2-Hydroxyethyl acrylate

116.11500

116.12

212-454-9

25GT92NY0C

1723

2927|1760

DTXSID2022123

Liquid|Clear colorless liquid

2916129000

46.53000

-0.2

Hydroxyethylacrylate appears as a clear colorless liquid. Less dense than water. Vapors heavier than air. Corrosive to tissue. May polymerize exothermically if heated or contaminated. If the polymerization takes place inside a container, the container may rupture violently. Used to make plastics.

1.011 g/cm³

-60ºC

220 °C

99ºC

1.449-1.451

H2O: soluble

Keep away from sources of ignition. Store in a cool place in the original container and protect from sunlight. Keep refrigerated

<0.1 mm Hg ( 20 °C)

>1 (vs air)

Lower flammable limit: 1.8% by volume at 100 deg C

Containers may explode in fire. /Inhibited/

Sweet pleasant odor

Henry's Law constant = 7.99X10-9 atm-cu m/mol at 25 °C (est)

Heat of polymerization: -218 Btu/lb = -121 cal/g= -5.06X10+5 J/kg (est)|React readily with electrophilic, free-radical, and nucleophilic agents /Acrylic acid & esters/|Hydroxyl radical reaction rate constant = 1.52X10-11 cu cm/molec-sec at 25 °C (est)

Flammable. Slightly soluble in water.

Alcohols and Polyols

Polymerizable

A functional monomer of thermosetting acrylic resins.

-10,800 Btu/lb = -6,000cal/g = -250X10+5 J/kg (est)

Lower flammable limit: 1.8% by volume at 100 °C

Corrosive to tissue

II

8

UN 2922

3

R20/22; R24; R34; R43; R50

S26-S36/37/39-S45-S61

AT1750000

T; N

Store only if stabilized. Keep in the dark. Cool. Ventilation along the floor. Provision to contain effluent from fire extinguishing. Store in an area without drain or sewer access.

Stable under recommended storage conditions. Contains the following stabilizer(s): Mequinol (>=200 - <=650 ppm)

P273-P280-P303 + P361 + P353-P304 + P340 + P310-P305 + P351 + P338-P333 + P313

H302-H311-H314-H317-H400

SRP: Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in air, soil or water; effects on animal, aquatic and plant life; and conformance with environmental and public health regulations. If it is possible or reasonable use an alternative chemical product with less inherent propensity for occupational harm/injury/toxicity or environmental contamination.|Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber. Contaminated packaging: Dispose of as unused product.

Homopolymers and copolymers of 2-hydroxyethyl acrylate are an indirect food additive for use only as a component of adhesives.

Organization for Economic Cooperation and Development; Screening Information Data Set for Hydroxyethyl acrylate, CAS No. 818-61-1 (April 2005). This OECD Initial Assessment of HPV Chemicals is part of a series of OECD SIDS documents published by UNEP Chemicals to facilitate the access to information needed for health and environmental risk assessments of chemicals.

Behavior in Fire: Containers may explode (USCG, 1999)|Combustible. Heating will cause rise in pressure with risk of bursting.|Corrosives, Reactive - 2nd degree

|Danger|H311: Toxic in contact with skin [Danger Acute toxicity, dermal]|P260, P261, P264, P272, P273, P280, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P310, P312, P321, P322, P333+P313, P361, P363, P391, P405, and P501|H302 (58.11%): Harmful if swallowed [Warning Acute toxicity, oral]|P260, P261, P262, P264, P270, P272, P273, P280, P301+P312, P301+P330+P331, P302+P350, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P310, P312, P321, P322, P330, P333+P313, P361, P363, P391, P405, and P501|Aggregated GHS information provided by 1321 companies from 24 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P260, P261, P264, P270, P272, P273, P280, P301+P312, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P310, P312, P321, P322, P330, P333+P313, P361, P363, P391, P405, and P501|P260, P261, P262, P264, P270, P271, P272, P280, P301+P312, P302+P350, P302+P352, P304+P312, P304+P340, P305+P351+P338, P310, P312, P314, P321, P322, P330, P332+P313, P333+P313, P361, P362, P363, P403+P233, P405, and P501

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]: As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]: ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS. (ERG, 2016)

Goggles or face shield; rubber gloves. (USCG, 1999)|2-hydroxyethyl acrylate penetrates both latex and vinyl gloves and elicits irritant/allergic reactions on the patient and irritant reactions on a control.|Protection required for safe handling of acrylic acid and esters commonly includes use of impervious gloves, shoe soles, and clothing; splash-proof goggles ... /Acrylic acid & derivatives/|Eye/face protection: Tightly fitting safety goggles. Faceshield (8-inch minimum). Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).|Body Protection: Complete suit protecting against chemicals, The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.|For more Personal Protective Equipment (PPE) (Complete) data for 2-Hydroxyethyl acrylate (6 total), please visit the HSDB record page.

Water or foam may cause frothing.|Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Soak up with inert absorbent material and dispose of as hazardous waste. Keep in suitable, closed containers for disposal.|SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.|Avoid contact with skin, eyes and clothing. Wash hands before breaks and immediately after handling the product.|Avoid contact with skin and eyes. Avoid inhalation of vapor or mist. For precautions see section|ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Wear respiratory protection. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.

The acute toxicity of the acrylates decreases with increasing molecular weight ... Acute inhalation of higher concentrations may cause marked irritation, salivation, conjunctival irritation, and pronounced pulmonary irritation or edema. ... /Acrylates/

Personal protection: chemical protection suit and filter respirator for organic gases and vapours adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Collect leaking liquid in covered containers. Absorb remaining liquid in sand or inert absorbent. Then store and dispose of according to local regulations.

Store only if stabilized. Keep in the dark. Cool. Ventilation along the floor. Provision to contain effluent from fire extinguishing. Store in an area without drain or sewer access.

A harmful contamination of the air can be reached very quickly on evaporation of this substance at 20 °C.

The substance is severely irritating to the eyes, skin and respiratory tract. If this liquid is swallowed, aspiration into the lungs may result in chemical pneumonitis.

Repeated or prolonged contact may cause skin sensitization.

NO open flames.

PREVENT GENERATION OF MISTS! AVOID ALL CONTACT!

Use ventilation (not if powder), local exhaust or breathing protection.

Protective gloves. Protective clothing.

Wear safety spectacles or eye protection in combination with breathing protection.

| 3 - Materials that, under emergency conditions, can cause serious or permanent injury.| 1 - Materials that must be preheated before ignition can occur. Materials require considerable preheating, under all ambient temperature conditions, before ignition and combustion can occur.| 2 - Materials that readily undergo violent chemical changes at elevated temperatures and pressures.

IDENTIFICATION AND USE: 2-Hydroxyethyl acrylate (HEA) is a liquid. HEA is used mainly either as a co-monomer in the manufacture of polymers or as a chemical reactant in the manufacture of chemical intermediates. In the manufacture of polymers, HEA can be co-polymerized with acrylic acid, acrylates, methacrylates, vinyl acetate, vinyl chloride, vinylidene chloride, styrene, butadiene, and the like. Co-reactants with HEA include aromatic and aliphatic isocyanates, anhydrides, and epoxides. The polymers and chemical intermediates made with HEA find applications in automotive top coatings, architectural coatings, photocure resins, and adhesives. Derivatives of HEA had been tested as experimental therapy. HUMAN STUDIES: Irritation of eyes and nose was observed at exposure concentrations of 3 ppm (nominal) and higher. The severity of irritation increased with concentration and could be tolerated for several minutes at 10 ppm. A summary of 15 years of experience of patch testing to (meth)acrylates presented the results in 440 patients with a history of exposures to (meth)acrylates. The most frequent positive test reactions were seen with 2-hydroxyethyl acrylate (9.6%). ANIMAL STUDIES: Undiluted HEA is severely irritating to the skin. Several studies have shown that undiluted HEA is severely irritating and can damage the eye. Inhalation data available for rats on HEA indicate that a 7 hour exposure of 264 ppm (1250 mg/cu m) had no lethal effect. Inhalation exposures to 333 to 394 ppm for 4 or 8 hours respectively caused irritation and were in the threshold area for lethality. At exposures at 500 ppm and above, close to 100% lethality was observed. The key study evaluating the acute dermal toxicity of HEA used rabbits and applied undiluted test material. Topical doses of 63, 130, 160, 200 or, 250 mg/kg bw were applied for 24 hours under a plastic occlusive bandage. Marked erythema and edema of the skin was seen in all treated animals and slight to moderate necrosis of the skin was observed in some animals. Clinical signs of toxicity were lethargy, decreased activity, loss of appetite and at 250 mg/kg bw only, rapid shallow breathing. The key study evaluating the acute oral toxicity of HEA administered as a 10% solution by gavage to groups of four rats at doses of 266.7, 400, 600, and 900 mg/kg bw. The animals were observed for 14 days post-dosing. The mortality was 0/4, 0/4, 3/4, and 4/4 at each dose level, respectively. Clinical signs included hypoactivity, rough fur, labored breathing, muscle weakness, GI tract hemorrhage in the animals that died. Neat material may burn the tissues of the mouth, throat and gastrointestinal tract. Positive responses have been reported in mice in the local lymph node assay indicating HEA dermal sensitization. There was no indication of significant chronic toxicity or a carcinogenic effect in either the 5 or 0.5 ppm treatment groups in rats in a chronic inhalation study (male and female were exposed to HEA 6 hours per day, 5 days/week for 18 months). HEA did not alter the histopathology of the testes or uterus in either dogs or rats (dogs up to 0.4% in the diet, rats up to 150 mg/kg bw/day). There were no treatment-related increases in the number of implants, embryo/fetal mortality, or fetal malformations observed in developmental study in rats. Neurotoxic potential of HEA appears to be minimal when tested in rats. HEA was not mutagenic in Salmonella typhimurium with or without metabolic activation. ECOTOXICITY STUDIES: Using the Warburg test, HEA was judged non-toxic to adapted sewage sludge.

LD50 Rat oral 548 mg/kg bw|LD50 Rat dermal > 1000 mg/kg bw|LD50 Rabbit skin 154 mg/kg bw

/AQUATIC SPECIES/ Using the Warburg test (development level 2), HEA was judged non-toxic to adapted sewage sludge at a concentration of EC0 > 250 mg/L ... For the protozoan Tetrahymena pyriformis, a 50% impairment of growth concentration (IGC50) of HEA was reported as the log (IGC50 -1) = 0.69 mM which is equivalent to 23.7 mg/L.

2-Hydroxyethyl acrylate's production and use in the manufacture of thermosetting acrylic resins(1) and chemical intermediates(2) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 1(SRC), determined from a structure estimation method(2), indicates that 2-hydroxyethyl acrylate is expected to have very high mobility in soil(SRC). Volatilization of 2-hydroxyethyl acrylate from moist soil surfaces is not expected(SRC) given an estimated Henry's Law constant of 8.0X10-9 atm-cu m/mole(SRC) based upon its vapor pressure, 0.0523 mm Hg(3), and assigned value for water solubility of 1X10+6 mg/L (miscible)(4). 2-Hydroxyethyl acrylate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(3). A 78% of Theoretical BOD using activated sludge in the Japanese MITI test(5) suggests that biodegradation is an important environmental fate process in soil(SRC). The degradation rate of 2-hydroxyethyl acrylate in soil was 3.6X10-7/s based on calculations using a chemical pollution footprint methodology(6).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 1(SRC), determined from a structure estimation method(2), indicates that 2-hydroxyethyl acrylate is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(3) based upon an estimated Henry's Law constant of 8.0X10-9 atm-cu m/mole(SRC) derived from its vapor pressure, 0.052 mm Hg(4), and assigned value for water solubility of 1X10+6 mg/L (miscible)(5). A hydrolysis half-life of >270 days at pH 7 for 2-hydroxyethyl acrylate was reported, the hydrolysis half-life decreases with increase pH indicating that 2-hydroxyethyl acrylate may undergo slow hydrolysis under basic conditions(5). According to a classification scheme(6), an estimated BCF of 3(SRC), from its log Kow of -0.21(7) and a regression-derived equation(2), suggests the potential for bioconcentration in aquatic organisms is low. Utilizing the Japanese MITI test, 78% of the Theoretical BOD was reached in 4 weeks(8) indicating that biodegradation is an important environmental fate process in water(SRC). Degradation rates of 2-hydroxyethyl acrylate in water and sediment were 7.2X10-7/s and 8.0X10-8/s, respectively, based on calculations using a chemical pollution footprint methodology(9).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 2-hydroxyethyl acrylate, which has a vapor pressure of 0.052 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase 2-hydroxyethyl acrylate is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals and ozone(SRC); the half-lives for these reactions in air are estimated to be 25 hours and 6.5 days(SRC), calculated from its respective rate constants of 1.5X10-11 and 1.7X10-18 cu cm/molecule-sec at 25 °C(SRC) that were derived using a structure estimation method(3). 2-Hydroxyethyl acrylate contains chromophores that absorb at wavelengths >290 nm(4) and, therefore, may be susceptible to direct photolysis by sunlight(SRC). The degradation rate of 2-hydroxyethyl acrylate in air was 1.3X10-5/s based on calculations using a chemical pollution footprint methodology(5).

The rate constant for the vapor-phase reaction of 2-hydroxyethyl acrylate with photochemically-produced hydroxyl radicals has been estimated as 1.5X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 25 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The rate constant for the vapor-phase reaction of 2-hydroxyethyl acrylate with ozone has been estimated as 1.7X10-18 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(1). This corresponds to an atmospheric half-life of about 6.5 days at an atmospheric concentration of 7X10+11 ozone molecules per cu cm(2). A base-catalyzed second-order hydrolysis rate constant of 0.024 L/mole-sec(SRC) was estimated using a structure estimation method(1); this corresponds to half-lives of 9 and 0.9 years at pH values of 7 and 8, respectively(1). Hydrolysis half-lives of >270 and 0.051 days were reported at respective pH values of 7.03 and 10.9 for a 2-hydroxyethyl acrylate(3). 2-Hydroxyethyl acrylate contains chromophores that absorb at wavelengths >290 nm(4) and, therefore, may be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 3 was calculated in fish for 2-hydroxyethyl acrylate(SRC), using a log Kow of -0.21(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of 2-hydroxyethyl acrylate can be estimated to be 1(SRC). According to a classification scheme(2), this estimated Koc value suggests that 2-hydroxyethyl acrylate is expected to have very high mobility in soil(SRC).

The Henry's Law constant for 2-hydroxyethyl acrylate is estimated as 8.0X10-9 atm-cu m/mole(SRC) derived from its vapor pressure, 0.0523 mm Hg(1), and assigned value for water solubility of 1X10+6 mg/L (miscible)(2). This Henry's Law constant indicates that 2-hydroxyethyl acrylate is expected to be essentially nonvolatile from water and moist soil surfaces(3). 2-Hydroxyethyl acrylate is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

According to the 2016 TSCA Inventory Update Reporting data, 14 reporting facilities estimate the number of persons reasonably likely to be exposed in the manufacturing, processing, or use of 2-hydroxyethyl acrylate in the United States may be as low as <10 workers up to the range of 500-999 workers per plant; the data may be greatly underestimated due to confidential business information (CBI) or unknown values(1).|NIOSH (NOES Survey 1981-1983) has statistically estimated that 2370 workers (354 of these are female) were potentially exposed to 2-hydroxyethyl acrylate in the US(1). Occupational exposure to 2-hydroxyethyl acrylate may occur through inhalation and dermal contact with this compound at workplaces where 2-hydroxyethyl acrylate is produced or used(SRC). The general population is not likely to be exposed to 2-hydroxyethyl acrylate(SRC).

/EXPL THER/ Electrospun fibrous membranes provide suitable physical anti-adhesion barriers for reducing tissue anti-adhesion following surgery. However, often during the biodegradation process, these barriers trigger inflammation and cause a foreign body reaction with subsequent decrease in anti-adhesion efficacy. Here, a facile strategy comprising the incorporation of ibuprofen (IBU) into implantable membranes and its sustained release was proposed in order to improve anti-adhesion effects and neurological outcomes, namely to prevent failed back surgery syndrome (FBSS). The combination of free IBU and a newly synthetized polymeric prodrug of IBU, namely poly(hydroxyethyl methacrylate) with ester-linked IBU, was successfully used in order to reduce initial burst drug release and provide sustained drug release from fibrous membranes throughout several weeks. Such release profile was shown useful in preventing both acute and chronic inflammation in rats following laminectomy and membrane implantation. Moreover, histological analysis provided evidence of an excellent anti-adhesion effect, while associated neurological deficits were effectively reduced. Furthermore, the assessment of macrophage density, neovascularization, and related gene expression at the lesion site revealed that a sustained anti-inflammatory effect was achieved with the IBU-loaded proposed fibrous membranes. Results suggested that the COX2 pathway plays an important role in the development epidural fibrosis and arachnoiditis. Overall, this study provided evidence that precisely engineered IBU-loaded electrospun fibrous membranes may be useful in preventing FBSS and able to potentially impact the outcome of patients undergoing spine surgery. /poly(hydroxyethyl methacrylate) with ester-linked ibuprofen/|/EXPL THER/ Protein aggregation into amyloid fibrils is a ubiquitous phenomenon across the spectrum of neurodegenerative disorders and type 2 diabetes. A common strategy against amyloidogenesis is to minimize the populations of toxic oligomers and protofibrils by inhibiting protein aggregation with small molecules or nanoparticles. However, melanin synthesis in nature is realized by accelerated protein fibrillation to circumvent accumulation of toxic intermediates. Accordingly, we designed and demonstrated the use of star-shaped poly(2-hydroxyethyl acrylate) (PHEA) nanostructures for promoting aggregation while ameliorating the toxicity of human islet amyloid polypeptide (IAPP), the peptide involved in glycemic control and the pathology of type 2 diabetes. The binding of PHEA elevated the beta-sheet content in IAPP aggregates while rendering a new morphology of "stelliform" amyloids originating from the polymers. Atomistic molecular dynamics simulations revealed that the PHEA arms served as rodlike scaffolds for IAPP binding and subsequently accelerated IAPP aggregation by increased local peptide concentration. The tertiary structure of the star nanoparticles was found to be essential for driving the specific interactions required to impel the accelerated IAPP aggregation. This study sheds new light on the structure-toxicity relationship of IAPP and points to the potential of exploiting star polymers as a new class of therapeutic agents against amyloidogenesis. /poly(2-hydroxyethyl acrylate) (PHEA) nanostructures/

2-hydroxyethyl acrylate (HEA) has been evaluated in a study that examined metabolism and excretion in male Fischer 344 rat using oral, intraperitoneal, dermal and inhalation routes of exposure ... For the oral and intraperitoneal routes of exposure the rats (four animals/dose level/route of exposure) received a single dose of (14)C-HEA at 2.5 or 50 mg/kg bw. For the inhalation exposure, six rats were exposed to a target concentration of 8 ppm (14)C-HEA for six hours in a head only inhalation chamber. For the dermal exposure, four rats were treated with (14)C-HEA at a dose of 50 mg/kg. No qualitative differences in urinary metabolites between routes were observed, indicating no marked route-dependent differences in the metabolic fate of HEA. The results of the study indicate that once the chemical becomes systemically available it is rapidly metabolized and eliminated from the body as either CO2 in the expired air or urinary metabolites with approximately equal percentage of administered/exposed dose eliminated by each route. The half-lives of elimination of radioactivity were approximately 14 hours for urine and 17 hours for CO2. The halflife of elimination of radioactivity from plasma was approximately 26 hours although the label was not associated with parent HEA. The available metabolic data on HEA is consistent with information on studies with other acrylates where hydrolysis of the ester functionality is the primary metabolic pathway. By analogy with ethyl acrylate and acrylic acid, it is expected that a minor metabolic pathway for HEA will be via conjugation with glutathione with the resulting mercapturic acid derivatives being excreted in the urine.|The metabolism and excretion of HEA has been examined in male Fischer 344 rat using oral, intraperitoneal, dermal and inhalation routes of exposure ... For the oral and intraperitoneal routes of exposure the rats (4 animals/dose level/route of exposure) received a single dose of 2.5 or 50 mg/kg bw (approx 15-20 uCi). For the inhalation exposure six rats were exposed to a target concentration of 8 ppm (14)C HEA for 6 hours in a head only inhalation chamber. For the dermal exposure 4 rats were treated with (14)C HEA at a dose of 12.5 mg/kg bw. No qualitative differences in urinary metabolites between routes were observed, indicating no marked route-dependent differences in the metabolic fate of HEA. The results of the study indicate that once the chemical becomes systemically available it is rapidly metabolized and eliminated from the body as either CO2 in the expired air or urinary metabolites. The available metabolic data on HEA is consistent with information on substances with other acrylates where hydrolysis of the ester functionality is the primary metabolic pathway. By analogy with ethyl acrylate and acrylic acid it is expected that a minor metabolic pathway for HEA will be via conjugation with glutathione with the resulting mercapturic acid derivatives being excreted in the urine. For the oral and intraperitoneal routes (2.5 mg/kg bw) 35-36% of the administered dose was expired as (14)CO2 and 43-47% of the dose excreted via the urine by 48 hours post-dosing. At 50 mg/kg bw 40-45% of the dose was expired as (14)CO2 and 33-36% of the dose was excreted in the urine. Following dermal administration 66% of the dose was absorbed within 48 hours of the application with remaining 33% being associated with the application site. Of the absorbed dose 27% was excreted in the urine as metabolites of HEA and 27% was excreted in the expired air as (14)CO2. For inhalation 39% of the absorbed dose was eliminated in the urine by 48 hr and 41% was expired as (14)CO2. For all routes, 9-16% was found in the tissues and carcass and less than 3% in the feces.|Following oral administration of (14)C-HEA to Fisher 344 male rats, between 91 and 95% of the administered radioactivity was recovered in the urine, CO2, feces, tissues and carcass, volatile organics and final cage wash. At the low dose of 2.5 mg (14)C-HEA/kg body weight, for the oral route of administration, approximately 43-47 % of the dose was eliminated in the urine, the primary elimination route, whereas 35-36% of the dose was expired as (14)CO2, and the tissues and carcass accounted for between 9-13 % of the dose. Less than 1.5% of the administered dose of radioactivity was recovered in the feces and less than 1% was found in the final cage wash. Less than 0.2% of the dose was recovered as volatile organics in the expired air. At the higher dose of 50 mg/kg (14)C-HEA/kg body weight, for the oral route of administration, 33-36% of the dose was eliminated in the urine, whereas 40-45% of the dose was expired as (14)CO2. At this higher dose there was a shift from the urinary pathway as the primary route of elimination to the exhalation of (14)CO2 as the primary route of elimination. As with the 2.5 mg/kg dose, the tissues and carcass accounted for 10-13% of the dose and less than 0.6% of the recovered radioactivity was in the final cage wash, less than 0.1% was recovered as volatile organics in the expired air and less than 2.5% of the dose was recovered in the feces. Following the oral route of administration, 0.3-1.5% of the dose was expired as (14)CO2 as early as 15 minutes post-dosing. The peak of CO2 excretion occurred during or before the 4-8 hr collection interval. By 12 hr post-dosing with 2.5 mg/kg for the oral route of administration, 31-32 of the dose was expired as (14)CO2. For this same collection interval following 50 mg/kg oral administration, 41 of the dose was expired as (14)CO2. The exhalation of (14)CO2 derived from (14)C-HEA appeared to follow first-order kinetics as a biphasic process, except following dermal administration. Following oral administration, greater than 92% of the total radioactivity excreted via the urine was excreted during the first 12 hr collection interval.

Following the 2.5 mg/kg and 50 mg/kg oral dose /in Fisher 344 male rats/, the half-lives for the terminal phase of elimination via (14)CO2 were determined to be approximately 15, and 14 hr, respectively. The half-lives for the initial phase of elimination were 1.9, and 1.8, respectively. The half life of elimination of radioactivity in the urine following oral administration were 10, and 9 hr for the 2.5 mg/kg bw oral and 50 mg/kg bw oral treatment groups, respectively.

96%, contains 200-650 ppm monomethyl ether hydroquinone as inhibitor.|Other esters < 2% w/w; dietylene glycol monoacrylate < or = 2.1% w/w; acrylic acid < or = 1% w/w; ethylene glycol approx 0.25% w/w; ethylene oxide approx 0.001% w/w

Inhalation causes irritation of nose and throat. Contact with liquid irritates eyes and skin. (USCG, 1999)

INHALATION: remove victim from exposure; support respiration; call physician if needed. EYES: wash with large amounts of water for 15 min.; call physician. SKIN: flush with water. (USCG, 1999)

Fresh air, rest. Half-upright position. Refer immediately for medical attention.

First rinse with plenty of water for at least 15 minutes, then remove contaminated clothes and rinse again. Refer immediately for medical attention.

Rinse with plenty of water (remove contact lenses if easily possible). Refer immediately for medical attention.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand-valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Organic acids and related compounds/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist respirations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Activated charcoal is not effective ... . Do not attempt to neutralize, because of exothermic reaction. Cover skin burns with dry, sterile dressings after decontamination ... . /Organic acids and related compounds/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Early intubation, at the first sign of upper airway obstruction, may be necessary. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if patient is hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Organic acids and related compounds/

/HUMAN EXPOSURE STUDIES/ It is generally thought that residual unpolymerized (meth)acrylic monomers commonly found in pressure sensitive adhesive tapes for medical use may cause dermal irritation, but a systematic study has never been carried out. Therefore, we assessed the potential dermal irritating effect of residual (meth)acrylic monomers. We studied seven acrylic monomers, acrylic acid (AA), methyl acrylate (MA), ethyl acrylate (EA), n-butyl acrylate (n-BA), n-hexyl acrylate (n-HA), 2-ethylhexyl acrylate (2-EHA) and 2-hydroxyethyl acrylate (HEA), as well as three methacrylic monomers, methacrylic acid (MAA), methyl methacrylate (MMA) and 2-hydroxyethyl methacrylate (2-HEMA). We first examined their cytotoxic effect on a cultured dermis model using the MTT method to determine their EC(50) and then performed a primary irritation test in rabbits using the monomers at three different concentrations (i.e., EC(50), one-tenth EC(50) and 10 times EC(50)). Marked variations were found in cytotoxic and dermal irritating activities among the (meth)acrylic monomers tested. HEA exhibited the most potent dermal irritation having the lowest erythema dose (the concentration which gives a primary dermal irritation index of 1.00) of 460 ppm. But the other monomers exhibited less potent dermal irritation (lowest erythema doses >/= 1000 ppm). For the monomers, significant correlation was found between cytotoxic activity and in vivo dermal irritating activity. Our results show that residual unpolymerized (meth)acrylic monomers in adhesive tapes are unlikely to induce skin irritation except for HEA. This study also suggests that cultured skin models are extremely useful as a screening method for chemical substances that could potentially cause dermal irritating activity.|/HUMAN EXPOSURE STUDIES/ BACKGROUND: Few US studies have reported results of patch testing with plastics and glues. OBJECTIVE: To report our institution's results of testing patients suspected of allergy to plastics and glues with a comprehensive plastics and glues series and to compare these results with previously published data. METHODS: Retrospective review of results of patch-testing with plastics and glues allergens at our institution between 2000 and 2007. In total, 444 patients were patch-tested with up to 56 plastics and glues allergens in the specialized series and up to five plastics and glues allergens in a baseline series. Positive-reaction rates were compared to other patch testing reports. RESULTS: Of patients, 97 (22%) had irritant reactions, and 201 (45%) had at least one allergic reaction. Bis(2-dimethylaminoethyl) ether 1%, benzoyl peroxide 1%, epoxy resin, bisphenol F 0.25%, 2-hydroxyethyl methacrylate 2%, and 2-hydroxyethyl acrylate 0.1% had the highest allergy reaction rates. Testing with specialized series identified 193 patients with plastics and glues allergy, of whom 162 were not identified by testing with baseline series alone. CONCLUSION: For patients suspected of allergy to plastics and glues, patch-testing with specialized series of plastics and glues allergens is an important adjunct to patch-testing with baseline series.|/HUMAN EXPOSURE STUDIES/ BACKGROUND: Acrylates constitute an important cause of occupational contact dermatitis. Isobornyl acrylate sensitization has been reported in only 2 cases. We encountered an industrial process operator with occupational contact dermatitis caused by isobornyl acrylate. OBJECTIVES: (i) To investigate whether it is relevant to add isobornyl acrylate to the (meth)acrylate test series. (ii) To report patients with (meth)acrylate contact allergy at an occupational dermatology clinic. PATIENTS/MATERIALS/METHODS: Our patch test database was screened for positive reactions to (meth)acrylates between 1993 and 2012. A selected group of 14 patients was tested with an isobornyl acrylate dilution series: 0.3%, 0.1%, 0.033%, and 0.01%. Readings were performed on D2, D3, and D7. RESULTS: One hundred and fifty-one patients were tested with our (meth)acrylate series; 24 had positive reactions. Most positive reactions were to 2-hydroxypropyl acrylate, 2-hydroxyethyl acrylate, 2-hydroxypropyl methacrylate, and diethyleneglycol diacrylate. Hypothetical screening with 2-hydroxypropyl acrylate, ethyleneglycol dimethacrylate, ethoxylated bisphenol A glycol dimethacrylate and trimethylolpropane triacrylate identified 91.7% of the 24 patients. No positive reactions were observed in 14 acrylate-positive patients tested with the isobornyl acrylate dilution series. The 0.3% isobornyl acrylate concentration induced irritant reactions in 3 patients. CONCLUSIONS: We report a rare case of allergic contact dermatitis caused by isobornyl acrylate. However, this study provides insufficient support for isobornyl acrylate to be added to a (meth)acrylate series.|/HUMAN EXPOSURE STUDIES/ BACKGROUND: (Meth)acrylates are important causes of contact allergy and allergic contact disease, such as dermatitis and stomatitis, with new and emerging sources resulting in changing clinical presentations. OBJECTIVES: To identify the (meth)acrylates that most commonly cause allergic contact disease, highlight their usefulness for screening, and examine their relationship with occupational and clinical data. METHODS: A retrospective review of results from patch tests performed between July 2002 and September 2015, in one tertiary Cutaneous Allergy Unit, was performed RESULTS: A series of 28 (meth)acrylates was applied to 475 patients. Results were positive in 52 cases, with occupational sources being identified in 24. Industrial exposures and acrylic nails were responsible for 13 and 10 cases, respectively, with wound dressings being implicated in 7. We found that four individual (meth)acrylates (2-hydroxyethyl acrylate, 2-hydroxypropyl methacrylate, bisphenol A glycerolate dimethacrylate, and ethyl acrylate), if used as a screening tool, could have identified 47 (90.4%) of our positive cases. CONCLUSIONS: Our 13-year experience indicates a changing landscape of (meth)acrylate contact allergy and allergic contact disease, with an observed shift in exposures away from manufacturing and towards acrylic nail sources. Wound dressings are highlighted as emerging sources of sensitization. Larger studies are required to establish the sensitivity and specificity of the four (meth)acrylates proposed for potential screening.|For more Human Toxicity Excerpts (Complete) data for 2-Hydroxyethyl acrylate (17 total), please visit the HSDB record page.

2-hydroxyethyl acrylate

The substance can be absorbed into the body by inhalation of its vapour, through the skin and by ingestion.

Cough. Sore throat. Burning sensation. Laboured breathing.

MAY BE ABSORBED! Redness. Pain.

Redness. Pain. Blurred vision.

Essentially 100% as comonomer in acrylic surface coatings (1976)

A typical commercial sample of HEA has a specified purity of >96.5% (w/w) and may contain diethyleneglycol monoacrylate (2.1% w/w), acrylic acid (< 1% w/w), other esters (< 2% w/w), ethylene glycol (0.25% w/w) and ethylene oxide (0.001% w/w). Methyl ether of hydroquinone may be added at 250 to 650 ppm as an inhibitor of spontaneous polymerization.|... Hydroquinone ... /is/ added to acrylic monomers to stabilize them ... . /Acrylic ester monomers/|Inhibitor of polymerization: monomethyl ether of hydroquinone, 400 ppm.

Adhesive manufacturing|2-Propenoic acid, 2-hydroxyethyl ester: ACTIVE|2-Propenoic acid, 2-hydroxyethyl ester, homopolymer: ACTIVE|XU - indicates a substance exempt from reporting under the Chemical Data Reporting Rule, (40 CFR 711).|Terpolymers for use as film-forming cmpd & coatings in cosmetics & pharmaceuticals contain: vinylpyrrolidine 10-40, vinyl acetate or vinyl propionate 20-50, & hydroxyethyl acrylate or methacrylate or hydroxypropyl acrylate 10-40% by wt. The polymers are especially useful as tablet binders & coatings in hair sprays & setting lotions. ...

A method for air sampling and analysis has been developed for vapors of acrylate monomers. Concentrations as low as 0.05 parts per million by volume (ppmv) can be measured, with the exception of 2-ethylhexyl acrylate which can be measured as low as 0.01 ppmv. These limits of sensitivity are based on a 60-minute sample at a flowrate of 500 cc per minute. The acrylate monomer vapor is adsorbed on activated silica gel, desorbed in acetone, and analyzed by gas chromatography using FFAP or OV-17 liquid phase columns. Three statistical studies show that this method is well within the accuracy and precision limits OSHA requires for methods of monitoring personnel exposure to air contaminants. Other parameters investigated were the effects of humidity, flowrate, and adsorption capacity, plus storage effects. This method has been applied to the following acrylate monomers; 2-ethylhexyl acrylate (2-EHA), hydroxyethyl acrylate (HEA), isodecyl acrylate (IDA), methylcarbamoyloxyethyl acrylate (MCEA), 2-henoxyethyl acrylate (PEA), esterdiol-204-diacrylate (ED-204-DA), and esterdiol-204-4-ethoxy-diacrylate (ED-204-4EO-DA).

Fire Hazards -> Corrosives, Reactive - 2nd degree