Pivalic acid

102.13

102.13

969480

200-922-5

813RE8BX41

0486

65449

3261

DTXSID8026432

Colorless cyrstals|Needles

29159000

37.3

1.5

Yellow to orange to tan Powder, Crystals and/or Chunks

0.905 g/cm³ @ Temp: 50 °C

35.5 °C

163.8 °C

147 °F

1.393

H2O: 25 g/L (20 ºC)

2-8°C

9.75 mm Hg ( 60 °C)

3.6 (vs air)

LD50 orally in Rabbit: 900 mg/kg LD50 dermal Rat 1900 mg/kg

1.6%(V)

2.78e-06 atm-m3/mole|Henry's Law constant = 2.78X10-6 atm-cu m/mole at 25 °C

pKa = 5.03 at 25 °C

Liquid. Density: 0.8580 at 18 °C/4 °C; bp 118.2 °C; index of refraction: 1.3922 at 18 °C/D /Ethyl ester/|Hydroxyl radical reaction rate constant = 5.9X10-13 cu cm/molec-sec at 25 °C (est)

With mixing, water soluble.

Acids, Carboxylic

TRIMETHYLACETIC 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.

560 °C

Ⅱ

8

UN 3261 8/PG 2

1

21/22-34

26-36/37/39-45

TO7700000

C

Separated from strong oxidants, bases and food and feedstuffs. Dry. Well closed. Ventilation along the floor.

P260, P261, P264, P270, P271, P280, P301+P312, P302+P352, P304+P340, P305+P351+P338, P309+P311, P312, P321, P322, P330, P332+P313, P337+P313, P362, P363, P403+P233, P405, P501

H302

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

EPA/Office of Pollution Prevention and Toxics; High Production Volume (HPV) Challenge Program's Robust Summaries and Test Plans. Available from the Database Query page at: http://www.epa.gov/hpv/pubs/hpvrstp.htm on Neoacids C5-C28 Category as of January 3, 2008.|European Chemicals Bureau; IUCLID Dataset, Pivalic acid (75-98-9) (2000 CD-ROM edition). Available from the Database Query page at: http://ecb.jrc.it/esis/esis.php as of January 3, 2008.

COMBUSTIBLE. Produces vapors irritating to eyes and skin. Decomposes to produce acrid smoke and fumes. (USCG, 1999)|Combustible. Above 64 °C explosive vapour/air mixtures may be formed.

|Danger|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|P260, P261, P264, P270, P271, P280, P301+P312, P301+P330+P331, P302+P352, P303+P361+P353, P304+P312, P304+P340, P305+P351+P338, P310, P312, P321, P322, P330, P332+P313, P337+P313, P362, P363, P405, and P501|Aggregated GHS information provided by 191 companies from 10 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|Warning|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P260, P261, P264, P270, P271, P280, P301+P312, P302+P352, P304+P340, P305+P351+P338, P309+P311, P312, P321, P322, P330, P332+P313, P337+P313, 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)

Avoid contact with solid and dust. Keep people away. Wear self-contained positive pressure breathing apparatus and full protective clothing. Stop discharge if possible. Shut off ignition sources. Call fire department. Isolate and remove discharged material. Notify local health and pollution control agencies. Issue warning - water contaminant Should be removed. Chemical and physical treatment. Dangerous to aquatic life in high concentrations. May be dangerous if it enter water intakes. Notify local health and wildlife officials. Notify operators of nearby water intakes. (USCG, 1999)

Wear self-contained positive breathing apparatus and full protective clothing. (USCG, 1999)|Personnel protection: ... Wear appropriate chemical protective gloves, boots and goggles.

Combustible.

Explosive limits , vol% in air: 1.6-?

Powder, alcohol-resistant foam, water spray, carbon dioxide.|If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped. Use water in flooding quantities as fog. Solid streams of water may be ineffective. Cool all affected containers with flooding quantities of water. Apply water from as far a distance as possible. Use "alcohol" foam, dry chemical, or carbon dioxide.

Collect leaking liquid in sealable containers. If solid: sweep spilled substance into containers; if appropriate, moisten first to prevent dusting. Wash away remainder with plenty of water. (Extra personal protection: A/P2 filter respirator for organic vapour and harmful dust).|Environmental considerations: Land spill: Dig a pit, pond, lagoon, holding area to contain liquid or solid material. Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash, cement powder, or commercial sorbents /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./|Environmental considerations: Water spill: Use natural barriers or oil spill control booms to limit spill travel. Remove trapped material with suction hoses.|Environmental considerations: Air spill: Apply water spray or mist to knock down vapors.

If material not on fire and not involved in fire: Keep sparks, flames, and other sources of ignition away. Keep material out of water sources and sewers. Build dikes to contain flow as necessary. Use water spray to disperse vapors and dilute standing pools of liquid..|Personnel protection: Avoid breathing vapors. Keep upwind. ... Do not handle broken packages unless wearing appropriate personal protective equipment. Wash away any material which may have contacted the body with copious amounts of water or soap and water.|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.

The substance irritates the eyes, the skin and the respiratory tract.

Personal protection: filter respirator for organic gases and particulates adapted to the airborne concentration of the substance. Collect leaking and spilled liquid in sealable containers as far as possible. Absorb liquid in sand or inert absorbent. If solid: sweep spilled substance into containers. If appropriate, moisten first to prevent dusting. Wash away remainder with plenty of water. Store and dispose of according to local regulations.

Separated from strong oxidants, bases and food and feedstuffs. Dry. Well closed. Ventilation along the floor.

No indication can be given about the rate at which a harmful concentration of this substance in the air is reached on evaporation at 20 °C.

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

NO open flames. Above 64 °C use a closed system and ventilation.

Use local exhaust.

Protective gloves.

Wear safety goggles.

This action promulgates standards of performance for equipment leaks of Volatile Organic Compounds (VOC) in the Synthetic Organic Chemical Manufacturing Industry (SOCMI). The intended effect of these standards is to require all newly constructed, modified, and reconstructed SOCMI process units to use the best demonstrated system of continuous emission reduction for equipment leaks of VOC, considering costs, non air quality health and environmental impact and energy requirements. Neopentanoic acid is produced, as an intermediate or a final product, by process units covered under this subpart.

2,2-Dimethylpropanoic acid was identified at a concn of 8 ppm in effluent from one of three New Jersey publicly owned treatment works (POTWs) located in an industrial area of the state(1).

LD50 Rat oral 2000 mg/kg /from table/|LD50 Rabbit dermal 3160 mg/kg /from table/|LC50 Rat (Wistar male) inhalation >4.0 mg/L/6 hr|LC50 Mouse (Swiss albino male) inhalation <4.0 mg/L/6 hr|LD50 Rat dermal 1900 mg/kg

2,2-Dimethylpropanoic acid's production and use in the production of polymers and resins, pharmaceuticals, agricultural chemicals, cosmetics, fuels, lubricants and transmission fluids(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 150(SRC), determined from a log Kow of 1.48(2) and a regression-derived equation(3), indicates that 2,2-dimethylpropanoic acid is expected to have high mobility in soil(SRC). The pKa of 2,2-dimethylpropanoic acid is 5.03(4), indicating that this compound will exist partially 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 2,2-dimethylpropanoic acid from moist soil surfaces is not expected to be an important fate process because anions do not volatilize. 2,2-Dimethylpropanoic acid is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 0.50 mm Hg(6). Several screening studies(7-11) suggest that under aerobic conditions, 2,2-dimethylpropanoic acid may biodegrade in soil with sufficient acclimation time, but no rate data were available.|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 150(SRC), determined from a log Kow of 1.48(2) and a regression-derived equation(3), indicates that 2,2-dimethylpropanoic acid is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon a Henry's Law constant of 2.78X10-6 atm-cu m/mole(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 13 and 100 days, respectively(SRC). According to a classification scheme(5), BCFs of <0.2-1.2 at a concentration of 1 ppb and <2.3 at a concentration of 0.1 ppb(6), suggest bioconcentration in aquatic organisms is low(SRC). Several screening studies(7-11) suggest that under aerobic conditions, 2,2-dimethylpropanoic acid may biodegrade in aquatic systems with sufficient acclimation time but no data were available. Aquatic oxidation with hydroxyl radicals is not likely to be an important fate process based on a half-life of 1.5 yrs in water under continuous sunlight(12).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), 2,2-dimethylpropanoic acid, which has a vapor pressure of 0.50 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase 2,2-dimethylpropanoic 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 27 days(SRC), calculated from its rate constant of 5.9X10-13 cu cm/molecule-sec at 25 °C(3).

The rate constant for the vapor-phase reaction of 2,2-dimethylpropanoic acid with photochemically-produced hydroxyl radicals has been measured as 5.9X10-13 cu cm/molecule-sec at 25 °C(1). This corresponds to an atmospheric half-life of about 27 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The aquatic oxidation rate for the reaction of the 2,2-dimethylpropanoic acid ion with photochemically produced hydroxyl radicals has been experimentally determined to be 1.5X10+9 L/mol-s (pH 9)(2). Based on this rate and a hydroxyl radical concn of 1X10-17 mol/L in water under continuous sunlight(3), the half-life for the aquatic oxidation of the 2,2-dimethylpropanoic acid ion can be estimated to be about 1.5 yrs(SRC). 2,2-Dimethylpropanoic acid is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(4).

2.29|The BCF of 2,2-dimethylpropanoic acid was <0.2-1.2 at a concentration of 1 ppb and <2.3 at a concentration of 0.1 ppb using carp (Cypinus carpio) which were exposed over a 6-week period(1). According to a classification scheme(2), these BCFs suggest bioconcentration in aquatic organisms is low(SRC).

The Koc of 2,2-dimethylpropanoic acid is estimated as 150(SRC), using a log Kow of 1.48(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that 2,2-dimethylpropanoic acid is expected to have high mobility in soil. The pKa of 2,2-dimethylpropanoic acid is 5.03(4), indicating that this compound will exist partially in 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 2,2-dimethylpropanoic acid is 2.78X10-6 atm-cu m/mole(1). This Henry's Law constant indicates that 2,2-dimethylpropanoic acid is expected to volatilize from water surfaces(2). 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)(2) is estimated as 13 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)(2) is estimated as 100 days. 2,2-Dimethylpropanoic acid's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). 2,2-Dimethylpropanoic acid is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 0.50 mm Hg(3).

DRINKING WATER: 2,2-Dimethylpropanoic acid was detected, not quantified in drinking water concentrate from New Orleans, LA on January 14, 1976, Philadelphia, PA on February 10, 1976, and Seattle, WA on November 5, 1976(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 1462 workers (996 of these were female) were potentially exposed to 2,2-dimethylpropanoic acid in the US(1). Occupational exposure to 2,2-dimethylpropanoic acid may occur through inhalation and dermal contact with this compound at workplaces where 2,2-dimethylpropanoic acid is produced or used. Use data indicate that the general population may be exposed to 2,2-dimethylpropanoic acid via ingestion of medications, and dermal contact with consumer products containing 2,2-dimethylpropanoic acid(SRC).

MEDICATION (VET): Pivalic acid was shown to possess musculotropic spasmolytic activity comparable or superior to papaverine hydrochloride on a Guinea pig ileum preparation. In addition, it exhibited neurotropic spasmolytic activity as well as hypotensive activity in rabbits.|Prodrugs that liberate pivalate (trimethylacetic acid) after hydrolysis have been developed to improve the bioavailability of therapeutic candidates. Catabolism of pivalate released by activation of a prodrug is limited in mammalian tissues. Pivalate can be activated to a coenzyme A thioester in cells. In humans, formation and urinary excretion of pivaloylcarnitine generated from pivaloyl-CoA is the major route of pivalate elimination. Because the total body carnitine pool is limited and can only slowly be replenished through normal diet or biosynthesis, treatment with large doses of pivalate prodrugs may deplete tissue carnitine content. Animal models and long-term treatment of patients with pivalate prodrugs have resulted in toxicity consistent with carnitine depletion. However, low plasma carnitine concentrations after pivalate prodrug exposure may not reflect tissue carnitine content and, thus, cannot be used as a surrogate for potential toxicity. The extent of tissue carnitine depletion will be dependent on the dose of pivalate, because carnitine losses may approximate the pivalate exposure on a stoichiometric basis. These concepts, combined with estimates of carnitine dietary intake and biosynthetic rates, can be used to estimate the impact of pivalate exposure on carnitine homeostasis. Thus, even in populations with altered carnitine homeostasis due to underlying conditions, the use of pivalate prodrugs for short periods of time is unlikely to result in clinically significant carnitine depletion. In contrast, long-term treatment with substantial doses of pivalate prodrugs may require administration of carnitine supplementation to avoid carnitine depletion.|The metabolism and clinical safety of the pivalic acid-containing antibiotic S-1108, an orally active pro-drug cephalosporin, were investigated to assess the clinical effects, with special emphasis on the influence of carnitine consumption in 15 patients with various infectious diseases receiving S-1108 three times a day at a 300- or 600-mg total daily dose for 3 to 7 days. The free carnitine concentrations in plasma were greatly reduced to approximately 65% of pretreatment levels, and the plasma pivaloylcarnitine (the main metabolite of pivaloyloxymethyl ester) concentrations were increased during the 200-mg (three times a day) regimens but returned to the pretreatment levels within 3 to 5 days after the cessation of treatment. In three elderly patients with declining renal function (creatinine clearance rate, 31 to 50 ml/min), the acylcarnitine/free carnitine ratio increased from 0.1 to 0.4 up to 0.7 to 1.5 at day 5 during the 7-day treatment, showed a tendency to decrease, and then returned to the pretreatment ratio 4 days after discontinuation of the drug. The degree of free carnitine reduction and increase of the acylcarnitine/free carnitine ratio depended mostly on the dose and the duration of S-1108 treatment. The increased acylcarnitine/free carnitine ratio in elderly patients was due to reduction of the free carnitine concentration in plasma and mainly to the retardation of nontoxic pivaloylcarnitine excretion. This study indicated that there was a decrease in free carnitine levels in plasma, but there were no clinical symptoms or adverse effects associated with carnitine reduction in patients during the 7-day multiple administration of S-1108.

14(C) labeled pivalic acid, administered orally in mice, was well absorbed and distributed in bone, kidneys, olfactory bulb, salivary gland, and some adipose tissues, and finally excreted in urine, primarily as its conjugated forms.|Both pivaloylesterified antibiotics and pivalic acid cause pivaloylcarnitine excretion into urine in the rat and human. In the present study, the formation of pivaloylcarnitine, expressed as short-chain acylcarnitines has been observed in rats. The carnitine pool of the rats was radiolabeled by injection of L-[3H]butyrobetaine 24 h prior to exposure to pivalic acid injected i.p. or pivampicillin administered orally. The presence of pivaloylcarnitine in liver, heart, kidney, stomach, small intestine, testis, muscle, brown fat, white fat and serum was determined at zero time, 0.5, 2, 8 and 24 h after exposure to pivalic acid. After injection of pivalic acid, pivaloylcarnitine calculated as percent of free carnitine and short-chain acylcarnitines amounted to (mean +/- SD) 1.1 +/- 0, 15.4 +/- 2.5, 33.4 +/- 0.7 and 37.5 +/- 1.5% in the heart and 1.2 +/- 0.2, 20.6 +/- 9.5, 29.8 +/- 7.6 and 22.5 +/- 1.6% in brown fat after 0, 0.5, 2 and 8 h, respectively. 2 h after administration, pivaloylcarnitine calculated as percent of free carnitine and short-chain acylcarnitines was highest in the heart (20.9 +/- 7.6%) and brown fat (19.0 +/- 8.5%) in the pivalic acid-treated rat, and highest in the kidney (12.4 +/- 3.1%) and brown fat (10.2 +/- 2.8%) in the pivampicillin-treated rat. Pivaloylcarnitine percent in the liver was 2.8 +/- 0.6 in the pivalic acid-treated rat, 3.5 +/- 1.2 in the pivampicillin-treated rat and 1.3 +/- 0.4 in the control group. Pivaloylcarnitine concentration, nmol/g and nmol/organ, was highest in the heart and brown fat in both treatment groups. The present study suggests that the heart and the brown fat, but not the liver, play important roles in pivaloylcarnitine formation in the rat.

Pivalic acid administered orally to mice was excreted in urine primarily in conjugated forms.|Three healthy volunteers were orally dosed with 100 and 200 mg of the test substance. More than 90% of pivalic acid is excreted as pivaloyl-carnitine and no measurable amount of free pivalic acid was present in the urine samples, indicating that pivalic acid was quantitatively conjugated with carnitine in the human body. /Pivaloyloxymethyl (+)-(6R,7R)-7-[(Z)-2-(2-amino-4-thiazolyl)-2-pentenamido]-3-carbamoyloxymethyl-8-oxo-5-thia-1-azabicyclo[4.2.0]oct-2-ene-2-carboxylate hydrochloride hydrate (S-1108), an oral cephem antibiotic/|Healthy volunteers in a Phase I clinical study were orally dosed with 200 mg of the test substance 3 times a day for 8 days. No clinical or abnormal signs. Pivalic acid is metabolized in the body to pivaloyl-carnitine. The urinary excretion of pivaloyl-carnitine and the plasma carnitine concentration of 50% indicates that there is enough carnitine store in the body to detoxify the pivalic acid. /Pivaloyloxymethyl (+)-(6R,7R)-7-[(Z)-2-(2-amino-4-thiazolyl)-2-pentenamido]-3-carbamoyloxymethyl-8-oxo-5-thia-1-azabicyclo[4.2.0]oct-2-ene-2-carboxylate hydrochloride hydrate (S-1108), an oral cephem antibiotic/|Freshly prepared rat hepatocytes from male Sprague-Dawley rats/ partly clofibrate treated, were exposed to 0, 0.5, 1.0, 5.0, and 10.0 mM of the test substance. Hepatocytes activate pivalate to pivaloyl-CoA, which can be used as a substrate for pivaloylcarnitine formation. the sequestration of hepatocyte CoA as pivaloyl-CoA is associated with the inhibition of pyruvate oxidation. /Pivalate/|For more Metabolism/Metabolites (Complete) data for 2,2-DIMETHYLPROPANOIC ACID (9 total), please visit the HSDB record page.

CALL FOR MEDICAL AID. SOLID: Irritating to eyes and skin. Harmful if swallowed. IF IN EYES OR ON SKIN, flush with running water for at least 15 minutes; hold eyelids open if necessary. Wash skin with soap and water. Remove and isolate contaminated clothing and shoes at the site. If SWALLOWED and victim is UNCONSCIOUS OR HAVING CONVULSIONS, do nothing except keep victim warm. Because of low volatility, it is relatively harmless when inhaled at normal ambient temperature (around 20°C). It is slightly toxic by ingestion or skin absorption. The vapor is irritating at elevated temperatures. Can cause considerable discomfort by oral routes; may cause reversible or irreversible changes to exposed tissue, not permanent injury or death. (USCG, 1999)

INHALATION: Remove victim to fresh air, get medical attention if irrtation persists. EYES: Hold eyelids open and flush with plenty of water for at least 15 minutes and get medical attention. SKIN: Contaminated skin should be washed with soap and water. (USCG, 1999)

Fresh air, rest. Refer for medical attention.

Rinse skin with plenty of water or shower. Refer for medical attention if skin irritation occurs.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer 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 as 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/ Treatment with pivalic acid containing prodrugs has been shown to cause carnitine depletion by loss of pivaloyl carnitine in urine. A 7-day standard pivmecillinam treatment of adults lead to a marked decrease of the free serum carnitine concentration (44.6 to 12.9 umol/L), whereas no change was seen in those given norfloxacine (40.0 to 40.5 umol/L). In some patients irrespective of age the free serum carnitine concentration was decreased to levels (around 10 umol/L) at which an impaired ketone-body production may occur.|/HUMAN EXPOSURE STUDIES/ Short-term administration of pivampicillin and pivmecillinam resulted in a reduction of serum carnitine concentration and an increase in excretion of acylcarnitine in urine. These changes persisted for more than ten days after cessation of therapy. In seven girls on long-term treatment with a mixture of pivampicillin and pivmecillinam the mean total serum carnitine concentration fell to 15% (7-27%) of pretreatment values. The acylcarnitine fraction was 11-57% of total carnitine, compared with less than 2% before treatment. Muscle carnitine concentrations in two girls treated with the antibiotics for 22 and 30 months were only 10% of the mean reference value. These concentrations in serum and muscle are in the range encountered in patients with carnitine deficiencies of other aetiologies in which life-threatening metabolic crises may arise. The risk of adverse effects from prodrugs that give rise to pivalic acid should be seriously considered, particularly in patients under metabolic stress.|/CASE REPORTS/ An 18-month-old boy was treated with an antibiotic containing pivalic acid for 6 months for intractable otitis media and then developed repeated convulsions and loss of consciousness. Laboratory data showed hypoglycemia and hypocarnitinemia. Intravenous administration of glucose was ineffective against the seizures and loss of consciousness. However, the patient regained consciousness and recovered soon after intravenous infusion of carnitine. To our knowledge, intravenous carnitine administration that contributed to marked improvements in neurologic deficit caused by administration of an antibiotic containing pivalic acid has not been reported previously.

2,2-dimethylpropionic acid

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

Cough. Sore throat.

Redness. Pain.

Redness. Pain.

>99% pure

All other basic organic chemical manufacturing|Propanoic acid, 2,2-dimethyl-: ACTIVE

GAS CHROMATOGRAPHY DETERMINATION OF VOLATILE, BASIC & ACID ORGANIC COMPONENTS IN EXHAUST GASES.

Fatty Acyls [FA] -> Fatty Acids and Conjugates [FA01] -> Branched fatty acids [FA0102]