化合物详情

Pesticide Ecotoxicity Data from EPA: 69

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

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...

The Koc of pirimicarb in soil was reported as 1,387(1), but no details of the soil conditions were provided and the adsorption of pirimicarb is greatly dependent upon the characteristics of the soil(SRC). The adsorption of pirimicarb in 21 different soils was studied(2). The greatest adsorption was observed in soils with a high clay content and low percentage of organic matter(2). Relatively weak adsorption was observed in soils containing a high percentage of organic carbon(2). Using the adsorption coefficient (Kd) and percentage of organic carbon present in the soil, Koc values ranging from about 56 to 270 were calculated for soils with organic carbon content of 1% or greater(SRC). The mobility of pirimicarb was significantly attenuated by soils with a large percentage of clay and a l...

Pirimicarb degraded in a cultivated and non-cultivated sandy loam obtained from Berlin, Germany(1). Following application of pirimicarb to the surface layer of the cultivated and uncultivated soil, approximately 66% (cultivated soil) and 60% degradation (uncultivated soil) was observed after 3 days(1). After 7 days approximately 75% (cultivated soil) and 73% (uncultivated soil) was observed(1). The half-life of pirimicarb is reported to range from 7-234 days, depending upon the conditions of the soil(2). The half-life of pirimicarb in soil was reported as 69 days(3). Pirimicarb has been classified as a persistent pesticide with a biodegradation half-life of 208 days in soil at 20 °C(4). The degradation of pirimicarb in 2 agricultural soils (a clay and silt loam) from the Netherlands was...

An estimated BCF of 4 was calculated for pirimicarb(SRC), using a log Kow of 1.7(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).

Pirimicarb is a weak base with pKa of 4.53(5). This pKa indicates that pirimicarb will partially exist in the protonated form in the environment(SRC). The Henry's Law constant for pirimicarb as the free base is estimated as 8.4X10-10 atm-cu m/mole(SRC) based upon its vapor pressure, 7.28X10-6 mm Hg(1), and water solubility, 2,700 mg/l(2). This Henry's Law constant and the fact that cations are non-volatile indicates that pirimicarb is expected to be essentially nonvolatile from water surfaces and soil surfaces(3). Pirimicarb is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1). Pirimicarb was applied to the surface of a soil and leaves of a French bean plant and studied in a fume hood (air velocity 2 m/s, 13-21 °C in plant experiments and 1 m/s, 19-...

The rate constant for the vapor-phase reaction of pirimicarb with photochemically-produced hydroxyl radicals has been estimated as 1.5X10-10 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 2 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Pirimicarb undergoes photolysis in the environment with a half-life of less than 1 day in aqueous solutions exposed to UV light(2). Hydrolysis occurs slowly in the environment with a measured half-life of over 23 days in a water/sediment system(2).

SURFACE WATER: Pirimicarb was detected at a concn of 4 ug/l in surface water near a barley field where it was applied(1). Pirimicarb was detected in water samples of a stream near an agricultural field in Sweden at mean concns of 0.22 ug/l (1990) and 0.02 ug/l (1991)(3). GROUND WATER: Pirimicarb was detected in 2 out of 12 groundwater samples of the Hojvads Rende catchment area, Denmark at concns of less than 0.1 ug/l(5). RAIN/SNOW: Pirimicarb was identified in 19% of the rainfall samples obtained in Germany(2). Pirimicarb was detected in rainfall samples from Greece at concns of 0.08-0.42 ug/l(4).

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).

/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.

Pirimicarb's production may result in its release to the environment through various waste streams; it's use as an insecticide(1) will result in its direct release to the environment(SRC).

Occupational exposure to pirimicarb may occur through inhalation and dermal contact with this compound at workplaces where pirimicarb is produced or used. Monitoring data indicate that the general population may be exposed to pirimicarb via ingestion of food products containing pirimicarb. (SRC)

Pirimicarb's production may result in its release to the environment through various waste streams; it's use as an insecticide will result in its direct release to the environment. If released to air, a vapor pressure of 7.28X10-6 mm Hg at 25 °C indicates pirimicarb will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase pirimicarb will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 2 hours. Particulate-phase pirimicarb will be removed from the atmosphere by wet and dry deposition. Pirimicarb absorbs light greater than 290 nm and may also be susceptible to photolysis in the environment. If released to soil, pirimicarb is expected to have high to low mo...

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)

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.

Thiram applied in an equitoxic mixture with pirimicarb evidently intensifies and prolongs the neurochemical effect of pirimicarb in the rat.

LC50 (rat) = 300 mg/m3/6h

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...

Other Poison - Carbamate

Inhalation (L793); oral (L793); dermal (L793)

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 estera...

No indication of carcinogenicity to humans (not listed by IARC).