Some inherited surfactant gene defects have also been implicated.
Respiratory Distress Syndrome (RDS) is one of the most common causes of morbidity in preterm neonates. It occurs worldwide with a slight male predominance [31]. Patients present shortly after birth with apnea, cyanosis, grunting, inspiratory stridor, nasal flaring, poor feeding, and tachypnea. There may also be intercostal or subcostal retractions. Radiological findings include a diffuse reticulogranular &#;ground glass&#; appearance (resulting from alveolar atelectasis) with superimposed air bronchograms [31]. The preterm infant who has RDS has low amounts of surfactant that contains a lower percent of disaturated phosphatidylcholine species, less phosphatidylglycerol, and less of all the surfactant proteins than surfactant from a mature lung. Minimal surface tensions are also higher for surfactant from preterm than term infants [19]. The diagnosis can be confirmed by biochemical evidence of surfactant deficiency or pathologically. Lungs of infants who have died from RDS show alveolar atelectasis, alveolar and interstitial edema and diffuse hyaline membranes in distorted small airways [45]. Prenatal corticosteroids and postnatal surfactant replacement therapy significantly reduce the incidence, severity and mortality associated with RDS, and surfactant therapy has become the standard of care in management of preterm infants with RDS [46].
Meconium Aspiration Syndrome (MAS) is an important cause of morbidity and mortality from respiratory distress in the perinatal period and affects an estimated 25,000 neonates in the United States each year [47]. Meconium staining of the amniotic fluid or fetus is an indication of fetal distress. Fetal respiration is associated with movement of fluid from the airways out into the amniotic fluid. However, in the presence of fetal distress, gasping may be initiated in utero leading to aspiration of amniotic fluid and its contents, which includes meconium, into the large airways [48]. Acute lung injury is characterized by airway obstruction, pneumonitis, pulmonary hypertension, ventilation/perfusion mismatch, acidosis and hypoxemia [49].
The mechanisms underlying surfactant inactivation by meconium are not fully understood, but it has been shown that meconium destroys the fibrillary structure of surfactant and decreases its surface adsorption rate [50]. MAS is associated with an inflammatory response characterized by the presence of elevated cell count and pro-inflammatory cytokines IL-1β, IL-6, and IL-8 as early as in the first 6 hours and significantly decreased by 96 hours of life [49]. Phospholipase-A2, (PLA2) present in meconium, has been found to inhibit the activity of surfactant in vitro in a dose-dependent manner, through the competitive displacement of surfactant from the alveolar film [51]. PLA2 is also known to induce hydrolysis of DPPC, releasing free fatty acids and lyso-PC which damage the alveolar capillary membrane and induce intrapulmonary sequestration of neutrophils [52]. Exogenous surfactant replacement either as bolus therapy or with a diluted surfactant lung lavage have been shown to reverse the hypoxemia and reduce pneumothoraces caused by meconium aspiration, decrease requirement for extracorporeal membrane oxygenation (ECMO), decrease duration of oxygen therapy and mechanical ventilation, and reduce the duration of hospital stays [47, 53]. A comparison of various surfactant treatment regimens in MAS did not find the superiority of one form of therapy over another, and may be related to the heterogeneous nature of this form of lung injury [54]. In an underpowered randomized trial comparing bolus (N=6) versus surfactant lavage (N=7) followed by inhaled nitric oxide, infants receiving surfactant lavage has significant improvements in oxygenation, decreases in mean airway pressure, and arterial-alveolar oxygen tension gradients; however there were no significant differences in duration of assisted ventilation, nitric oxide therapy, or hospitalization[55].
Pulmonary hemorrhage may also be associated with Respiratory Distress Syndrome (RDS) and can be difficult to differentiate from it by radiography [46]. It occurs subsequent to a rise in lung capillary pressure due to the effects of hypoxia, volume overload, congestive heart failure, or it may be induced by trauma from mechanical suctioning of the newborn airway. There is a strong association between significant left to right ductal shunting and pulmonary hemorrhage in preterm babies [45, 56]. There is a build up of the capillary filtrate in the interstitial space which can then burst through into the airspaces through the pulmonary epithelium. Neutrophils are released following endothelial damage and they, in turn, express proteases, oxygen free-radicals and cytokines. These free oxygen molecules damage the Type II cells that produce SPs, thus inhibiting production of the proteins. Elastase, one of these proteases, damages and degrades SP-A, thereby inhibiting SP-A mediated surfactant lipid aggregation and adsorption in vitro [2]. Pulmonary hemorrhage is also considered a rare adverse event associated with surfactant replacement therapy [45, 46].
Acute Respiratory Distress Syndrome (ARDS) is a significant cause of morbidity and mortality in all age groups following sepsis, hemorrhage, or other forms of lung injury. It is defined as a severe form of acute lung injury (ALI) and a syndrome of acute pulmonary inflammation. ALI/ARDS is characterized by sudden onset, impaired gas exchange, decreased static compliance, and by a non-hydrostatic pulmonary edema [57].
Infection is the most common cause of development of ARDS in children [58]. The lungs appear particularly vulnerable in the first year of life. Premature neonates with chronic lung disease who develop viral pneumonia, older children with immune deficiency syndromes, and those with childhood malignancies are especially at risk [58].
The hallmark in the pathophysiology of the acute event is an increase in the permeability of the alveolar-capillary barrier as a result of injury to the endothelium and/or alveolar lining cells. Damage to the alveolar Type I cells leads to an influx of protein-rich edema-fluid into the alveoli, as well as decreased fluid clearance from the alveolar space. Neutrophils are attracted into the airways by host bacterial and chemotactic factors and express enzymes and cytokines which further damage the alveolar epithelial cells [2]. Type II epithelial cell injury leads to a decrease in surfactant production, with resultant alveolar collapse.
Four clinical criteria must be met to establish a clinical diagnosis of ARDS: (i) acute disease onset, (ii) bilateral pulmonary infiltrates on chest radiograph, (iii) pulmonary capillary wedge pressure < 18 mmHg or absence of clinical evidence of left atrial hypertension, and (iv), ratio between arterial oxygen partial pressure (PaO2) and the fraction of inspired oxygen (FiO2) < 200 [57]. In contrast, patients that meet the first three criteria, but exhibit a PaO2/FiO2 ratio between 200 and 300, are defined as having ALI.
Despite the introduction of novel treatments, the mortality from ARDS in the pediatric age group still remains high. Attempts to treat ARDS with an SP-C surfactant, Venticute® (Altana Pharma, Germany), were ineffective [59]. However, the use of calfactant (Infasurf®) in younger children with ALI was effective in reducing ventilator days and increasing survival [60].
Pulmonary Alveolar Proteinosis (PAP) is a rare lung disease in which the alveoli fill with PL-rich proteinaceous material. This substance stains for periodic acid-Schiff and is nearly identical to surfactant [61]. PAP occurs in three clinically distinct forms; congenital, secondary and acquired. Congenital PAP is an uncommon cause of respiratory failure in full-term newborns known to be caused by inborn errors of surfactant protein metabolism [62]. Lysinuric protein intolerance has also been implicated as a secondary cause of congenital/infantile PAP [63]. Although the specific cellular pathogenesis is unknown, recent observations in genetically altered mice have led to the speculation that either absolute deficiency of alveolar cells or hypo-responsiveness of the alveolar cells to Granulocyte-Macrophage Colony Stimulating Factor (GM-CS F) is etiologic to PAP [61]. However, the role of GM-CSF in congenital PAP is not clear as antibodies against GM-CSF have not been identified in infants with this condition. The standard of care is the use of whole lung lavage to relieve the symptoms [61]. The prognosis for infants with congenital PAP has been uniformly poor and they die within the first year of life, despite maximal medical therapy [62, 64]. However, a recent report also showed successful treatment of congenital PAP with monthly doses of intravenous Immunoglobulin with the patient remaining free of respiratory symptoms for more than 3 years [65].
Schematic diagram of a micelle of oil in aqueous suspension, such as might occur in an emulsion of oil in water. In this example, the surfactant molecules' oil-soluble tails project into the oil (blue), while the water-soluble ends remain in contact with the water phase (red).
Surfactants are chemical compounds that decrease the surface tension or interfacial tension between two liquids, a liquid and a gas, or a liquid and a solid. The word "surfactant" is a blend of surface-active agent,[1] coined c.&#;.[2] As they consist of a water-repellent and a water-attracting part, they enable water and oil to mix; they can form foam and facilitate the detachment of dirt.
Surfactants are among the most widespread and commercially important chemicals. Private households as well as many industries use them in large quantities as detergents and cleaning agents, but also for example as emulsifiers, wetting agents, foaming agents, antistatic additives, or dispersants.
Surfactants occur naturally in traditional plant-based detergents, e.g. horse chestnuts or soap nuts; they can also be found in the secretions of some caterpillars. Today the most commonly used surfactants, above all anionic linear alkylbenzene sulfates (LAS), are produced from petroleum products. However, surfactants are (again) increasingly produced in whole or in part from renewable biomass, like sugar, fatty alcohol from vegetable oils, by-products of biofuel production, or other biogenic material.[3]
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Most surfactants are organic compounds with hydrophilic "heads" and hydrophobic "tails." The "heads" of surfactants are polar and may or may not carry an electrical charge. The "tails" of most surfactants are fairly similar, consisting of a hydrocarbon chain, which can be branched, linear, or aromatic. Fluorosurfactants have fluorocarbon chains. Siloxane surfactants have siloxane chains.
Many important surfactants include a polyether chain terminating in a highly polar anionic group. The polyether groups often comprise ethoxylated (polyethylene oxide-like) sequences inserted to increase the hydrophilic character of a surfactant. Polypropylene oxides conversely, may be inserted to increase the lipophilic character of a surfactant.
Surfactant molecules have either one tail or two; those with two tails are said to be double-chained.[4]
Surfactant classification according to the composition of their head: non-ionic, anionic, cationic, amphoteric.Most commonly, surfactants are classified according to polar head group. A non-ionic surfactant has no charged groups in its head. The head of an ionic surfactant carries a net positive, or negative, charge. If the charge is negative, the surfactant is more specifically called anionic; if the charge is positive, it is called cationic. If a surfactant contains a head with two oppositely charged groups, it is termed zwitterionic, or amphoteric. Commonly encountered surfactants of each type include:
Anionic: sulfate, sulfonate, and phosphate, carboxylate derivatives[
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Anionic surfactants contain anionic functional groups at their head, such as sulfate, sulfonate, phosphate, and carboxylates. Prominent alkyl sulfates include ammonium lauryl sulfate, sodium lauryl sulfate (sodium dodecyl sulfate, SLS, or SDS), and the related alkyl-ether sulfates sodium laureth sulfate (sodium lauryl ether sulfate or SLES), and sodium myreth sulfate.
Others include:
Carboxylates are the most common surfactants and comprise the carboxylate salts (soaps), such as sodium stearate. More specialized species include sodium lauroyl sarcosinate and carboxylate-based fluorosurfactants such as perfluorononanoate, perfluorooctanoate (PFOA or PFO).
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pH-dependent primary, secondary, or tertiary amines; primary and secondary amines become positively charged at pH < 10:[5] octenidine dihydrochloride.
Permanently charged quaternary ammonium salts: cetrimonium bromide (CTAB), cetylpyridinium chloride (CPC), benzalkonium chloride (BAC), benzethonium chloride (BZT), dimethyldioctadecylammonium chloride, and dioctadecyldimethylammonium bromide (DODAB).
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Zwitterionic (ampholytic) surfactants have both cationic and anionic centers attached to the same molecule. The cationic part is based on primary, secondary, or tertiary amines or quaternary ammonium cations. The anionic part can be more variable and include sulfonates, as in the sultaines CHAPS (3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate) and cocamidopropyl hydroxysultaine. Betaines such as cocamidopropyl betaine have a carboxylate with the ammonium. The most common biological zwitterionic surfactants have a phosphate anion with an amine or ammonium, such as the phospholipids phosphatidylserine, phosphatidylethanolamine, phosphatidylcholine, and sphingomyelins.
Lauryldimethylamine oxide and myristamine oxide are two commonly used zwitterionic surfactants of the tertiary amine oxides structural type.
Non-ionic surfactants have covalently bonded oxygen-containing hydrophilic groups, which are bonded to hydrophobic parent structures. The water-solubility of the oxygen groups is the result of hydrogen bonding. Hydrogen bonding decreases with increasing temperature, and the water solubility of non-ionic surfactants therefore decreases with increasing temperature.
Non-ionic surfactants are less sensitive to water hardness than anionic surfactants, and they foam less strongly. The differences between the individual types of non-ionic surfactants are slight, and the choice is primarily governed having regard to the costs of special properties (e.g., effectiveness and efficiency, toxicity, dermatological compatibility, biodegradability) or permission for use in food.[6]
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Alkylphenol ethoxylates (APEs or APEOs)[
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Fatty acid ethoxylates are a class of very versatile surfactants, which combine in a single molecule the characteristic of a weakly anionic, pH-responsive head group with the presence of stabilizing and temperature responsive ethyleneoxide units.[7]
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Ethoxylated amines and/or fatty acid amides[
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Contact us to discuss your requirements of Surfactants Fabrication. Our experienced sales team can help you identify the options that best suit your needs.
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Gemini amino acid-based surfactant (based on cysteine)[
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Schematic diagram of a micelle &#; the lipophilic tails of the surfactant ions remain inside the oil because they interact more strongly with oil than with water. The polar "heads" of the surfactant molecules coating the micelle interact more strongly with water, so they form a hydrophilic outer layer that forms a barrier between micelles. This inhibits the oil droplets, the hydrophobic cores of micelles, from merging into fewer, larger droplets ("emulsion breaking") of the micelle. The compounds that coat a micelle are typically amphiphilic in nature, meaning that micelles may be stable either as droplets of aprotic solvents such as oil in water, or as protic solvents such as water in oil. When the droplet is aprotic it is sometimes[when?
] known as a reverse micelle.Surfactants are usually organic compounds that are akin to amphiphilic, which means that this molecule, being as double-agent, each contains a hydrophilic "water-seeking" group (the head), and a hydrophobic "water-avoiding" group (the tail).[9] As a result, a surfactant contains both a water-soluble component and a water-insoluble component. Surfactants diffuse in water and get adsorbed at interfaces between air and water, or at the interface between oil and water in the case where water is mixed with oil. The water-insoluble hydrophobic group may extend out of the bulk water phase into a non-water phase such as air or oil phase, while the water-soluble head group remains bound in the water phase.
The hydrophobic tail may be either lipophilic ("oil-seeking") or lipophobic ("oil-avoiding") depending on its chemistry. Hydrocarbon groups are usually lipophilic, for use in soaps and detergents, while fluorocarbon groups are lipophobic, for use in repelling stains or reducing surface tension.
World production of surfactants is estimated at 15 million tons per year, of which about half are soaps. Other surfactants produced on a particularly large scale are linear alkylbenzene sulfonates (1.7 million tons/y), lignin sulfonates (600,000 tons/y), fatty alcohol ethoxylates (700,000 tons/y), and alkylphenol ethoxylates (500,000 tons/y).[6]
Sodium stearate, the most common component of most soap, which comprises about 50% of commercial surfactants 4-(5-Dodecyl) benzenesulfonate, a linear dodecylbenzenesulfonate, one of the most common surfactants[
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In the bulk aqueous phase, surfactants form aggregates, such as micelles, where the hydrophobic tails form the core of the aggregate and the hydrophilic heads are in contact with the surrounding liquid. Other types of aggregates can also be formed, such as spherical or cylindrical micelles or lipid bilayers. The shape of the aggregates depends on the chemical structure of the surfactants, namely the balance in size between the hydrophilic head and hydrophobic tail. A measure of this is the hydrophilic-lipophilic balance (HLB). Surfactants reduce the surface tension of water by adsorbing at the liquid-air interface. The relation that links the surface tension and the surface excess is known as the Gibbs isotherm.
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The dynamics of surfactant adsorption is of great importance for practical applications such as in foaming, emulsifying or coating processes, where bubbles or drops are rapidly generated and need to be stabilized. The dynamics of absorption depend on the diffusion coefficient of the surfactant. As the interface is created, the adsorption is limited by the diffusion of the surfactant to the interface. In some cases, there can exist an energetic barrier to adsorption or desorption of the surfactant. If such a barrier limits the adsorption rate, the dynamics are said to be &#;kinetically limited'. Such energy barriers can be due to steric or electrostatic repulsions. The surface rheology of surfactant layers, including the elasticity and viscosity of the layer, play an important role in the stability of foams and emulsions.
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Interfacial and surface tension can be characterized by classical methods such as the -pendant or spinning drop method. Dynamic surface tensions, i.e. surface tension as a function of time, can be obtained by the maximum bubble pressure apparatus
The structure of surfactant layers can be studied by ellipsometry or X-ray reflectivity.
Surface rheology can be characterized by the oscillating drop method or shear surface rheometers such as double-cone, double-ring or magnetic rod shear surface rheometer.
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Surfactants play an important role as cleaning, wetting, dispersing, emulsifying, foaming and anti-foaming agents in many practical applications and products, including detergents, fabric softeners, motor oils, emulsions, soaps, paints, adhesives, inks, anti-fogs, ski waxes, snowboard wax, deinking of recycled papers, in flotation, washing and enzymatic processes, and laxatives. Also agrochemical formulations such as herbicides (some), insecticides, biocides (sanitizers), and spermicides (nonoxynol-9).[10] Personal care products such as cosmetics, shampoos, shower gel, hair conditioners, and toothpastes. Surfactants are used in firefighting (to make "wet water" that more quickly soaks into flammable materials[11][12]) and pipelines (liquid drag reducing agents). Alkali surfactant polymers are used to mobilize oil in oil wells.
Surfactants act to cause the displacement of air from the matrix of cotton pads and bandages so that medicinal solutions can be absorbed for application to various body areas. They also act to displace dirt and debris by the use of detergents in the washing of wounds[13] and via the application of medicinal lotions and sprays to surface of skin and mucous membranes.[14] Surfactants enhance remediation via soil washing, bioremediation, and phytoremediation.[15]
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In solution, detergents help solubilize a variety of chemical species by dissociating aggregates and unfolding proteins. Popular surfactants in the biochemistry laboratory are sodium lauryl sulfate (SDS) and cetyl trimethylammonium bromide (CTAB). Detergents are key reagents to extract protein by lysis of the cells and tissues: They disorganize the membrane's lipid bilayer (SDS, Triton X-100, X-114, CHAPS, DOC, and NP-40), and solubilize proteins. Milder detergents such as octyl thioglucoside, octyl glucoside or dodecyl maltoside are used to solubilize membrane proteins such as enzymes and receptors without denaturing them. Non-solubilized material is harvested by centrifugation or other means. For electrophoresis, for example, proteins are classically treated with SDS to denature the native tertiary and quaternary structures, allowing the separation of proteins according to their molecular weight.
Detergents have also been used to decellularise organs. This process maintains a matrix of proteins that preserves the structure of the organ and often the microvascular network. The process has been successfully used to prepare organs such as the liver and heart for transplant in rats.[16] Pulmonary surfactants are also naturally secreted by type II cells of the lung alveoli in mammals.
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Surfactants are used with quantum dots in order to manipulate their growth,[17] assembly, and electrical properties, in addition to mediating reactions on their surfaces. Research is ongoing in how surfactants arrange themselves on the surface of the quantum dots.[18]
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Surfactants play an important role in droplet-based microfluidics in the stabilization of the droplets, and the prevention of the fusion of droplets during incubation.[19]
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Janus-type material is used as a surfactant-like heterogeneous catalyst for the synthesis of adipic acid.[20]
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Agents that increase surface tension are "surface active" in the literal sense but are not called surfactants as their effect is opposite to the common meaning. A common example of surface tension increase is salting out: adding an inorganic salt to an aqueous solution of a weakly polar substance will cause the substance to precipitate. The substance may itself be a surfactant, which is one of the reasons why many surfactants are ineffective in sea water.
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The human body produces diverse surfactants. Pulmonary surfactant is produced in the lungs in order to facilitate breathing by increasing total lung capacity, and lung compliance. In respiratory distress syndrome or RDS, surfactant replacement therapy helps patients have normal respiration by using pharmaceutical forms of the surfactants. One example of a pharmaceutical pulmonary surfactant is Survanta (beractant) or its generic form Beraksurf, produced by Abbvie and Tekzima respectively. Bile salts, a surfactant produced in the liver, play an important role in digestion.[21]
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Most anionic and non-ionic surfactants are non-toxic, having LD50 comparable to table salt. The toxicity of quaternary ammonium compounds, which are antibacterial and antifungal, varies. Dialkyldimethylammonium chlorides (DDAC, DSDMAC) used as fabric softeners have high LD50 (5 g/kg) and are essentially non-toxic, while the disinfectant alkylbenzyldimethylammonium chloride has an LD50 of 0.35 g/kg. Prolonged exposure to surfactants can irritate and damage the skin because surfactants disrupt the lipid membrane that protects skin and other cells. Skin irritancy generally increases in the series non-ionic, amphoteric, anionic, cationic surfactants.[6]
Surfactants are routinely deposited in numerous ways on land and into water systems, whether as part of an intended process or as industrial and household waste.[22][23][24]
Anionic surfactants can be found in soils as the result of sewage sludge application, wastewater irrigation, and remediation processes. Relatively high concentrations of surfactants together with multimetals can represent an environmental risk. At low concentrations, surfactant application is unlikely to have a significant effect on trace metal mobility.[25][26]
In the case of the Deepwater Horizon oil spill, unprecedented amounts of Corexit were sprayed directly into the ocean at the leak and on the sea-water's surface. The apparent theory was that the surfactants isolate droplets of oil, making it easier for petroleum-consuming microbes to digest the oil. The active ingredient in Corexit is dioctyl sodium sulfosuccinate (DOSS), sorbitan monooleate (Span 80), and polyoxyethylenated sorbitan monooleate (Tween-80).[27][28]
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Because of the volume of surfactants released into the environment, for example laundry detergents in waters, their biodegradation is of great interest. Attracting much attention is the non-biodegradability and extreme persistence of fluorosurfactant, e.g. perfluorooctanoic acid (PFOA).[29] Strategies to enhance degradation include ozone treatment and biodegradation.[30][31] Two major surfactants, linear alkylbenzene sulfonates (LAS) and the alkyl phenol ethoxylates (APE) break down under aerobic conditions found in sewage treatment plants and in soil to nonylphenol, which is thought to be an endocrine disruptor.[32][33] Interest in biodegradable surfactants has led to much interest in "biosurfactants" such as those derived from amino acids.[34] Biobased surfactants can offer improved biodegradation. However, whether surfactants damage the cells of fish or cause foam mountains on bodies of water depends primarily on their chemical structure and not on whether the carbon originally used came from fossil sources, carbon dioxide or biomass.[3]
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