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Acrolein
Acrolein
Acrolein
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Not to be confused with Propanol, Acyloin, or Propanal.
Acrolein
Names
Preferred IUPAC name
Prop-2-enal
Other names
Acraldehyde[1]
Acrylic aldehyde[1]
Allyl aldehyde[1]
Ethylene aldehyde
Acrylaldehyde[1]
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
ECHA InfoCard 100.003.141 Edit this at Wikidata
EC Number
  • 203-453-4
KEGG
RTECS number
  • AS1050000
UNII
UN number 1092
  • InChI=1S/C3H4O/c1-2-3-4/h2-3H,1H2 checkY
    Key: HGINCPLSRVDWNT-UHFFFAOYSA-N checkY
  • InChI=1/C3H4O/c1-2-3-4/h2-3H,1H2
    Key: HGINCPLSRVDWNT-UHFFFAOYAQ
  • O=CC=C
  • C=CC=O
Properties
C3H4O
Molar mass 56.064 g·mol−1
Appearance Colorless to yellow liquid. Colorless gas in smoke.
Odor Acrid, Foul, Irritating
Density 0.839 g/mL
Melting point −88 °C (−126 °F; 185 K)
Boiling point 53 °C (127 °F; 326 K)
Appreciable (> 10%)
Vapor pressure 210 mmHg[1]
Hazards[3]
Occupational safety and health (OHS/OSH):
Main hazards
 Highly poisonous. Causes severe irritation to exposed membranes. Extremely flammable liquid and vapor.
GHS labelling:
GHS02: Flammable GHS05: Corrosive GHS06: Toxic GHS08: Health hazard GHS09: Environmental hazard
Danger
H225, H300, H311, H314, H330, H410
P210, P233, P240, P241, P242, P243, P260, P264, P270, P271, P273, P280, P284, P301+P310, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P310, P312, P320, P321, P322, P330, P361, P363, P370+P378, P391, P403+P233, P403+P235, P405, P501
NFPA 704 (fire diamond)
NFPA 704 four-colored diamondHealth 4: Very short exposure could cause death or major residual injury. E.g. VX gasFlammability 3: Liquids and solids that can be ignited under almost all ambient temperature conditions. Flash point between 23 and 38 °C (73 and 100 °F). E.g. gasolineInstability 3: Capable of detonation or explosive decomposition but requires a strong initiating source, must be heated under confinement before initiation, reacts explosively with water, or will detonate if severely shocked. E.g. hydrogen peroxideSpecial hazards (white): no code
4
3
3
Flash point −26 °C (−15 °F; 247 K)
278 °C (532 °F; 551 K)
Explosive limits 2.8–31%[1]
Lethal dose or concentration (LD, LC):
875 ppm (mouse, 1 min)
175 ppm (mouse, 10 min)
150 ppm (dog, 30 min)
8 ppm (rat, 4 hr)
375 ppm (rat, 10 min)
25.4 ppm (hamster, 4 hr)
131 ppm (rat, 30 min)[2]
674 ppm (cat, 2 hr)[2]
NIOSH (US health exposure limits):
PEL (Permissible)
 TWA 0.1 ppm (0.25 mg/m3)[1]
REL (Recommended)
 TWA 0.1 ppm (0.25 mg/m3) ST 0.3 ppm (0.8 mg/m3)[1]
IDLH (Immediate danger)
 2 ppm[1]
Safety data sheet (SDS) Sigma-Aldrich SDS
Related compounds
Related alkenals
 Crotonaldehyde

cis-3-Hexenal
(E,E)-2,4-Decadienal

Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
checkY verify (what is checkY☒N ?)

Acrolein (systematic name: propenal) is the simplest unsaturated aldehyde. It is a colorless liquid with a foul and acrid aroma. The smell of burnt fat (as when cooking oil is heated to its smoke point) is caused by glycerol in the burning fat breaking down into acrolein. It is produced industrially from propene and mainly used as a biocide and a building block to other chemical compounds, such as the amino acid methionine.

History

[edit]

Acrolein was first named and characterized as an aldehyde by the Swedish chemist Jöns Jacob Berzelius in 1839. He had been working with it as a thermal degradation product of glycerol, a material used in the manufacture of soap. The name is a contraction of 'acrid' (referring to its pungent smell) and 'oleum' (referring to its oil-like consistency). In the 20th century, acrolein became an important intermediate for the industrial production of acrylic acid and acrylic plastics.[4]

Production

[edit]

Acrolein is prepared industrially by oxidation of propene. The process uses air as the source of oxygen and requires metal oxides as heterogeneous catalysts:[5]

About 500,000 tons of acrolein are produced in this way annually in North America, Europe, and Japan. Additionally, all acrylic acid is produced via the transient formation of acrolein.

Propane represents a promising but challenging feedstock for the synthesis of acrolein (and acrylic acid).The main challenge is in fact the overoxidation to this acid.

When glycerol (also called glycerin) is heated to 280 °C, it decomposes into acrolein

This route is attractive when glycerol is co-generated in the production of biodiesel from vegetable oils or animal fats. The dehydration of glycerol has been demonstrated but has not proven competitive with the route from petrochemicals.[6][7]

Niche or laboratory methods

[edit]

The original industrial route to acrolein, developed by Degussa, involves aldol condensation of formaldehyde and acetaldehyde:

Acrolein may also be produced on lab scale by the action of potassium bisulfate on glycerol (glycerine). [8]

Reactions

[edit]

Acrolein is a relatively electrophilic compound and a reactive one, hence its high toxicity. It is a good Michael acceptor, hence its useful reaction with thiols. It forms acetals readily, a prominent one being the spirocycle derived from pentaerythritol, diallylidene pentaerythritol. Acrolein participates in many Diels-Alder reactions, even with itself. Via Diels-Alder reactions, it is a precursor to some commercial fragrances, including myrac aldehyde ("lyral") and norbornene-2-carboxaldehyde.[5] The monomer 3,4-epoxycyclohexylmethyl-3',4'-epoxycyclohexane carboxylate is also produced from acrolein via the intermediacy of tetrahydrobenzaldehyde.

Uses

[edit]

Military uses

[edit]

Acrolein was used in warfare due to its irritant and blistering properties. The French used the chemical in their hand grenades and artillery shells[9] during World War I under the name "Papite".[10]

Biocide

[edit]

Acrolein is mainly used as a contact herbicide to control submersed and floating weeds, as well as algae, in irrigation canals. It is used at a level of 10 ppm in irrigation and recirculating waters. In the oil and gas industry, it is used as a biocide in drilling waters, as well as a scavenger for hydrogen sulfide and mercaptans.[5]

Chemical precursor

[edit]

A number of useful compounds are made from acrolein, exploiting its bifunctionality. The amino acid methionine is produced by addition of methanethiol followed by the Strecker synthesis. Acrolein condenses with acetaldehyde and amines to give methylpyridines.[11] It is also an intermediate in the Skraup synthesis of quinolines.

Acrolein will polymerize in the presence of oxygen and in water at concentrations above 22%. The color and texture of the polymer depends on the conditions. The polymer is a clear, yellow solid. In water, it will form a hard, porous plastic.[citation needed]

Acrolein has been used as a fixative in preparation of biological specimens for electron microscopy.[12]

Health risks

[edit]

Acrolein is toxic and is a strong irritant for the skin, eyes, and nasal passages.[5] The main metabolic pathway for acrolein is the alkylation of glutathione. The WHO suggests a "tolerable oral acrolein intake" of 7.5 μg per day per kg of body weight. Although acrolein occurs in French fries (and other fried foods), the levels are only a few μg per kg.[13] In response to occupational exposures to acrolein, the US Occupational Safety and Health Administration has set a permissible exposure limit at 0.1 ppm (0.25 mg/m3) at an eight-hour time-weighted average.[14] Acrolein acts in an immunosuppressive manner and may promote regulatory cells,[15] thereby preventing the generation of allergies on the one hand, but also increasing the risk of cancer.

Acrolein was identified as one of the chemicals involved in the 2019 Kim Kim River toxic pollution incident.[16]

Cigarette smoke

[edit]

Connections exist between acrolein gas in the smoke from tobacco cigarettes and the risk of lung cancer.[17] Acrolein is one of seven toxicants in cigarette smoke that are most associated with respiratory tract carcinogenesis.[18] The mechanism of action of acrolein appears to involve induction of increased reactive oxygen species and DNA damage related to oxidative stress.[19]

Acrolein is the most significant contributor to non-cancer related health risks in cigarette smoke, contributing 40 times more than the next component, hydrogen cyanide.[20] The acrolein content in cigarette smoke depends on the type of cigarette and added glycerin, making up to 220 μg acrolein per cigarette.[21][22] Importantly, while the concentration of the constituents in mainstream smoke can be reduced by filters, this has no significant effect on the composition of the side-stream smoke where acrolein usually resides, and which is inhaled by passive smoking.[23][24] E-cigarettes, used normally, only generate "negligible" levels of acrolein (less than 10 μg "per puff").[25][26]

Chemotherapy metabolite

[edit]

Cyclophosphamide and ifosfamide treatment results in the production of acrolein.[27] Acrolein produced during cyclophosphamide treatment collects in the urinary bladder and if untreated can cause hemorrhagic cystitis.

Endogenous production

[edit]

Acrolein is a component of reuterin.[28] Reuterin can be produced by gut microbes when glycerol is present. Microbe-produced reuterin is a potential resource of acrolein.[29]

Analytical methods

[edit]

The "acrolein test" is for the presence of glycerin or fats. A sample is heated with potassium bisulfate, and acrolein is released if the test is positive. When a fat is heated strongly in the presence of a dehydrating agent such as potassium bisulfate (KHSO
4), the glycerol portion of the molecule is dehydrated to form the unsaturated aldehyde, acrolein (CH2=CH–CHO), which has the odor peculiar to burnt cooking grease. More modern methods exist.[13]

In the US, EPA methods 603 and 624.1 are designed to measure acrolein in industrial and municipal wastewater streams.[30][31]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Acrolein

View on Grokipedia
from Grokipedia

Acrolein, with the IUPAC name prop-2-enal, is the simplest α,β-unsaturated , characterized by the C₃H₄O and the CH₂=CHCHO. It exists as a colorless to pale yellow volatile liquid with a pungent, , exhibiting high reactivity due to its conjugated and . Acrolein polymerizes readily and is typically stabilized for storage and handling. Industrially, acrolein is primarily produced through the selective of with air, involving metal oxide catalysts in a process that also generates byproducts like . Alternative routes include the of , particularly from renewable sources, though these are less dominant. As a versatile chemical intermediate, it is employed in the synthesis of resins, plastics, pharmaceuticals, and pesticides, including its role in producing and . Despite its utility, acrolein poses significant and environmental risks, acting as a potent irritant and lachrymator that causes severe to the eyes, , and upon exposure. or dermal contact can lead to , including , while chronic exposure is linked to carcinogenic potential; it is also highly toxic to aquatic life. Acrolein occurs naturally in processes, such as in smoke and heated fats, contributing to their irritancy.

Properties

Chemical Structure and Formula

Acrolein has the molecular formula C₃H₄O. Its IUPAC name is prop-2-enal. The compound consists of a three-carbon featuring a of a carbon-carbon and an group, represented structurally as H₂C=CH–CHO. This arrangement makes acrolein the simplest α,β-unsaturated . In the gas phase, acrolein predominantly exists in the s-trans conformation, where the aldehyde group and the are trans about the intervening C–C , due to its lower energy compared to the s-cis form by approximately 1.7 kcal/mol as determined by calculations. The s-trans geometry minimizes steric interactions and stabilizes the conjugated π-system. The InChI representation is InChI=1S/C3H4O/c1-2-3-4/h2-3H,1H2, and the SMILES notation is C=CC=O.

Physical Characteristics

Acrolein appears as a colorless to pale yellow liquid at standard conditions, often exhibiting upon standing or exposure to , which imparts a yellow tint. It possesses a sharp, acrid reminiscent of burnt fat or , detectable at low concentrations and contributing to its recognition as a lachrymator. The compound has a melting point of -88 °C and a boiling point of 53 °C at atmospheric pressure, rendering it a volatile liquid that readily evaporates. Its density is 0.839 g/cm³ at 20 °C, with a vapor density of 1.94 relative to air, facilitating rapid dispersion in gaseous phases. Acrolein is freely soluble in to the extent of approximately 20 g/100 mL at 20 °C, and it mixes readily with organic solvents such as , , and . Its is notably high at around 210 mmHg at 20 °C, underscoring its volatility and tendency to form explosive mixtures with air.
PropertyValueConditions
Melting point-88 °CStandard pressure
Boiling point53 °C1 atm
Density0.839 g/cm³20 °C
Water solubility20 g/100 mL20 °C
210 mmHg20 °C

Chemical Reactivity

Acrolein, with the formula CH₂=CHCHO, displays pronounced electrophilicity arising from the conjugation between its carbonyl and the adjacent carbon-carbon , rendering the β-carbon and carbonyl carbon susceptible to nucleophilic attack. This structural feature facilitates Michael-type (1,4-conjugate) additions, where nucleophiles such as thiols, amines, and enolates add preferentially to the β-position, forming stable adducts. For instance, acrolein reacts rapidly with biological nucleophiles like or protein residues (e.g., , ), depleting cellular antioxidants and modifying biomolecules. Such reactivity underpins its use as a synthetic intermediate but also necessitates careful handling to prevent unintended side reactions. In addition to conjugate additions, acrolein participates in reactions typical of aldehydes, including oxidation to and reduction to , though the unsaturated system often directs selectivity toward 1,4-pathways over direct 1,2-addition to the carbonyl. It also undergoes Diels-Alder cycloadditions as a dienophile, leveraging the electron-deficient . However, its instability manifests in a strong propensity for , which can occur violently under heat (above 50 °C), light, or by acids, bases, or initiators, yielding insoluble polyacrolein. Commercial acrolein is thus stabilized with inhibitors like to mitigate exothermic self-polymerization or dimerization. Acrolein is incompatible with strong oxidizing agents, which can trigger explosive reactions, and with alkaline materials or amines, promoting or addition products. Its high reactivity with and alcohols leads to or formation, further complicating storage and transport. These properties demand inert atmospheres and low temperatures during manipulation to preserve monomeric integrity.

History

Discovery and Early Identification

Acrolein was first characterized as an aldehyde in 1839 by Swedish chemist Jöns Jacob Berzelius during experiments involving the thermal degradation of glycerol, yielding a light-yellow liquid with a highly pungent, acrid odor. Berzelius named the compound "acrolein," combining the Latin terms acris (acrid) for its irritating smell and oleum (oil) for its viscous nature, distinguishing it from saturated aldehydes like those derived from alcohols. This identification marked the initial recognition of acrolein as a distinct chemical entity, produced via dehydration of glycerol, though its exact structure as propenal (CH₂=CHCHO) was not fully elucidated at the time. In 1843, Austrian chemist Joseph Redtenbacher independently prepared acrolein through the of animal fats at high temperatures, confirming its presence as a volatile in such processes. Redtenbacher's work provided empirical evidence of acrolein's formation from lipid decomposition and noted its tendency to polymerize into a resinous material, termed "disacryl," when exposed to or , highlighting its and reactivity early on. These observations built on Berzelius's findings by demonstrating reproducible isolation methods and foreshadowing acrolein's challenges in handling due to its lachrymatory and self-reactive properties. Subsequent early analyses in the mid-19th century refined acrolein's and confirmed its unsaturated nature through reactions with oxidizing agents, though systematic structural determination awaited advanced spectroscopic techniques. These foundational efforts, grounded in direct and experiments, established acrolein as a key intermediate in organic degradation pathways, with applications initially limited by its and instability.

Development of Industrial Synthesis

The initial industrial synthesis of acrolein was established through the vapor-phase aldol condensation of formaldehyde and acetaldehyde, developed by Degussa in Germany, with commercial production commencing in 1942. This process involved heating the aldehydes over catalysts such as sodium silicate or phosphate at temperatures around 300–400 °C, yielding acrolein alongside byproducts like water and hydrogen. It represented the first scalable method for acrolein manufacture, driven by demand for intermediates in chemical synthesis during the early 20th century. By the late 1950s, economic pressures and the post-World War II abundance of petroleum-derived led to a pivotal shift toward direct of . Commercial implementation of this -based process began in 1959, utilizing air or oxygen over metal oxide catalysts like cuprous oxide or , achieving conversions exceeding 90% with high selectivity to acrolein. Pioneered by companies such as Shell Chemical, this method supplanted the route due to lower raw material costs and improved efficiency, rendering the older process virtually obsolete by the . Worldwide acrolein production via oxidation reached approximately 59,000 tonnes of isolated product by 1975, underscoring its dominance. Subsequent refinements in catalyst technology, including multicomponent oxides, further enhanced yields and selectivity, solidifying propylene oxidation as the standard industrial pathway. This evolution reflected broader trends in integration, where acrolein served increasingly as an intermediate for and production.

Production Methods

Industrial Processes

The primary industrial production of acrolein involves the selective of (propene) with molecular oxygen from air, typically in the presence of to moderate the reaction and prevent hotspots. This gas-phase process operates at temperatures around 300–400 °C and , using multi-component catalysts such as bismuth-molybdate (Bi-Mo-O) systems, which promote allylic oxidation while minimizing complete to carbon oxides and . Yields of acrolein can reach 80–90% based on propylene conversion of about 10–15% per pass, with unreacted recycled after separation. The reaction mixture, comprising propylene, air (providing 10–15% oxygen), and steam (ratio often 1:10:1 propylene:O2:H2O), passes through fixed-bed tubular reactors filled with the catalyst. Post-reaction, the effluent is cooled and quenched to stabilize acrolein, followed by absorption in water or fractionation to recover the product, which is then purified by distillation under reduced pressure to avoid polymerization. Byproducts include acrylic acid, acetaldehyde, and trace amounts of carbon monoxide and dioxide, necessitating efficient separation to achieve commercial-grade acrolein purity exceeding 95%. Historically, acrolein was manufactured via vapor-phase condensation of and over alkali catalysts, but this method has been largely supplanted by oxidation due to higher efficiency and lower costs associated with petroleum-derived feedstocks. Emerging processes, such as of —a byproduct—over acid catalysts like metal oxides or zeolites at 250–350 °C, offer a bio-based alternative with acrolein yields up to 80%, though these remain niche or developmental rather than dominant industrial routes as of 2025.

Laboratory and Niche Syntheses

Acrolein is commonly prepared in settings through the acid-catalyzed of , a method dating back to early practices. This involves heating in the presence of dehydrating agents such as or to facilitate the elimination of two molecules of , yielding acrolein as the distillate. In a standard procedure, a mixture of and anhydrous is gradually heated to temperatures around 180–220 °C, with acrolein collected by at its of approximately 52.5 °C at . Yields typically range from 40–60%, though purification via fractionation or formation of addition compounds like the bisulfite adduct is often required to separate acrolein from byproducts such as , , and polymeric residues. An alternative laboratory route employs the oxidation of allyl alcohol using palladium(II) chloride in aqueous media at ambient temperatures (around 25 °C), producing acrolein through selective dehydrogenation of the allylic alcohol. This method affords acrolein in yields of about 30%, accompanied by 15% α-hydroxyacetone as a coproduct, and is noted for its mild conditions suitable for small-scale preparations. For niche applications, alkyl allyl ethers can be oxidized with atmospheric oxygen in the presence of palladium chloride at 50–60 °C, providing another pathway to acrolein via allylic rearrangement and dehydrogenation. Historically significant but less common in modern labs, acrolein can be synthesized via the of and , where the of adds to to form 3-hydroxypropanal, which spontaneously or under acidic/basic conditions dehydrates to acrolein. This crossed , often conducted in vapor phase over oxide catalysts like ZnO or MgO at elevated temperatures (270–330 °C), achieves selectivities dependent on catalyst composition but is adaptable to liquid-phase conditions for use. Such methods highlight acrolein's derivation from simpler aldehydes, though they require careful control to minimize self-condensation of .

Chemical Reactions

Electrophilic Addition

Acrolein participates in reactions across its α,β-unsaturated carbon-carbon double bond, where the conjugated influences by stabilizing an intermediate through . The β-carbon (terminal CH₂) acts as the initial site of attachment, following principles analogous to , leading to the electrophile positioning at the α-carbon adjacent to the . This reactivity is documented in standard contexts for α,β-unsaturated aldehydes, though acrolein's high electrophilicity as a Michael acceptor often competes with these additions. In , hydrogen halides such as HCl or HBr add to acrolein to form 2-halopropanal derivatives. occurs at the β-carbon, generating a resonance-stabilized at the α-carbon: the primary form is CH₃-CH⁺-CHO, which delocalizes to CH₃-CH=CH-OH⁺, facilitating subsequent nucleophilic attack by the halide ion at the α-position. The product is thus 2-halopropanal (e.g., CH₃CHXCHO, where X is Cl or Br), as confirmed by balanced reaction and . Halogenation with Br₂ proceeds via electrophilic addition, typically yielding the vicinal dihalide 2,3-dibromopropanal (BrCH₂CHBrCHO). The mechanism involves formation of a bromonium ion intermediate bridged across the double bond, with the second bromide attacking the more substituted α-carbon due to partial positive charge distribution influenced by the carbonyl. This compound has been identified in studies of reactive metabolites and genotoxicity assays, underscoring the addition's occurrence under controlled conditions. Experimental demonstrations, such as vapor-phase bromination, highlight rapid reaction kinetics, often requiring low temperatures to isolate products without polymerization side reactions. These additions are generally conducted in inert solvents or gas phase to minimize competing nucleophilic conjugate additions or , with yields varying based on concentration and ; for instance, HBr addition proceeds efficiently but may require catalysts like peroxides for anti-Markovnikov orientation in non-conjugated analogs, though conjugation favors the 1,2-mode here. The electron-withdrawing reduces the double bond's nucleophilicity compared to simple alkenes, slowing rates but preserving via the stabilized allylic-like or .

Polymerization and Other Transformations

Acrolein undergoes spontaneous in the absence of inhibitors, particularly when exposed to , air, or oxygen at , leading to highly exothermic reactions that form insoluble, cross-linked polymers whose color and texture vary with conditions such as concentration and . In aqueous solutions above 22% concentration, occurs readily, often catalyzed by initiators like peroxodiphosphate or free radical species. proceeds via initiation by peroxides or , propagating through 1,4-addition to the , yielding polyacrolein with pendant vinyl and groups that enable further reactivity, including Michael additions and carbonyl condensations. Anionic favors 3,4-addition modes, producing branched structures suitable for microsphere synthesis used in biomedical applications like cell labeling and immobilization. Polyacrolein microspheres, typically 0.1–5 μm in , exhibit high reactivity for covalent attachment of biomolecules due to their functionalities, with stability enhanced by crosslinking. Beyond , acrolein serves as a dienophile in Diels-Alder cycloadditions with conjugated dienes such as or 1,3-butadiene, forming derivatives with the group retained in the ; these reactions exhibit endo selectivity in uncatalyzed cases but can be modulated by catalysts like iron-exchanged clays for improved yields at ambient temperatures. Hetero-Diels-Alder variants, including oxa-Diels-Alder with allylic alcohols, enable asymmetric synthesis of dihydropyrans when catalyzed by chiral oxazaborolidinium ions, achieving high enantioselectivity (up to 99% ee) via activation of α-bromoacrolein derivatives. transforms acrolein to over molybdenum-based oxides (e.g., MoVTeNb), while ammoxidation yields , sharing a common Mars-van Krevelen mechanism involving lattice oxygen regeneration. Organocatalytic self-trimerization of acrolein produces trialkylated cyclohexenals, as demonstrated in total syntheses like that of montiporyne F III, proceeding through sequential aldol and cyclization steps. These transformations highlight acrolein's utility in constructing complex carbon frameworks, though risks necessitate stabilizers like in storage and handling.

Applications

Industrial and Chemical Synthesis Uses

Acrolein is predominantly utilized as an intermediate in the industrial production of , where it undergoes selective with air or oxygen over supported metal oxide catalysts, such as molybdenum-bismuth or iron-molybdate systems, at temperatures around 250–350°C, yielding high-purity for subsequent esterification into acrylates used in polymers, adhesives, and coatings. This process accounts for the majority of acrolein's commercial demand, with acrylic acid derivatives forming the basis for superabsorbent polymers and water-treatment chemicals. A substantial portion of acrolein is directed toward the synthesis of DL-methionine, a critical feed additive for , involving its reaction with methyl mercaptan to form 3-(methylthio), followed by cyanohydrin formation with and , often conducted in integrated facilities to minimize handling of the reactive . This route leverages acrolein's α,β-unsaturation for efficient carbon chain building in production. Additional synthetic applications include the manufacture of through successive of acrolein to and then , though this is less dominant than direct propylene routes; the formation of and resins via Diels-Alder or Michael addition reactions; and as a precursor for herbicides like 2,4-D derivatives and certain pharmaceuticals through aldol condensations or cyclization reactions. In , acrolein participates in the for production by condensing with anilines and related heterocycles, and in forming methylpyridines via reactions with and amines, supporting and flavor intermediates. These uses exploit its electrophilic reactivity, though stringent safety protocols are required due to its volatility and toxicity.

Biocidal and Agricultural Applications

Acrolein functions as a potent contact due to its reactivity with proteins and enzymes, making it effective against a range of microorganisms, , and aquatic vegetation at low concentrations typically ranging from 0.1 to 10 mg/L. In agricultural contexts, it is registered as a restricted-use , primarily under the trade name Magnacide H, for controlling submerged and floating weeds, as well as , in canals and ditches. This application is particularly prevalent in the and , where it prevents vegetation-induced flow restrictions that reduce efficiency and capacity, with injections achieving rapid lethality to target species while minimizing persistence in treated water. Its high volatility and water solubility (approximately 215,000 ppm) facilitate even distribution in flowing systems, though use requires supervision by licensed applicators due to its . In non-agricultural biocidal roles, acrolein is employed in industrial recirculating water systems, such as cooling towers and paper mills, for slime, , weed, and control. It is also applied in oilfield operations to suppress , hydrogen sulfide production, and biogenic iron sulfides, enhancing asset integrity and reducing risks. These uses leverage acrolein's broad-spectrum action, which disrupts cellular processes in prokaryotes and eukaryotes alike, though environmental discharge is regulated to limit ecological impacts on non-target organisms.

Military and Specialized Uses

Acrolein has been utilized in military contexts for its potent irritant and lacrimatory effects, as well as its foul, pungent odor that can serve as a detectable warning. During , the French military deployed acrolein, codenamed "Papite," in shells and hand grenades as a agent to incapacitate enemy forces through severe eye and respiratory irritation. However, its practical effectiveness as a agent was limited by inherent instability during storage and deployment, preventing widespread or sustained use. Scottish chemist proposed acrolein to the British in the early as a potential war gas, highlighting its capacity to cause blistering and incapacitation, though this did not lead to adoption. Beyond direct combat applications, acrolein has been incorporated into poison gas mixtures to enhance detectability and irritancy. Its inclusion in such formulations dates to early 20th-century efforts, where the compound's volatility and complemented other agents, though logistical challenges like reduced reliability. In specialized non-combat applications, acrolein functions as an odorant additive or warning agent in hazardous industrial gases, such as methyl chloride refrigerants, alerting personnel to leaks via its acrid smell at concentrations as low as 0.5 parts per million. In the offshore oil and gas sector, it is applied as a dual-phase biocide to penetrate oil-coated iron sulfide solids and sessile bacteria in pipelines and reservoirs, mitigating microbiologically influenced corrosion and souring; treatments typically involve concentrations of 50-200 ppm, injected continuously or in slugs for efficacy in both aqueous and hydrocarbon phases. These uses exploit acrolein's reactivity without relying on its full-scale industrial synthesis role.

Toxicology and Health Effects

Acute Toxicity Mechanisms

Acrolein, an , induces through its electrophilic reactivity, primarily via Michael addition to nucleophilic residues in proteins, particularly sulfhydryl groups, and to , depleting cellular defenses. This adduction disrupts protein function, including enzymes critical for cellular , and generates (ROS) by overwhelming the system, leading to oxidative damage in exposed tissues. Acrolein also forms cross-links with and other amines, further contributing to protein misfolding and aggregation. In acute inhalation exposures, the primary route of concern, acrolein reacts rapidly with mucosal surfaces in the , causing sensory via activation of transient receptor potential ankyrin 1 () channels and subsequent neurogenic . This triggers vagal reflex-mediated and , with histological evidence of epithelial and sloughing observed in animal models at concentrations as low as 1-10 ppm for short durations. Ocular and dermal exposures similarly result from direct adduction to corneal or skin proteins, manifesting as severe and burns due to the compound's high and , which facilitate penetration and local . At the cellular level, acute high-dose exposure inhibits mitochondrial respiration by adducting thiol-dependent complexes in the , exacerbating ATP depletion and necrotic , particularly in alveolar cells. Unlike saturated aldehydes, acrolein's conjugated enhances its reactivity toward thiols by approximately 1000-fold, making it the most potent 2-alkenal among structurally related compounds. These mechanisms collectively underlie the low LC50 values reported in , such as 66 ppm for 1-hour , reflecting rapid onset of systemic effects including from vascular endothelial damage.

Chronic Exposure Risks

Chronic exposure to acrolein at concentrations as low as 1-3 ppm has been associated with histological alterations and in the of experimental animals, including epithelial , , and ulceration in the and trachea. In rats and mice exposed to acrolein vapors for up to two years, chronic effects included forestomach lesions and increased incidences of nasal squamous cell carcinomas, with no-observed-adverse-effect levels (NOAELs) around 0.1-0.6 ppm depending on and duration. These findings indicate a primary site of action in the upper due to acrolein's reactivity as an α,β-unsaturated , leading to protein adduction and . In humans, direct evidence for chronic acrolein-specific toxicity is limited, but long-term exposure through environmental tobacco smoke or occupational settings correlates with exacerbated respiratory conditions such as (COPD) and , where acrolein contributes to airway inflammation and mucus hypersecretion. Epidemiological data from smokers show elevated urinary biomarkers of acrolein exposure (e.g., 3-hydroxypropylmercapturic acid) linked to reduced lung function over time, suggesting a role in progressive . Systemic effects from chronic exposure remain understudied, though animal models report mild inflammatory changes in organs like the liver and kidneys at higher doses, without clear thresholds for non-respiratory . Regarding carcinogenicity, the International Agency for Research on Cancer (IARC) classifies acrolein as "probably carcinogenic to humans" (Group 2A), based on sufficient evidence of nasal tumors in from chronic inhalation and strong mechanistic data showing DNA adduct formation, , and inhibition of . However, human cancer data are inadequate for direct attribution, with no consistent epidemiological links to specific malignancies beyond tobacco-related risks; the U.S. EPA considers the evidence inconclusive for human carcinogenicity. Chronic exposure risks are thus dominated by non-cancer respiratory endpoints, with cancer potential inferred primarily from animal and in vitro studies.

Human Exposure Sources and Epidemiology

Human exposure to acrolein primarily occurs via , with secondary routes including of contaminated or and dermal contact in occupational settings. In the general , dominates due to ubiquitous sources such as tobacco smoke (3–220 μg per smoked, higher in marijuana at 92–145 μg per and e-cigarettes at ~150 μg per device), cooking fumes from overheated oils and fats, indoor wood burning, and building materials emitting volatile compounds. Ambient outdoor air contributes smaller amounts from vehicle exhaust, wildfires, and , with measured concentrations ranging 0.062–0.591 ppbv. via foods averages ≤1 μg/g (up to 40 μg/g in some), while exposures are typically low but can reach 115 μg/L in contaminated sources. Occupational exposures are higher and inhalation-focused in industries including (e.g., acrylates, pharmaceuticals), plastics and resin production, oil refining, and fuel , where workplace air levels range 0.004–0.25 ppm. Professions like involve acute spikes, with post-incident air concentrations up to 31.64 μg/m³ and elevated urinary mercapturic acid metabolites (e.g., 3-HPMA). Overall U.S. releases totaled 415,288 pounds to air in 2023, primarily from industrial facilities. Epidemiological relies heavily on like urinary 3-HPMA, which is markedly higher in smokers versus nonsmokers and correlates with exposure intensity. In a cohort of 211 adults with moderate-to-high cardiovascular , elevated 3-HPMA levels associated with platelet-leukocyte aggregation, suppressed circulating angiogenic cells, and higher Framingham Risk Scores, effects observed in both smokers and nonsmokers. Cross-sectional and longitudinal studies link acrolein exposure to pulmonary function decline, mediated partly by . levels also correlate with increased all-cause, , and cancer mortality . carcinogenicity data remain limited, supporting IARC's Group 2A classification (probably carcinogenic) based mainly on tumors and mechanistic from smoking-related contexts, without direct population-level incidence studies isolating acrolein. Acute population exposures, such as from fires, consistently report respiratory irritation thresholds at 0.26–0.43 ppm.

Biological and Endogenous Aspects

Metabolic Production in Organisms

Acrolein is generated endogenously in mammalian cells primarily through oxidative processes associated with cellular stress. One major pathway involves , where attack polyunsaturated fatty acids in cell membranes, leading to the formation of α,β-unsaturated aldehydes including acrolein. This occurs ubiquitously during conditions of oxidative damage, such as or ischemia, with acrolein yields depending on the extent of peroxidation; for instance, studies on oxidized low-density lipoproteins have quantified free acrolein release alongside protein conjugates. Another key route stems from polyamine catabolism, where enzymes like spermine oxidase (SMO) and acetylpolyamine oxidase (APAO) oxidize and spermidine, producing acrolein alongside and 3-aminopropanal. This pathway is active in various tissues, with elevated activity linked to pathological states; for example, SMO-mediated spermine oxidation has been measured to generate micromolar levels of acrolein in cell models under stress. Polyamine-derived acrolein contributes significantly to intracellular pools, particularly in neurons and vascular cells. Myeloperoxidase (MPO), released by activated neutrophils, catalyzes acrolein formation from hydroxy-amino acids such as via hypochlorous acid-dependent reactions. This enzymatic process predominates during acute , with MPO activity correlating to acrolein levels in inflammatory exudates; quantitative assays have detected acrolein at concentrations up to 10-50 μM in MPO-exposed solutions. In the , commensal and pathogenic gut harboring glycerol/ dehydratase (encoded by pduCDE genes) metabolize to 3-hydroxypropionaldehyde, which spontaneously dehydrates to acrolein. This microbial pathway represents an endogenous source in humans, with in vitro studies showing acrolein release during on glycerol-rich media, potentially exacerbating host via absorption. Basal acrolein production from these routes maintains low physiological levels (nanomolar range in tissues), but dysregulation amplifies toxicity in diseases like and neurodegeneration.

Role in Cellular Processes and Pathology

Acrolein, as an α,β-unsaturated aldehyde, acts as a reactive in cellular environments, forming Michael addition adducts primarily with nucleophilic residues such as , , and in proteins, as well as in DNA. These adducts disrupt protein function, including inhibition of enzymes like in mitochondria, leading to impaired cellular signaling and energy production. Protein-bound acrolein serves as a biomarker for , reflecting long-term damage in conditions involving . At the cellular level, acrolein depletes through conjugation, exacerbating and causing mitochondrial dysfunction, membrane damage, and accumulation. Low concentrations inhibit and enhance susceptibility to secondary stressors, while higher doses trigger oncosis or via growth arrest and inhibition. Acrolein-derived DNA adducts, such as γ-hydroxy-1,N²-propano-2'-deoxyguanosine, are mutagenic and persist due to impaired nucleotide excision and pathways. In inflammatory contexts, it activates pathways like and modulates T-cell responses, contributing to epithelial cell damage in airways. In , endogenous acrolein from and polyamine oxidation accumulates in neurodegenerative diseases, promoting neuronal damage, synaptic dysfunction via RhoA/ROCK2 activation, and disruption in and . It exacerbates through vascular endothelial injury and oxidative pathways, and correlates with via adduct formation on plasma proteins. In trauma and ischemia, elevated acrolein levels perpetuate and , underscoring its causal role in secondary injury cascades across cardiovascular, pulmonary, and oncogenic processes.

Environmental Impact

Environmental Sources and Occurrence

Acrolein enters the environment primarily through processes and industrial activities, with both natural and anthropogenic contributions. Natural sources include wildfires and controlled vegetation burning, which release acrolein via incomplete oxidation of , as well as minor contributions from photochemical degradation of atmospheric hydrocarbons and biological processes like in soils or matter. Anthropogenic sources dominate emissions, stemming from vehicle exhaust, in power plants, and industrial processes such as synthesis, production, and paper milling; acrolein also forms secondarily from the atmospheric breakdown of pollutants like 1,3-butadiene. In ambient air, acrolein occurs ubiquitously but at low concentrations due to its high reactivity and atmospheric of 15–20 hours, primarily via oxidation. Median background levels in remote or coastal areas are approximately 0.04 μg/m³ during summer, with urban concentrations 3- to 8-fold higher, averaging 0.07–0.69 μg/m³ and maxima up to 3.23 μg/m³ in recent U.S. monitoring (2022–2023); national U.S. averages from 2006–2009 ranged from non-detect to 2.05 μg/m³. In , acrolein is detected infrequently at low levels (e.g., 1.16–4.44 μg/L averages in 20% of U.S. samples from 2005–2015), often linked to applications like Magnacide in canals, but it degrades rapidly ( <1–3 days) and is rarely found in or . and detections are minimal, with no quantifiable levels in most U.S. samples (e.g., absent in 2005–2009 surveys and only up to 1.9 μg/kg in select sediments). Overall, air represents the dominant environmental compartment for acrolein occurrence, with outdoor levels typically orders of magnitude lower than indoor sources.

Fate, Persistence, and Ecological Effects

Acrolein is released into the environment primarily through industrial emissions, combustion processes, and its use as an aquatic herbicide, where it partitions variably across air, water, and soil based on its high water solubility (approximately 200 g/L at 20°C) and moderate volatility (vapor pressure of 210 mmHg at 20°C). In air, acrolein undergoes rapid photochemical degradation and reacts with hydroxyl radicals, limiting long-range transport; it does not bioaccumulate significantly due to its reactivity. In water, it hydrolyzes to form gem-diols and undergoes volatilization to air, with dilution and advection further reducing concentrations in flowing systems. Soil sorption is low (Koc ≈ 10–100), favoring leaching or runoff into aquatic environments rather than strong retention. Persistence of acrolein is short across media owing to abiotic and biotic degradation. Atmospheric half-life estimates range from 3 to 20 hours, driven by oxidation. In , half-lives are typically <1–3 days under aerobic conditions, influenced by (faster at higher pH via hydration to 3-hydroxypropanal) and microbial activity; anaerobic sediment half-lives extend to 10 days. half-lives, based on reactivity models, are 30–100 hours, with predominating in aerobic upper layers but slower anaerobic processes in deeper sediments. Acrolein does not persist long-term, as it is not detected in sources despite potential runoff, and field applications as a show dissipation within hours to days via downstream dilution and transformation. Ecological effects of acrolein center on acute and to aquatic organisms, reflecting its via protein adduction, inhibition, and disruption. It is highly toxic to (e.g., LC50 of 0.05–0.69 mg/L for over 96 hours) and (e.g., LC50 of 0.39–2.7 mg/L for ), with estuarine/marine species showing similar sensitivity (LC50 ≈0.1–1 mg/L). Chronic exposures reduce survival, growth, and reproduction in and at concentrations as low as 0.003–0.05 mg/L, though rapid dissipation limits prolonged impacts in lotic systems. Terrestrial effects are less documented, but high reactivity suggests minimal in ; no significant avian or mammalian ecological risks are reported beyond direct exposure. As an aquatic herbicide, acrolein controls weeds without leaving phytotoxic residues, but non-target mortality occurs at application rates exceeding 0.1–1 mg/L.

Regulations and Risk Assessment

Acrolein is classified as a hazardous air pollutant under the U.S. Clean Air Act, subjecting industrial emissions to National Emissions Standards for Hazardous Air Pollutants (NESHAP) from sources such as combustion processes and chemical manufacturing. The U.S. Environmental Protection Agency (EPA) has restricted the use of acrolein-containing pesticides, requiring registration review that includes ecological risk assessments evaluating impacts on non-target aquatic and terrestrial organisms. These assessments identify potential risks to aquatic life from direct applications as a or , with mitigation measures such as buffer zones recommended to protect sensitive ecosystems. For , the EPA's national recommended criteria for the protection of aquatic life specify that the one-hour average concentration should not exceed 6.0 µg/L more than once every three years to prevent acute effects on freshwater and saltwater organisms, while the four-day average should not exceed 3.0 µg/L more than once every three years to avoid chronic effects. Human health criteria, updated in 2009, recommend a concentration of 6 µg/L for consumption of and aquatic organisms, reflecting acrolein's carcinogenic potential and irritant properties based on oral and inhalation reference doses. Solid wastes containing acrolein concentrations above specified thresholds are designated as hazardous under the (RCRA), mandating specialized handling, treatment, and disposal to prevent environmental release. In the , acrolein is registered under regulation for uses in and biocides, with safety sheets emphasizing environmental hazard classifications due to its high aquatic toxicity (H400: very toxic to aquatic life). The approval for acrolein in biocidal products (type 12, non-agricultural pesticides) was not renewed by Commission Implementing Decision () 2023/1424, citing unacceptable risks to non-target organisms and the environment after re-evaluation of and exposure . Risk assessments under REACH and the Biocidal Products Regulation highlight acrolein's rapid in water ( ~5-20 hours at neutral pH) but persistent local effects in effluents, leading to derived no-effect concentrations (PNECs) for aquatic compartments around 0.3-3 µg/L based on chronic toxicity for , , and . Ecological risk assessments by the EPA and international bodies consistently note acrolein's high reactivity and irritancy, with lowest-observed-adverse-effect levels (LOAELs) for aquatic species as low as 0.3 ppm in exposure studies, underscoring the need for emission controls and monitoring in combustion-derived sources like wildfires and exhaust. Despite its environmental instability, episodic releases can exceed protective thresholds, prompting state-level guidelines stricter than federal criteria in areas with high industrial activity.

Analytical Methods

Detection Techniques

Acrolein's volatility and reactivity necessitate specialized sampling and stabilization techniques in detection methods, often involving derivatization to form stable derivatives like oxazolidines or use of graphitized sorbents to minimize losses. In ambient and indoor air, the U.S. EPA Method TO-15 utilizes evacuated canisters for whole-air sampling, followed by cryogenic preconcentration, desorption, and analysis by (GC/MS), enabling detection limits around 0.1–0.5 ppb with reduced artifacts compared to sorbent-based methods. Alternative air sampling employs solid sorbents such as graphitized , with desorption-GC/MS (TD-GC/MS) providing robust quantification in environmental chambers and workplaces, achieving limits of detection (LODs) as low as 0.05 μg/m³ after 1–4 hours of sampling. For occupational exposure, NIOSH Method 2501 involves collection on tubes derivatized with 2-(hydroxymethyl), solvent extraction, and GC with nitrogen-phosphorus detection, resolving acrolein-derived oxazolidine peaks from interferents like , with a sampler capacity exceeding 0.1 mg. In water matrices, EPA Method 603 employs purge-and-trap extraction with /flame ionization detection (GC/FID), separating acrolein via temperature-programmed columns for concentrations above 1 μg/L in and . More sensitive approaches for environmental waters use (SPE) with activated charcoal sorbents, followed by liquid chromatography-tandem (LC-MS/MS), detecting acrolein at 0.2–5 ng/L in and samples while minimizing matrix interferences. Biological fluids like urine require headspace sampling to volatilize acrolein, followed by GC/MS for precise measurement of endogenous or exposure-derived levels, with LODs reaching 1–10 ng/mL after derivatization. Emerging spectroscopic alternatives, such as Fourier-transform infrared (FTIR) or differential optical absorption spectroscopy (DOAS), offer real-time, non-destructive air monitoring but are less common due to lower selectivity in complex mixtures. Method validation emphasizes recovery rates above 80% and calibration with certified standards to account for acrolein's instability.

Quantification and Monitoring

Acrolein is quantified in air samples using EPA Compendium Method TO-15, which involves collecting samples in passivated canisters followed by preconcentration and analysis via gas chromatography-mass spectrometry (GC-MS) in selected ion monitoring mode, achieving detection limits in the low parts-per-billion range. This method has been validated for ambient and source monitoring without modification, addressing previous artifacts from derivatization approaches like (DNPH) cartridges. For occupational exposure, OSHA Method 52 employs activated 13X molecular sieves for sampling acrolein vapor, with subsequent solvent desorption and GC analysis using flame ionization detection, targeting the of 0.1 ppm (0.25 mg/m³) as an 8-hour time-weighted average. In indoor and environmental chamber air, solid sorbent sampling tubes packed with Tenax or similar materials, coupled with thermal desorption and GC-MS, enable quantitative determination at concentrations as low as 0.1 ppb, offering robustness against interferences from co-occurring volatile organic compounds. (SPME) variants, including cold fiber techniques, provide sensitive preconcentration for trace-level acrolein in air, with limits of detection reaching 0.05 μg/m³ after headspace extraction and GC-MS detection. These methods prioritize minimal artifact formation, as acrolein's high reactivity can lead to underestimation in traditional impinger-based sampling with or derivatives. For aqueous environmental samples, such as , (SPE) using activated charcoal cartridges followed by liquid chromatography-tandem (LC-MS/MS) allows direct quantification without derivatization, yielding method detection limits of 0.1 μg/L and recoveries exceeding 90% even in complex matrices. In biological fluids like , acrolein is often indirectly quantified via its mercapturic metabolite, 3-hydroxypropylmercapturic (3-HPMA), using SPE cleanup and LC-MS/MS, with typical exposure biomarkers ranging from 100-500 μg/g in smokers. Monitoring programs, such as those under the EPA's ambient air networks, integrate these techniques into routine , reporting annual averages below 1 ppb in urban areas but flagging exceedances near industrial sources. Continuous or real-time monitoring employs proton transfer reaction-mass spectrometry (PTR-MS) for acrolein in air, providing sub-minute resolution at ppb levels, though calibration challenges persist due to humidity interference. Overall, method selection balances sensitivity, specificity, and matrix effects, with GC-MS and LC-MS/MS dominating peer-reviewed validations for .

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