3,5-Bis(1,1-dimethylethyl)phenol methylcarbamate

263.38

263.38

48SLE5Y118

DTXSID0041690

WHITE CRYSTALLINE SOLID

2924199090

41.82000

4.20420

0.978g/cm3

102.5-103.3 °C

406.62°C (rough estimate)

143.4ºC

1.49

15mg/L(20 ºC)

Store in cool, dry place away from feed and food.

1.98X10-6 mm Hg at 20 deg C

Oral-Rat LD50: 1800 mg/kg; Oral-Mouse LD50: 3200 mg/kg

Combustion produces toxic nitrogen oxide gas

Henry's Law constant = 4.6X10-8 atm-cu m/mol at 25 °C /Estimated/

Hydroxyl radical reaction rate constant: 15X10-12 cu cm/molec-sec at 25 °C /Estimated/

The warehouse is ventilated, low temperature and dry; stored and transported separately from food materials

Stable to light, heat and hydrolysis under normal conditions

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.

Approved respirator. chemical resistant footwear plus socks. Long-sleeved shirts and long pants. Waterproof gloves.

SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants.|SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at end of shift, but should remain at employee's place of work for cleaning.|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 protective clothing should be kept in separate places where it cannot be contaminated with toxic chemicals. It should be forbidden to keep this clothing in living quarters. Protective clothing must be washed at least once a week and each time it is contaminated with pesticides. Before washing the clothing should be soaked for several hours in a calcium carbonate solution. /Pesticides/|Smoking, eating, and drinking before washing should be absolutely prohibited when any pesticide ... is being handled or used. /Pesticides/

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./|The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials.|The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.

Carbamates produce slight to moderate skin and eye irritation, depending on the vehicle used, duration of contact, and on whether the substance is applied to the abraided or intact skin. From the available data, it cannot be excluded that some of the carbamates will have a slight to moderate sensitization potential. /Carbamate Pesticides/

moderately toxic

...Feature of insecticidal action of... carbamates is pronounced synergism shown by addition of methylenedioxy compound such as piperonyl butoxide, sesoxane, and propyl isome... these prevent in vivo detoxication of carbamates by inhibiting "mixed function oxidase" detoxification system. /Carbamates/

LD50 Dog oral 1000 mg/kg|LD50 Mouse oral 3200 mg/kg|LD50 Rat oral 1800 mg/kg|LD50 Rabbit dermal 13000 mg/kg|LC50 Rat inhalation >4.7 mg/kg 4hr

Butacarb's former production may have resulted in its release to the environment through various waste streams; its former use as a cholinesterase inhibitor insecticide(1) resulted in its direct release to the environment.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 980(SRC), determined from a water solubility of 15 mg/L(2) and a regression-derived equation(3), indicates that butacarb is expected to have low mobility in soil(SRC). Volatilization of butacarb from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 4.6X10-8 atm-cu m/mole(SRC), derived from its vapor pressure, 1.98X10-6 mm Hg(4), and water solubility(2). Butacarb is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(4). Biodegradation data were not available(SRC, 2005).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 980(SRC), determined from a water solubility of 15 mg/L(2) and a regression-derived equation(3), indicates that butacarb 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 4.57X10-8 atm-cu m/mole(SRC), derived from its vapor pressure, 1.98X10-6 mm Hg(4), and water solubility(2). According to a classification scheme(5), an estimated BCF of 130(SRC), from its water solubility(2) and a regression-derived equation(3), suggests the potential for bioconcentration in aquatic organisms is moderate(SRC). Biodegradation data were not available(SRC, 2005).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), butacarb, which has a vapor pressure of 1.98X10-6 mm Hg at 25 °C(2) is expected to exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase butacarb 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 26 hours(SRC), calculated from its rate constant of 14X10-12 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase butacarb may be removed from the air by wet and dry deposition(SRC). Butacarb does not contain chromophores that absorb at wavelengths >290 nm and would not be expected to be susceptible to direct photolysis by sunlight(SRC).

The rate constant for the vapor-phase reaction of butacarb with photochemically-produced hydroxyl radicals has been estimated as 14X10-12 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 26 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). A base-catalyzed second-order hydrolysis rate constant of 1.5 L/mole-sec(SRC) was estimated using a structure estimation method(2); this corresponds to half-lives of 55 days and 5.5 days at pH values of 7 and 8, respectively(2). Butacarb does not contain chromophores that absorb at wavelengths >290 nm and would not be expected to be susceptible to direct photolysis by sunlight(SRC).

An estimated BCF of 130 was calculated for butacarb(SRC), using a water solubility of 15 mg/L(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is moderate(SRC), provided the compound is not altered physically or chemically once released into the environment(SRP).

The Koc of butacarb is estimated as 980(SRC), using a water solubility of 15 mg/L(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that butacarb is expected to have low mobility in soil(SRC).

The Henry's Law constant for butacarb is estimated as 4.57X10-8 atm-cu m/mole(SRC) derived from its vapor pressure, 1.98X10-6 mm Hg(1), and water solubility, 15.0 mg/L(2). This Henry's Law constant indicates that butacarb is expected to be essentially nonvolatile from water surfaces(3). Butacarb's estimated Henry's Law constant indicates that volatilization from moist soil surfaces will not occur(SRC). Butacarb is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

Occupational exposure and general population exposure is expected to be low or non-existent since butacarb is no longer produced or used in the US (May, 2005). (SRC)

3. 3= moderately toxic: probable oral lethal dose (human) 0.5-5 g/kg, between 1 oz & 1 pint (or 1 lb) for 70 kg person (150 lb).

In vivo studies have shown that carbamates are almost completely absorbed during normal transit through the gastrointestinal tract. ...In mice, all carbamates were rapidly distributed to the tissues and organs. The half-life values of penetration ranged from 8-17 min for carbamates. ...In animals, oxidation of carbamates often, but not always, results in detoxification. Oxidative metabolism generally leads to products of greater polarity and water solubility, and these can be more readily eliminated through the urine and feces than the parent compound. /Carbamate pesticides/|Little information is available on the distribution of carbamates in the various organs and tissues in mammals following exposure by inhalation or the oral route. The organs in which residues have been reported are the liver, kidneys, brain, fat, and muscle. The half-life in the rat is of the order of 3-8 hr. It seems that the excretion of carbamates via urine is also rapid in man, and that the metabolic pathways in man are the same as those in the rat. /Carbamate pesticides/

When butacarb was incubated with mouse liver 10,000xg supernatant, eleven metabolites were detected. Hydrolysis produced only 6 phenols. One of these, the major metabolite, was identified as 3,5-di-tert-butylphenol. Other metabolites were characterized but not all were completely identified: two acid metabolites containing a carboxyl & carbamoyl group; two containing a carbamoyl & two hydroxy groups (but not dihydroxybenzenoid); a hydroxybutylphenol; one containing a carbamoyl & hydroxy group; two dihydroxybutylphenols; n-hydroxymethyl butacarb; & n-hydroxymethyl hydroxybutyl analog. Studies with housefly (musca domestica), blowfly (lucilia sericata) & grass grubs (costelytra zealandica) gave results quant similar to those with mouse liver enzymes.|...Butacarb.../is/ cleaved to phenolic products by enzyme system in liver microsomes, which requires nadph & is inhibited by carbon monoxide...it is likely that this...microsomal mono-oxygenation is very important in 'hydrolysis' of carbamates.|The principal route of metabolism of insecticidal carbamate esters is oxidative and is generally associated with the mixed-function oxidase (MFO) enzymes, which are present in several tissues. /Carbamate pesticides/|The metabolism of 3,5-di-tert-butylphenyl-N-methylcarbamate (butacarb) was studied in insects and mouse liver enzymes. Tritium (H-3) labeled butacarb was incubated with 10,000 times the force of gravity supernatants from mouse liver or housefly and blowfly enzyme preparations, obtained from their abdomens. The reaction mixtures were analyzed for metabolites. Eleven oxidation products were detected in each species. In-vivo, adult houseflies and blowflies were dosed topically with H-3 labeled butacarb. The insects were then extracted by grinding them with sand and ether. Ether extracts were examined for metabolites. The water soluble fraction was also examined. Both fractions consisted of complex mixtures. The ether fraction was hydrolyzed with sodium-hydroxide, and the water soluble portion was analyzed. Six phenolic metabolites were detected. The major phenolic product was 3,5-di-tert-butylphenol, which accounted for more than half of the dose.

The carbamates alone weakly activated estrogen- or progesterone-responsive reporter genes in breast and endometrial cancer cells. All of the carbamates decreased estradiol- or progesterone-induced reporter gene activity in the breast and endometrial cancer cells. In whole cell competition binding assays, the carbamates demonstrated a limited capacity to displace radiolabeled estrogen or progesterone from /estrogen receptor/ or /progesterone receptor/. /Carbamates/|Carbamates are effective insecticides by virtue of their ability to inhibit acetylcholinesterase (AChE) in the nervous system. They also inhibit other esterases. The carbamylation of the enzyme is unstable, and the regeneration of AChE is relatively rapid compared with that from a phosphorylated enzyme. Thus, carbamate pesticides are less dangerous with regard to human exposure than organophosphorus pesticides. The ratio between the dose required to produce death and the dose required to produce minimum symptoms of poisoning is substantially larger for carbamate compounds than for organophosphorus compounds. /Carbamate Pesticides/|The carbamate insecticides are reversible cholinesterase-inhibitors. They cause this effect by reversible carbamylation of the enzyme acetylcholinesterase, allowing accum of acetylcholine, as with the organophosphate insecticides. ... While the organophosphate insecticides cause irreversible inhibition of the cholinesterase enzymes, the carbamyl-enzyme complex is reversible & dissociates far more readily than the organophosphate complex. The clinical syndrome is more benign & of much shorter duration with the carbamate insecticides. /Carbamate insecticides/

Maintain an open airway and assist ventilation if necessary. Pay careful attention to respiratory weakness; sudden respiratory arrest may occur. This is often preceded by increasing weakness of neck flexion muscles. If intubation is required, note the potential for interaction between neuromuscular blockers and cholinesterase inhibitors. Administer supplemental oxygen. Treat hydrocarbon pneumonitis, seizures, and coma if they occur. Observe asymptomatic patients for at least 8-12 hours to rule out delayed onset symptoms especially after extensive skin exposure or ingestion of a highly fat-soluble agent. Specific treatment includes the antimuscarinic agent atropine and the enzyme reactivator pralidoxime. ... Do not induce vomiting because of the risk of abrupt onset of toxicity. ... Administer activated charcoal (cathartics are not necessary if the patient already has diarrhea ). Consider inserting a small flexible gastric tube to aspirate liquid gastric contents, if this procedure can be carried out safely and within 1-2 hours of ingestion. The inadvertent introduction of hydrocarbon solvents into the lungs through overly aggressive gastric lavage may kill the patient.) /Organophosphorus and Carbamate insecticides/|Basic treatment: Establish a patent airway. Suction if necessary. Aggressive airway control may be needed. Watch for signs of respiratory insufficiency and assist ventilations 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 ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline 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. Administer activated charcoal ... . /Carbamates and related compounds/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. For hypotension if signs of hypovolemia are present, administer fluid cautiously. Watch for signs of pulmonary edema ... . Administer atropine. Correct hypoxia before administration ... . In severely poisoned patients, administer pralidoxime chloride (2 PAM). DIRECT PHYSICIAN ORDERS ONLY ... . Treat seizures with adequate atropinization and correction of hypoxia. Rarely is diazepam necessary ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Carbamates and related compounds/|Elimination Enhancement: No methods are recommended, because of the short clinical effect of carbamates and the presence of an effective antidote (atropine). /Carbamates/|For more Antidote and Emergency Treatment (Complete) data for BUTACARB (32 total), please visit the HSDB record page.

/SIGNS AND SYMPTOMS/ Symptomatology: Nausea, vomiting, abdominal cramps, diarrhea & excessive salivation... sweating. Lassitude & weakness. Rhinorrhea and sensation of tightness in chest may occur with inhalation exposure. Blurring or dimness of vision. Miosis ... tearing, ciliary muscle spasm, loss of accommodation and ocular pain. None of these ... signs ... is dependable for diagnosis. Mydriasis may be seen ... Loss of muscle coordination, slurring of speech, fasciculation & twitching of muscles. Difficulty in breathing, excessive secretions of saliva and of respiratory tract mucus, oronasal frothing, cyanosis, pulmonary rales & rhonchi, and hypertension. ... Jerky movements, incontinence, convulsions and coma. Death ... due to respiratory arrest of central origin, paralysis of respiratory muscles, intense bronchoconstriction or all three.|/SIGNS AND SYMPTOMS/ The clinical picture of carbamates intoxication results from accumulation of ACh at nerve endings. ...The signs and symptoms can be categorized into the following 3 groups: (a) Muscarinic manifestations - increased bronchial secretion, excessive sweating, salivation, and lachrymation; pinpoint pupils, bronchoconstriction, abdominal cramps (vomiting and diarrhea); and bradycardia. (b) Nicotinic manifestations - fasciculation of fine muscles (in severe cases, diaphragm and respiratory muscles also involved); and tachycardia. (c) Central nervous system manifestations- headache, dizziness, anxiety, mental confusion, convulsions, and coma; and depression of respiratory center. All these signs and symptoms can occur in different combinations and can vary in onset and sequence, depending on the chemical, dose, and route of exposure. The duration of symptoms is usually shorter than that observed in organophosphorus poisoning. Mild poisoning might include muscarinic and nicotinic signs only. Severe cases always show central nervous system involvement; the clinical picture is dominated by the respiratory failure sometimes leading to pulmonary edema due to the combination of the above mentioned symptoms. /Carbamate pesticides/

butacarb

Emulsifiable concentrate, granules

Very effective against larval stages of sheep blow fly. In sheep dips at 50 g ai/100 l gives protection from blow fly strike 10 to 12 weeks.|Compatible with most other pesticides|Not marketed in /United States/|FRASER, HARRISON, BRITISH PATENT 987,254 (1965 TO BOOTS PURE DRUG); KAEDING ET AL, J AGR FOOD CHEM 13, 215 (1965).|Discontinued by The Boots Co Ltd

Analysis: Hydrolysis and determination of methylamine produced; acetylation and determination of product by gas-liquid chromatography.