2-Ethylhexanoic acid

144.21100

144.21

262-971-9

0477

8881

1993

DTXSID9025293

Clear liquid

29159080

37.30000

2.6

Ethylhexoic acid is a colorless to light yellow liquid with a mild odor. It will burn though it may take some effort to ignite. It is slightly soluble in water. It is corrosive to metals and tissue. It is used to make paint dryers and plasticizers.

0.9031 g/cm³ @ Temp: 25 °C

-59 °C

228 °C

114ºC

1.424-1.426

Solubility in water, g/100ml: 0.14 (very poor)

Keep container closed when not in use. Store in a cool, dry, well-ventilated area away from incompatible substances.

<0.01 mm Hg ( 20 °C)

4.98 (vs air)

Lower flammable limit: 0.8% by volume; Upper flammable limit: 6.0% by volume

vol% in air: 0.8

Mild odor

Henry's Law constant = 2.8X10-6 atm-cu m/mol at 25 °C (est)

Hydroxyl radical reaction rate constant = 8.18X10-12 cu cm/molec-sec at 25 °C (est)

No rapid reaction with air. No rapid reaction with water.

Acids, Carboxylic

ETHYLHEXOIC ACID is a carboxylic acid. Carboxylic acids donate hydrogen ions if a base is present to accept them. They react in this way with all bases, both organic (for example, the amines) and inorganic. Their reactions with bases, called "neutralizations", are accompanied by the evolution of substantial amounts of heat. Neutralization between an acid and a base produces water plus a salt. Carboxylic acids with six or fewer carbon atoms are freely or moderately soluble in water; those with more than six carbons are slightly soluble in water. Soluble carboxylic acid dissociate to an extent in water to yield hydrogen ions. The pH of solutions of carboxylic acids is therefore less than 7.0. Many insoluble carboxylic acids react rapidly with aqueous solutions containing a chemical base and dissolve as the neutralization generates a soluble salt. Carboxylic acids in aqueous solution and liquid or molten carboxylic acids can react with active metals to form gaseous hydrogen and a metal salt. Such reactions occur in principle for solid carboxylic acids as well, but are slow if the solid acid remains dry. Even "insoluble" carboxylic acids may absorb enough water from the air and dissolve sufficiently in it to corrode or dissolve iron, steel, and aluminum parts and containers. Carboxylic acids, like other acids, react with cyanide salts to generate gaseous hydrogen cyanide. The reaction is slower for dry, solid carboxylic acids. Insoluble carboxylic acids react with solutions of cyanides to cause the release of gaseous hydrogen cyanide. Flammable and/or toxic gases and heat are generated by the reaction of carboxylic acids with diazo compounds, dithiocarbamates, isocyanates, mercaptans, nitrides, and sulfides. Carboxylic acids, especially in aqueous solution, also react with sulfites, nitrites, thiosulfates (to give H2S and SO3), dithionites (SO2), to generate flammable and/or toxic gases and heat. Their reaction with carbonates and bicarbonates generates a harmless gas (carbon dioxide) but still heat. Like other organic compounds, carboxylic acids can be oxidized by strong oxidizing agents and reduced by strong reducing agents. These reactions generate heat. A wide variety of products is possible. Like other acids, carboxylic acids may initiate polymerization reactions; like other acids, they often catalyze (increase the rate of) chemical reactions.

699 °F (USCG, 1999)|700 °F (371 °C)|371 °C

Lower flammable limit: 0.8% by volume; Upper flammable limit: 6.0% by volume

Critical temperature: 615.2 K

II

6.1

UN 3265 8/PG 2

1

R63

S36/37

MO7700000

Xn

Separated from strong oxidants. Store in an area without drain or sewer access.

Stable. Combustible. Incompatible with strong oxidizing agents, reducing agents, bases.

P280

H361d

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. 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 soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

The substance is a strong reducing agent and reacts with oxidants.

BG Chemie; Toxicological Evaluation No. 275. 2-Ethyl-hexanoic acid (CAS No. 149-57-5). 84 p. (2000) BG Chemie, Heidelberg, Germany. Report available from a search of the BG Chemie website, www.bechemie.de/toxicologicalevaluations as of July 31, 2007. An evaluation of the toxicological information on the subject chemical prepared and reviewed by experts on behalf of BG Chemie.|EPA; Robust Summaries & Test Plans: Metal Carboxylates; Revised Summaries (September 22, 2004) Appendix 1.0. Robust Summaries and SIDS Dossier for 2-Eethvlhexanoic acid. Describes information submitted to the U.S. EPA by industry participating in the HPV Challenge Program.|European Chemicals Bureau; IUCLID Dataset, 2-Ethylhexanoic acid (149-57-5) (2000 CD-ROM edition). Describes information on usage patterns, ecotoxicity and toxicity supplied to the European Union by industry.

This chemical is combustible. (NTP, 1992)|Combustible.

|Warning|H361d ***: Suspected of damaging the unborn child [Warning Reproductive toxicity]|P201, P202, P281, P308+P313, P405, and P501|H361 (100%): Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]|Aggregated GHS information provided by 1888 companies from 21 notifications to the ECHA C&L Inventory.|H315 (93.3%): Causes skin irritation [Warning Skin corrosion/irritation]|P264, P273, P280, P302+P352, P321, P332+P313, P362, and P501|Aggregated GHS information provided by 235 companies from 5 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H315: Causes skin irritation [Warning Skin corrosion/irritation]|P201, P202, P264, P280, P281, P302+P352, P308+P313, P321, P332+P313, P362, P405, and P501|Danger|H312: Harmful in contact with skin [Warning Acute toxicity, dermal]|P201, P202, P260, P264, P270, P280, P281, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P308+P313, P309+P311, P310, P312, P321, P322, P337+P313, P363, P405, and P501|H303: May be harmful if swallowed [Warning Acute toxicity, oral]|P201, P202, P260, P264, P280, P281, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P308+P313, P310, P312, P321, P322, P363, P405, and P501

Respirator, chemical safety goggles, rubber boots, heavy rubber gloves, and impervious apron. (USCG, 1999)

Explosive limits, vol% in air: 0.8-6|Explosive limits , vol% in air: 0.8-6

Combustible. Water may be ineffective on fire. Wear self-contained breathing apparatus and protective clothing. Extinguish with dry chemical, alcohol foam, or carbon dioxide.

Collect leaking and spilled liquid in sealable containers as far as possible. Absorb remaining liquid in sand or inert absorbent and remove to safe place. Do NOT absorb in saw-dust or other combustible absorbents. Do NOT let this chemical enter the environment.

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Vapor irritating to eyes, nose, and throat.

Personal protection: 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 sealable containers. Absorb remaining liquid in sand or inert absorbent. Do NOT absorb in saw-dust or other combustible absorbents. Then store and dispose of according to local regulations.

Separated from strong oxidants. Store in an area without drain or sewer access.

A harmful contamination of the air will be reached on evaporation of this substance at 20 °C; on spraying or dispersing, however, much faster.

The substance is irritating to the eyes, skin and respiratory tract.

Animal tests show that this substance possibly causes toxicity to human reproduction or development.

NO open flames.

AVOID ALL CONTACT!

Use local exhaust or breathing protection.

Protective gloves.

Wear safety goggles.

| 1 - Materials that, under emergency conditions, can cause significant irritation.| 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.| 0 - Materials that in themselves are normally stable, even under fire conditions.

2-Ethylhexanoic acid was detected in groundwater from a landfill well near Norman, OK at an estimated concn of 4.2 ug/L(1). 2-Ethylhexanoic acid was identified as a volatile compound emitted from bonded urethane carpet cushions(2). 2-Ethylhexanoic acid was identified as a byproduct of chlorine dioxide disinfection of drinking water at a pilot plant in Evansville, IN(3). Leachate samples collected from a Swedish municipal landfill in May 1990 contained 2-ethylhexanoic acid at an unreported concn(4). Water samples from several sampling stations in the "Valley of the Drums" near Louisville, KY were found to contain ethyl hexanoic acid(5). Groundwater samples collected near an area known to be contaminated by wood-preserving chemicals in Pensacola, FL contained 2-ethylhexanoic acid at concns of 0.17, 5.79, and 1.44 mg/L 6.1, 3.3, and 5.8 m below the surface, respectively(6). 2-Ethylhexanoic acid was identified in trench leachate from low-level radioactive waste disposal sites in Maxey Flats, KY and West Valley, NY at an average concn of 5.9 and 140 mg/L, respectively(7). 2-Ethylhexanoic acid was detected in the leachate of a sanitary landfill located in Barcelona, Spain at an unreported concn(8). 2-Ethylhexanoic acid was detected in emissions from a municipal waste incineration plant at a concn of 0.60 ug/cu m(9).|2-Ethylhexanoic acid has been identified in municipal landfill leachate samples from Gryta, Vasteras, Sweden, sampled in May, 1990; the compounds was detected not quantified in 1 of 3 samples(1). The possible origins were identified as detergents and as a hydrolysis product of phthalates(1). The compound was present at a concentration of 155 ug/L in leachate from a landfill for municipal wastes in Japan(2).

URBAN/SUBURBAN: 2-Ethylhexanoic acid was identified but not quantitated in air samples collected along the Niagara River in Sept 1982(1).

2-Ehtylhexanoic acid was identified, not quantified one sample of volatile emissions from different types of furniture coatings(1). The compound was detected not quantified as a volatile emission from bonded-urethane carpet cushions(2). Ten commercially available coffee filter papers were tested for various semi-volatile compounds; 2-ethylhexanoic acid was detected in one chlorine-bleached type sample at a concentration of 1.6 ug/g(3).

LD50 Rat oral 1.6 to 3 g/kg|LD50 Rabbit oral 1.3 g/kg|LD50 Guinea pig dermal 5690 mg/kg|LD50 Rabbit dermal 1260 mg/kg|For more Non-Human Toxicity Values (Complete) data for 2-ETHYLHEXANOIC ACID (6 total), please visit the HSDB record page.

/AQUATIC SPECIES/ Earlier work with pure cultures had shown that the interaction of microbes with plasticizers leads to the formation of metabolites including 2-ethylhexanoic acid and 2-ethylhexanol that resist further degradation. The presence of these metabolites is now reported in a variety of environmental samples. Thus, even in a complex ecosystem, when plasticizers are degraded, the breakdown is not complete and significant amounts of 2-ethylhexanoic acid and 2-ethylhexanol are observed. These compounds have been shown to exhibit acute toxicity using Microtox, Daphnia, rainbow trout and fathead minnow toxicity assays. Since it is already well established that plasticizers are ubiquitous in the environment, it is expected that their recalcitrant metabolites will also be ubiquitous. This is of concern because, while the plasticizers do not exhibit acute toxicity, their metabolites do.

2-Ethylhexanoic acid's production and use as a chemical intermediate and use in the manufacture of resins used for baking enamels, lubricants, detergents, flotation aids, and corrosion inhibitors, as catalysts for polyurethane foaming, for solvent extraction, and for dye granulation(1) 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 650(SRC), determined from a log Kow of 2.64(2) and a regression-derived equation(3), indicates that 2-ethylhexanoic acid is expected to have low mobility in soil(SRC). The estimated pKa of 2-ethylhexanoic acid is 4.70(4), indicating that this compound will partially exist in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5). Volatilization of 2-ethylhexanoic acid from moist soil surfaces is expected to be a slow fate process(SRC) given an estimated Henry's Law constant of 2.8X10-6 atm-cu m/mole(SRC), derived from its vapor pressure, 0.03 mm Hg(6), and water solubility, 2,000 mg/L(7). 2-Ethylhexanoic acid is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(6). A biodegradation half-life of approximately 5 days when incubated in river sediment(8) suggests that biodegradation may be an important environmental fate process in soil(SRC).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 650(SRC), determined from a log Kow of 2.64(2) and a regression-derived equation(3), indicates that 2-ethylhexanoic acid is 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 2.8X10-6 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4), derived from its vapor pressure, 0.03 mm Hg(5), and water solubility, 2,000 mg/L(6). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 15 and 120 days, respectively(SRC). According to a classification scheme(7), an estimated BCF of 3(SRC), from its log Kow(2) and a regression-derived equation(8), suggests the potential for bioconcentration in aquatic organisms is low(SRC). A biodegradation half-life of approximately 5 days when incubated in river sediment(9) suggests that biodegradation may be an important environmental fate process in water(SRC).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 2-ethylhexanoic acid, which has a vapor pressure of 0.03 mm Hg at 20 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase 2-ethylhexanoic acid is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 2 days(SRC), calculated from its rate constant of 8.2X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). 2-Ethylhexanoic acid does not contain chromophores that absorb at wavelengths >290 nm(4) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of 2-ethylhexanoic acid with photochemically-produced hydroxyl radicals has been estimated as 8.2X10-12 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 2 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). 2-Ethylhexanoic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(3). 2-Ethylhexanoic acid does not contain chromophores that absorb at wavelengths >290 nm(3) and therefore is not expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 3 was calculated in fish for 2-ethylhexanoic acid(SRC), using a log Kow of 2.64(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).

The Koc of 2-ethylhexanoic acid is estimated as 650(SRC), using a log Kow of 2.64(1)((1,SRC) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that 2-ethylhexanoic acid is expected to have low mobility in soil. The estimated pKa of 2-ethylhexanoic acid is 4.70(4), indicating that this compound will partially exist in the anion form in the environment and anions generally do not adsorb more strongly to soils containing organic carbon and clay than their neutral counterparts(5).

The Henry's Law constant for 2-ethylhexanoic acid is estimated as 2.8X10-6 atm-cu m/mole(SRC) derived from its vapor pressure, 0.03 mm Hg(1), and water solubility, 2,000 mg/L(2). This Henry's Law constant indicates that 2-ethylhexanoic acid is expected to volatilize from water surfaces(3). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(3) is estimated as 15 days(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(3) is estimated as 120 days(SRC). 2-Ethylhexanoic acid's estimated Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). 2-Ethylhexanoic acid is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

DRINKING WATER: 2-Ethylhexanoic acid was detected, not quantified in drinking water samples from: Cincinnati, OH in Oct 1978 and Jan 1980; Miami, FL in Feb 1976; New Orleans, LA in Jan 1976; Philadelphia, PA in Feb 1976; Ottumwa, IA in Sept 1976; and Seattle, WA in Nov 1976(1).|RAIN/SNOW/FOG: Snow samples collected in early March from 6 rural areas in Russia and 4 rural areas in Finland were tested for 2-ethylhexanoic acid; 2 of 10 samples tested positive at concentrations of 0.12 and 0.14 ug/kg from Levi, (Lapland), Finland and Butovo (clean city area, southern end of Moscow) Russia, respectively(1).

After simultaneous distillation-extraction (SDE) of commercial baby foods (n = 20) and fruit juices (n = 15) (among them 15 and eight products labelled 'organic', respectively) from 11 different suppliers, analyses performed by coupled capillary gas chromatography-mass spectrometry (GC-MS) revealed the presence of 2-ethylhexanoic acid (2-EHA), a known teratogenic compound. 2-EHA was found in 80 and 73% of the baby foods and fruit juices, respectively. Amounts ranged from 0.25 to 3.2 mg kg(-1)(average, 0.55 mg kg(-1)) and from 0.01 to 0.59 mg L(-1) (average, 0.18 mg L(-1)) in baby foods and fruit juices, respectively. GC-MS analysis of the SDE extracts obtained from the plastic gaskets inside the metal lids of the samples under study revealed the gaskets to be the origin of 2-EHA.|2-Ethylhexanoic acid was identified as a volatile component in raw beef; the compound may not be representative of raw beef but rather more akin to products produced in cooked fat(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 176,189 workers (20,117 of these are female) are potentially exposed to 2-ethylhexanoic acid in the US(1). Occupational exposure to 2-ethylhexanoic acid may occur through inhalationand dermal contact with this compound at workplaces where 2-ethylhexanoic acid is produced or used. Monitoring data indicate that the general population may be exposed to 2-ethylhexanoic acid via ingestion of food and drinking water, and dermal contact with this compound and other consumer products containing 2-ethylhexanoic acid(SRC).

The disposition of di-2-(ethylhexyl)adipate in humans following administration of the stable isotope labeled test substance was investigated. Blood and urine samples were collected from six male volunteers following the administration of 46 mg of 2H10 labeled di-2-(ethylhexyl)adipate. Blood was collected at 0.5, 1, 2, 3, 4, 5, 6, 8, and 12 hours after administration. Urine was collected for up to 96 hours after administration. No adverse effects were observed in any of the volunteers and no significant changes in biochemical or hematological parameters were seen. The plasma contained no parent molecule; however, the metabolite 2-ethylhexanoic-acid was detected, but levels were below the limit of quantitation. 2-ethylhexanoic-acid, as a conjugated product, was also the principal metabolite detected in urine. Urinary elimination of the di-2-(ethylhexyl)adipate metabolites peaked within 8 hours of dosing in all volunteers; beyond 36 hours, no metabolites were detected in urine. The conjugated 2-ethylhexanoic acid in urine accounted for an average of 8.6% of the administered dose. A further 3.5% of the dose was accounted for by 2-ethyl-5-hydroxyhexanoic acid, 2-ethylhexanedioic acid, 2-ethyl-5-keto-hexanoic acid, and 2-ethylhexanol. /It was/ concluded that 2-ethylhexanoic acid is an appropriate marker for biological monitoring in estimating the dietary di-2-(ethylhexyl)adipate intake as it is the major metabolite identified and as its rate of elimination is similar to that of other measured di-2-(ethylhexyl)adipate metabolites.|... 2-(14)C-ethylhexanoic acid in rat blood, brain, liver and kidney was quantitated by liquid scintillation analysis and by wholebody autoradiography in mice. A single intraperitoneal dose of 2-(14)C-ethylhexanoic acid was injected in both species. Animals were sacrificed 30 min, 2 and 6 hr after the administration of 2-(14)C-ethylhexanoic acid in autoradiography experiments. The highest uptake of 2-(14)C-ethylhexanoic acid was observed in the liver, kidney and blood in mice. In contrast, low uptake of 2-(14)C-ethylhexanoic acid was seen in the brain. 2-(14)C-ethylhexanoic acid was well detectable in the olfactory bulb and in the salivary gland. In rats, at 2 hr after administration the highest concentration of 2-(14)C-ethylhexanoic acid occurred in blood (0.3%; of the total dose/g tissue). The radioactivity in the liver (0.2%) and kidney (0.1%) was also relatively high. The concentrations of 2-(14)C-ethylhexanoic acid was low in the brain (0.02%). By 6 hr, the radioactivity had decreased rapidly and was hardly measurable at 24 hr after the administration. The results suggest that 2-ethylhexanoic acid is rapidly cleared from the tissues.|[2-14(C)-Hexyl]2-ethylhexanoic acid in corn oil was administered to female Fischer 344 rats either as a single oral gavage at 100 or 1000 mg/kg, or after 14 days of oral unlabeled 2-ethylhexanoic acid (100 mg/kg only). An aqueous solution of [2-14(C)-hexyl]2-ethylhexanoic acid was applied topically at either 100 or 1000 mg/kg and another group of rats received 2-ethylhexanoic acid by intravenous injection (1 mg/kg). Urine, feces, and blood were collected at various intervals for 96 hr. Approximately 72 to 75 percent of the oral dose was excreted in the urine within 24 hr, and <10 percent was excreted after 24 hr. About 50% of the 14(C) was excreted in the first 8 hr after the 100-mg/kg dose versus 20 percent after the 1000 mg/kg dose. Fecal excretion accounted for 7 to 12 percent of both doses. After intravenous injection, 64 percent of the l4(C) was excreted in the urine and 2 percent in the feces. Repeated dosing with unlabeled 2-ethylhexanoic acid (100 mg/kg) appeared to reduce the urinary elimination of 14(C) slightly to 55 percent in urine, whereas the fecal excretion increased to 15 percent in the first 24 hr. After dermal application, approximately 30 percent of the applied dose was excreted in the urine during the first 24 hr, followed by an additional 8 and 17 percent from 24 to 96 hr for the 100- and 1000-mg/kg doses, respectively. Fecal excretion was 7 percent for both dose levels. Dermal absorption was estimated to be 63 to 70 percent relative to intravenous administration. After dermal application, peak blood levels of 14C occurred about 5.7 hr after application and the absorption half-life was 3.2 hr. Major urinary metabolites included the glucuronide of 2-ethylhexanoic acid, the glucuronides of 2-ethyl-6-hydroxyhexanoic acid and 2-ethyl-1,6-hexanedioic acid, and unmetabolized 2-ethylhexanoic acid. The proportions of each metabolite changed with the dose and route of administration.|Nine sawmill workers were divided into two groups according to their exposure to 2-ethylhexanoic acid, a pesticide which has replaced the older pentachlorophenol. The men with lower exposure excreted 30 + or - 10 nmol 2-ethylhexanoic acid/mmol creatinine (mean SD, n = 4) in urine samples taken after the workshift, whereas men with higher exposure excreted 1.8 + or - 1.6 umol 2-ethylhexanoic acid/mmol creatinine (mean + - SD, n = 5, p < 0.01). The urinary ornithine and arginine concentrations were at the lower exposure 1.4 0.4 and 1.5 + or - 0.8 umol/mmol creatinine, respectively (mean + or - SD, n = 4), and they increased significantly (p < 0.01) to 4.5 2.5 and 3.2 + or - 1.5 umol/mmol mean + or - SD, n = 5), respectively, at the higher exposure. This might have been caused by the inhibitory effect of 2-ethylhexanoic acid on urea synthesis which was partially compensated for by elevated arginine and ornithine concentrations to drive the urea cycle more efficiently.|... The hypothesis that infants undergoing exchange transfusion are exposed to toxic levels of di-(2-ethylhexyl)-phthalate and the presumed metabolite 2-ethylhexanoic acid was tested by measuring serum levels of di-(2-ethylhexyl)-phthalate in 16 newborn infants (gas-liquid-chromatography) and urine concentrations of 2-ethylhexanoic acid in 6 of these infants (gas chromatography-mass spectrometry). Di-(2-ethylhexyl)-phthalate levels were undetectable (< 1 ug/mL) before exchange but ranged from 6.1 to 21.6 ug/mL of serum (average, 12.5 to 6.2 ug/mL) after a single exchange transfusion. Di-(2-ethylhexyl)-phthalate uptake did not result in cholestasis. 2-Ethylhexanoic acid peak levels were 127 to 416 ng per mL of urine, with a median of 174 ng per mL. Concentrations of 2-ethylhexanoic acid were lower than anticipated, which indicates that 2-ethylhexanoic acid is not a major metabolite in the neonatal infant.

Male Wistar rats receiving 2-ethylhexanoic acid in drinking water (600 mg/kg daily) for 9 weeks eliminated 10 different metabolites, including 2-ethyl-1,6-hexanedioic acid, 2-ethyl-6-hydroxyhexanoic acid, five other hydroxylated metabolites and two lactones, the unsaturated 5,6-dehydro-2-ethylhexanoic acid, and parent compound (partly as the glucuronic acid conjugate).|Major urinary metabolites included the glucuronide of 2-ethylhexanoic acid, the glucuronides of 2-ethyl-6-hydroxyhexanoic acid and 2-ethyl-1,6-hexanedioic acid, and unmetabolized 2-ethylhexanoic acid. The proportions of each metabolite changed with the dose and route of administration.|... Liver microsomes were extracted from male Han/Wistar rats, male DBA/2N/Kuo mice, and humans undergoing liver surgery. 2-Ethylhexanoic acid metabolism was determined in-vitro by incubating the microsomes in the presence and absence of the cytochrome P450 inhibitors triacetyloleandomycin, metyrapone, quinidine, and SKF-525A. In-vivo, 2-ethylhexanoic acid metabolism was determined by administering 2-ethylhexanoic acid to rats with and without the cytochrome P450 inhibitors, and by assessing metabolite levels in human urine samples taken from 2-ethylhexanoic acid exposed sawmill workers. The main 2-ethylhexanoic acid metabolite produced in all microsomes was 2-ethyl-1,6-hexanedioic acid. Production of this metabolite was prevented by triacetyloleandomycin, metyrapone, quinidine, and SKF-525A. /It was/ concluded that some cytochrome P450s may contribute to 2-ethylhexanoic acid metabolism in the liver, that the same 2-ethylhexanoic acid metabolites are formed in rats and humans, and that 2-ethylhexanoic acid resembles the hepatotoxicant 2-envalproic acid.|The metabolites of 2-ethylhexanoic acid ... were investigated in rat urine. Male Wister rats were give 2-ethylhexanoic acid in drinking water 1600 mg/kg daily for nine weeks, and then urine specimens were collected and analysed. ... In addition to 2-(ethylhexyl)adipate, ten different 2-(ethylhexyl)adipate related metabolites were found in the urine of 2-(ethylhexyl)adipate treated rats. The main metabolite was 2-ethyl-1,6-hexanedioic acid. Urine also contained 2-ethyl-6-hydroxyhexanoic acid and five other hydroxylated metabolites and two lactones, the detailed structures of which have not yet been elucidated. The unsaturated 5,6-dehydro-di-2-(ethylhexyl)adipate was also identified; this is the metabolite corresponding to 2-n-propyl-4-pentenoic acid, the hepatotoxic metabolite of valproic acid. At least part of the 2-(ethylhexyl)adipate is present in urine as a glucuronide conjugate.|For more Metabolism/Metabolites (Complete) data for 2-ETHYLHEXANOIC ACID (6 total), please visit the HSDB record page.

/In female FIscher rats/ Blood levels after iv injection appear to decay in a triphasic manner with half-lives of 0.19 +/- 0.11 hrs, 6.6 +/- 3.9 hrs, and 117 +/- 47 hrs. After oral administration, peak blood levels were achieved after 15 or 30 minutes, and also declined triphasically with half-lives similar to what had been estimated from intravenous administration (0.32 +/- 0.04 hrs, 6.8 +/- 3.5 hrs, and 98.2 +/- 32.8 hrs). Dermal application resulted in slower absorption with peak blood levels occurring 5.7 +/- 0.4 hours after application and a half-life of 3.2 +/- 0.1 hr. Elimination was biphasic with half-lives of 4.2 +/- 0.2 and 251 +/- 135 hrs.

A mouse model for the induction of exencephaly with sodium (+ or -)-2-ethylhexanoate has been developed using multiple administration regimes. With three consecutive administrations one-half-day intervals, the most sensitive time to induce exencephaly was Gestational Days 8-9. Using the racemic substance it was determined that the SWV strain was more sensitive to the induction of exencephaly than the C57BL/6NCrlBR strain. The enantiomers of 2-ethylhexanoic acid were separated via preparative HPLC to greater than 99.8% optical purity, and greater than 99% purity according to a gas chromatographic analysis. It was demonstrated that the (R)-enantiomer is a more potent teratogen than the (S)-enantiomer for the induction of exencephaly as well as malformations of other organ systems. Pharmacokinetic analyses for each of the enantiomers were performed in maternal plasma, maternal muscle, and embryo. The pharmacokinetics showed that the peak concentration (Cmax) for both enantiomers in the three compartments was approximately equivalent and was attained within 15 min following the third administration. The area under the concentration versus time curve values for the two enantiomers were approximately 10 higher for the (R)-antipode because of a slightly slower elimination of this compound. There was negligible (or no) racemization of the two enantiomers in the biological samples. The results suggest that teratologic differences in the enantiomers of sodium 2-ethylhexanoate are not due to differences in the concentrations of these antipodes in the embryo, but more likely result from the specific interaction of the enantiomers with chiral molecules in the embryo.

Harmful if swallowed, inhaled or absorbed through skin. Material is extremely destructive to tissues of mucous membranes and upper respiratory tract, eyes and skin. Inhalation may be fatal as a result of spasm, inflammation and edema of the larynx, bronchii, chemical pneumonitis and pulmonary edema. Symptoms of exposure may include burning sensation, coughing, wheezing, laryngitis, shortness of breath, headache, nausea and vomiting. (USCG, 1999)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

Fresh air, rest.

Remove contaminated clothes. Rinse skin with plenty of water or shower.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Call for medical aid. Vapor irritating to eyes, nose, and throat. If inhaled, will cause coughing or difficult breathing. If breathing stopped, give artificial respiration. If breathing is difficult, give oxygen. Liquid will burn skin and eyes. If swallowed will cause nausea and vomiting. Remove contaminated clothing and shoes. Flush affected areas with plenty of water. If in eyes, hold eyelids open, and flush with plenty of water.|/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/

/SIGNS AND SYMPTOMS/ Harmful if swallowed, inhaled, or absorbed through skin. Material is extremely destructive to tissues of mucous membranes and upper respiratory tract, eyes, and skin. Inhalation may be fatal as a result of spasm, inflammation, and edema of the larynx, and bronchi, chemical pneumonitis, and pulmonary edema. Symptoms of exposure may include burning sensation, coughing, wheezing, laryngitis, shortness of breath, headache, nausea, and vomiting.|/SIGNS AND SYMPTOMS/ /Following ingestion/ abdominal pain; burning sensation; diarrhea. /from table/|/CASE REPORTS/ ... Case of corneal injury, with prompt healing, has been reported.|/ALTERNATIVE and IN VITRO TESTS/ ... Human polymorphonuclear leukocytes (PMNL) /were exposed/ to 2-Ethylhexanoic acid (2-EHA) in vitro and /the authors/ measured the production of reactive oxygen species (ROS) and explored the associated cellular mechanisms. 2-EHA (10-2000 uM) inhibited dose-dependently formyl-methionyl-leucyl-phenylalanine (FMLP)-induced respiratory burst in PMNL. Moreover, 2-EHA decreased oxidative burst evoked by the protein kinase C (PKC) activators, phorbol myristate acetate (PMA) and dioctanoyl-s,n-glycerol (DIC(8)). 2-EHA affected neither the levels of free intracellular calcium nor inhibited PKC. The results indicate that 2-EHA inhibits activation of PMNL to produce ROS, i.e. has an immunosuppressive effect in vitro. The site of action in the PKC is after activation of this enzyme.|/BIOMONITORING/ Sawmill workers in Finland were monitored for urinary excretion of 2-ethylhexanoic acid used in a wood preservative. Excretion ranged from 30 + or - 10 nmol 2-ethylhexanoic acid/mmol creatinine in urine samples taken from four workers with lower exposures to 1.8 + or - 1.6 umol 2-ethylhexanoic acid/mmol creatinine in five men from the group designated as having higher exposure.

2-ethylhexanoic acid

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

Cough.

Redness.

Redness. Pain.

All other basic inorganic chemical manufacturing|Hexanoic acid, 2-ethyl-: ACTIVE|Hexanoic acid, 2-ethyl-, rare earth salts: ACTIVE|After simultaneous distillation-extraction (SDE) of commercial baby foods (n = 20) and fruit juices (n = 15) (among them 15 and eight products labelled 'organic', respectively) from 11 different suppliers, analyses performed by coupled capillary gas chromatography-mass spectrometry (GC-MS) revealed the presence of 2-ethylhexanoic acid (2-EHA), a known teratogenic compound. 2-EHA was found in 80 and 73% of the baby foods and fruit juices, respectively. Amounts ranged from 0.25 to 3.2 mg/kg (average, 0.55 mg/kg and from 0.01 to 0.59 mg/L (average, 0.18 mg/L) in baby foods and fruit juices, respectively. GC-MS analysis of the SDE extracts obtained from the plastic gaskets inside the metal lids of the samples under study revealed the gaskets to be the origin of 2-EHA.|2-Ethylhexanoic acid (2-EHA), is an industrial chemical and a toxic biotransformation product of the plasticizer di(2-ethylhexyl)phthalate.

Food additives -> Flavoring Agents|Fatty Acyls [FA] -> Fatty Acids and Conjugates [FA01] -> Branched fatty acids [FA0102]|Cosmetics -> Emollient; Skin conditioning

Flavoring Agents