N,N-ジメチルカルバミド酸2-ジメチルアミノ-5,6-ジメチルピリミジン-4-イル

Biological Exposure Indices (BEI) [ACGIH] - Acetylcholinesterase activity in red blood cells = 70% of individual's baseline; Butylcholinesterase activity in serum or plasma = 60% of individual's baseline; Sample at end of shift; [TLVs and BEIs]

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.

If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.

Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Chronically high (>10 years) exposure leads to neuropsychological consequences including disturbances in perception and visuo-motor processing (A15321).

LD50 Mallard ducks oral 17.2 mg/kg

LD50 Bobwhite quail oral 8.2 mg/kg

LC50 (96 hr) Rainbow trout 29 mg/L /conditions of bioassay not specified/

LC50 (96 hr) Bluegill sunfish 55 mg/L /condition of bioassay not specified/

TERRESTRIAL FATE: Based on a classification scheme(1), Koc values in the range of 56-800(2,3), indicate that pirimicarb is expected to have high to low mobility in soil(SRC). Soils with a high clay content and low percentage of organic matter tend to sorb pirimicarb stronger than do soils with a high content of organic matter(SRC). Pirimicarb is a weak base with a pKa of 4.54(4), suggesting that it will partially exist in the protonated form in moist soils(SRC). Volatilization of pirimicarb from moist soil surfaces is not expected to be an important fate process(SRC) because cations do not volatilize and given an estimated Henry's Law constant for the free base of 8.4X10-10 atm-cu m/mole(SRC), based upon its vapor pressure, 7.28X10-6 mm Hg(4), and water solubility, 2,700 mg/l(4). Pirimicarb is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure of 7.28X10-6 mm Hg(4). Biodegradation data on pirimicarb in soils suggests that the rate of degradation varies greatly depending upon the conditions of the soil(SRC), with half-lives ranging from several days to several months(4,6-8).

AQUATIC FATE: Based on a classification scheme(1), Koc value ranging from 56-800, measured in different soils(2,3), indicates that pirimicarb is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(4) based upon an estimated Henry's Law constant of 8.4X10-10 atm-cu m/mole(SRC), based upon its vapor pressure, 7.28X10-6 mm Hg(5), and water solubility, 2,700 mg/l(6). Furthermore, pirimicarb is a weak base with a pKa of 4.53(12). This pKa indicates that pirimicarb will partially exist in the protonated form in the environment and cations do not volatilize(SRC). According to a classification scheme(7), an estimated BCF of 4(SRC), from a measured log Kow of 1.7(5) and a regression-derived equation(8), suggests the potential for bioconcentration in aquatic organisms is low(SRC). No biodegradation data exist for pirimicarb in water(SRC), but data in soil shows that biodegradation varies greatly by location and type of soil, with half-lives ranging from several days to several months(5,9-11). Photolysis in sunlit surface water may be an important fate process for pirimicarb based on a photolysis half-life of less than 1 day in aqueous solution(5). Hydrolysis occurs slowly in the environment with a measured half-life of over 23 days in a water/sediment system(5).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), pirimicarb, which has a vapor pressure of 7.28X10-6 mm Hg at 25 °C(2), is expected to exist in both the vapor and particulate phases in the particulate phase in the ambient atmosphere. Vapor-phase pirimicarb 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 hours(SRC), calculated from its rate constant of 1.5X10-10 cu cm/molecule-sec at 25 °C(SRC) determined using a structure estimation method(3). Particulate-phase pirimicarb may be removed from the air by wet and dry deposition(SRC). Pirimicarb undergoes photolysis in aqueous solutions exposed to UV light with a half-life of less than 1 day(2), which suggests direct photolysis in the atmosphere is also possible(SRC).

Pirimicarb was detected in lettuce at concns of 0.04-15.65 ppm(1) and grapes at a concn of 0.11 ppm(2). Pirimicarb was detected in 3 agricultural commodities at a concn of 0.1 ppm and 1 commodity at a concn of 0.05 ppm during a 1982-1986 study on domestic and imported food products(3).

Pirimicarb is a cholinesterase or acetylcholinesterase (AChE) inhibitor. Carbamates form unstable complexes with chlolinesterases by carbamoylation of the active sites of the enzymes. This inhibition is reversible. A cholinesterase inhibitor suppresses the action of acetylcholine esterase. Because of its essential function, chemicals that interfere with the action of acetylcholine esterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop.

/AQUATIC SPECIES/ Tadpoles of Rana perezi were kept for 14 weeks in water containing two sublethal levels of the carbamate insecticide ZZ-Aphox or the organophosphate Folidol. Approx concns of their active ingredients were 0.25 and 1 mg/l. Resulting malformations were studied by skeletal analysis and histological and histochemical investigation of the rear limbs of the tadpoles. The pesticides caused the animals to have malformations of the spinal column (scoliosis) and/or limbs (short and thick long bones with the epiphyses grossly twisted). Histochemical study showed differences in the composition of the connective matrix, and microscopic exam of the long bones indicated alterations in the thickness of the uncalcified bone matrix (osteoid) and the presence of abundant vascularised connective tissue in the region of the periosteum. The results confirmed changes in the composition of the connective tissue matrix as the cause of the defects observed in bone formation which are also discussed in relation to vitamin D absorption and calcium homeostasis.

/AQUATIC SPECIES/ In tests with newborn and 1-wk-old Daphnia magna, 48-hr EC50 values of 21-24 ug/L and 16 ug/L pirimicarb, respectively, were found.

/FIELD STUDIES/ Pirimicarb is registered for use within cereals ... /and was/ field-tested for toxicity to beneficial nontarget invertebrate groups important as food for farmland birds. Compared to the control, pirimicarb was the least toxic for most invertebrate groups examined. ...Toxicity was further tested on larvae of graminivorous sawflies, an important chick- food group, using field-sprayed plants in laboratory and semifield trials. None of the pyrethroid and carbamate compounds and mixtures was as toxic as the organophosphate, but all were more toxic than the control. The semifield experiments provided a useful way of determining potential insecticide impact on this nontarget group where field populations are often too low for field trials to have statistically conclusive results.

As with organophosphates, the signs and symptoms are based on excessive cholinergic stimulation. Unlike organophosphate poisoning, carbamate poisonings tend to be of shorter duration because the inhibition of nervous tissue acetylcholinesterase is reversible, and carbamates are more rapidly metabolized. Muscle weakness, dizziness, sweating and slight body discomfort are commonly reported early symptoms. Headache, salivation, nausea, vomiting, abdominal pain and diarrhea are often prominent at higher levels of exposure. Contraction of the pupils with blurred vision, incoordination, muscle twitching and slurred speech have been reported. (L795)

Pirimicarb (2-dimethylamino-5,6-dimethylpyrimidin-4-yldimethylcarbamate ) is used as insecticide in agriculture & fruit growing. During its metabolism in mammals the carbamate moiety is hydrolyzed & subsequent demethylation at the dimethylaminogroup which is attached to the heterocyclic moiety results in the following major metabolites which are excreted in urine: 2-dimethylamino-5,6-dimethyl-4-hydroxypyrimidine (DDHP), 2-methylamino-5,6-dimethyl-4-hydroxypyrimidine (MDHP), & 2-amino-5,6-dimethyl-4-hydroxypyrimidine (ADHP). These metabolites were detected in every urine sample of seven workers who had applied pirimicarb. Concns of the 2-methylamino-5,6-dimethyl-4-hydroxypyrimidine & 2-amino-5,6-dimethyl-4-hydroxypyrimidine were much higher than that of 2-dimethylamino-5,6-dimethyl-4-hydroxypyrimidine indicating a considerable demethylation capacity in humans. No metabolites were found in urine specimens of controls. The investigated pyrimidines represent sensitive & specific parameters for biological monitoring of exposure to pirimicarb.

New Active Ingredients ... includes pesticide active ingredients initially registered after November 1, 1984, that currently have active product registrations. By law, these newer pesticides are not subject to the reregistration program. They must, however, meet the new safety standard of the FQPA, and will be reviewed on a 15-year cycle under the registration review program. ... Active Ingredient Number: 106101; Tpye of Pesticide: insecticide; Use Site: food use (alfalfa); Year: 1997.

Used as insecticide (selective aphicide); [Merck Index] Registered for use on alfalfa grown for seed (non-food) in the states of Idaho, Nevada, Oregon, and Washington; [Reference #1]

Farming (Pesticides) [Category: Industry]

For Pirimicarb (USEPA/OPP Pesticide Code: 106101) ACTIVE products with label matches. /SRP: Registered for use in the U.S. but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

Insecticide

Pirimicarb is widely used as an insecticide or pesticide in homes, gardens and agricultural applications. It is a synthetic compound.

USEPA/OPP Pesticide Code 106101; Trade Names: Pirimor, PP 062, Pirimicarb technical.

Abol /trade name/

Aficida /trade name/

Aphox /trade name/

For more Formulations/Preparations (Complete) data for PIRIMICARB (7 total), please visit the HSDB record page.

Insecticides

Environmental transformation -> Pesticides (parent, predecessor)