파라옥손

Pesticide -> EPA IRIS

Pesticides -> Organophosphate Insecticides

Pesticide (Parathion oxygen analog) -> USDA PDB

Pesticide degradation product

log Kow = 1.98

1.98

SLIGHT ODOR

Odorless

1.274 at 68 °F (NTP, 1992) - Denser than water; will sink

1.2683 at 25 °C/4 °C

OILY LIQUID

REDDISH-YELLOW OIL

Sparingly soluble (NTP, 1992)

Freely soluble in ether and other organic solvents

In water, 3,640 mg/l at 20 °C.

3.64 mg/mL at 20 °C

336 to 338 °F at 760 mmHg (NTP, 1992)

169-170 °C at 1.0 mm Hg

0.0000011 [mmHg]

1.1X10-6 mm Hg at 25 °C.

Danger

H300 (100%): Fatal if swallowed [Danger Acute toxicity, oral]

P260, P262, P264, P270, P271, P273, P280, P284, P301+P316, P302+P352, P304+P340, P316, P320, P321, P330, P361+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 43 reports by companies from 4 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

SYMPTOMS: Symptoms of related compounds include anorexia, headache, dizziness, weakness, anxiety, tremors of the tongue and eyelids; miosis, impairment of visual acuity; nausea, salivation, tearing, abdominal cramps, vomiting, sweating, slow pulse, muscular fasciculations, diarrhea, pinpoint and nonreactive pupils; respiratory difficulty, pulmonary edema, cyanosis, loss of sphincter, convulsions, coma and heart block.

The oxygen analog of parathion; A cholinesterase inhibitor; [Hawley] May have detrimental effects on immune and hematopoietic systems; Mutagenic effects to Salmonella and Schizosaccharomyces pombe and sister chromatid exchanges in hamster ovary cells; No evidence of delayed neurotoxicity in study with hens; [HSDB] The average of two baseline respective cholinesterase activity determinations three days apart, with no exposures to enzyme inhibiting pesticides for at least 30 days, is recommended for each worker prior to exposure to cholinesterase inhibitors because of large inter-individual differences in published baseline values. To be established at least once a year. Removal from workplace exposures is recommended until the cholinesterase activity returns to within 20% of baseline. [TLVs and BEIs] See Parathion.

Willems JL et al; Fate of Organophosphorus Compounds in Animals And Man. Naunyn-Schmiedemberg's Arch Pharmacol 330 (Suppl) (1985)

Govt Reports Announcements & Index (GR&I) 24: 172 (1985) NTIS/AD-A157 923/4

P041; As stipulated in 40 CFR 261.33, when paraoxon, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to federal and/or state hazardous waste regulations. Also defined as a hazardous waste is any container or inner liner used to hold this waste or any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5(e)).

Organophosphates are susceptible to formation of highly toxic and flammable phosphine gas in the presence of strong reducing agents such as hydrides. Partial oxidation by oxidizing agents may result in the release of toxic phosphorus oxides.

Paraoxon

Marine pollutant

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.

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]

If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped or safely confined. 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, carbon dioxide or dry chemical. /Organophosphorus pesticides, liquid, NOS/

If material on fire or involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) Use water in flooding quantities as fog. Use "alcohol" foam, carbon dioxide or dry chemical. /Organophosphorus pesticides, solid, NOS/

Pesticides containers must be provided with labels indicating the degree of toxicity of the product they contain. The labels must not only give a short description of how to use the prepn, but also state basic precautions to be taken when applying it. /Organophosphorus pesticides/

SMALL SPILLS AND LEAKAGE: If you spill this chemical, FIRST REMOVE ALL SOURCES OF IGNITION, then use absorbent paper to pick up liquid spill material. Your contaminated clothing and absorbent paper should be sealed in a vapor-tight plastic bag for eventual disposal. Solvent wash all contaminated surfaces with toluene followed by washing with a soap and water solution. Do no reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned.

Special aircraft should preferably be used for spraying or dusting toxic organophosphorus pesticides. ... aerial spraying or dusting gives rise to clouds which spread over larger surfaces than clouds produced by ground application. Aerial spraying should therefore be carried out on windless days only. Residential areas, water supply sources, etc must be avoided. ... When aircraft approaches, signalmen /guiding the aircraft/ should leave the windward side. ... The local population should be informed about the site & time of aerial pesticide treatment. Access of unauthorized persons & especially children to the area to be treated must be ... forbidden. Warning signs should be placed at the limits of the area. Ground spraying must be carried out with compressed-air spraying equipment towed by tractors with closed cabs. /Organophosphorus pesticides/

Small packages of pesticides are preferable for individual application in order to limit the quantities to be weighed & metered. A special vessel with long stirring rod for dilution & suspension of the poison must be available in order to reduce manual handling to a minimum. The strict observance of hygiene rules--no smoking & no food intake during work. Thorough washing with soap after work, changing protective clothing before going home--is of utmost importance. /Organophosphorus pesticides/

Containers ... should be cleaned with a suspension of bleaching powder in water or with other alkaline soln after soaking for 24 hr and then be rinsed with hot water. /Organophosphorus pesticides/

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 knock-down vapors. /Organophosphorus pesticides, liquid, NOS/

For more Preventive Measures (Complete) data for PARAOXON (8 total), please visit the HSDB record page.

MINIMUM PROTECTIVE CLOTHING: If Tyvek-type disposable protective clothing is not worn during handling of this chemical, wear disposable Tyvek-type sleeves taped to your gloves.

WORKERS HANDLING AND APPLYING ORGANOPHOSPHATE PESTICIDES (OPP) MUST ... BE GIVEN PERSONAL PROTECTIVE EQUIPMENT COMPRISING OVERALLS MADE OF A TIGHT FABRIC OR POLYVINYL CHLORIDE, GLOVES, AND RUBBER BOOTS. THEY MUST WEAR A RESPIRATOR WITH AN ACTIVATED-CARBON GAS FILTER CARTRIDGE AFFORDING PROTECTION FOR A DETERMINED NUMBER OF WORKING HOURS. THE EYES SHOULD BE PROTECTED BY GOGGLES. THE SIGNALMEN FOR AERIAL DUSTING OPERATIONS SHOULD BE EQUIPPED WITH A HAT AND CAPE MADE OF POLYVINYL CHLORIDE OR A FABRIC IMPREGNATED WITH A WATER REPELLENT. /PESTICIDES, ORGANOPHOSPHORUS/

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.

... PARAOXON INHIBITS THE METABOLISM OF BENZO(A) PYRENE IN VIVO.

... THE QUANTITATIVE IMPORTANCE OF NADPH-DEPENDENT O-DEALKYLATION OF ORGANOPHOSPHATE INSECTICIDES, EG PARAOXON ... MAY BE MODIFIED BY 1,1,1-TRICHLORO-2,2-BIS(P-CHLOROPHENYL)ETHANE OR 1,1-DICHLORO-2,2-BIS(P-CHLOROPHENYL)ETHENE.

Incubation of both parathion and chlorpyrifos at various concn with mouse hepatic microsomes resulted in the inhibition of production of paraoxon, p-nitrophenol, chlorpyrifos oxon, and 3,5,6-trichloro-2-pyridinol, which was characteristic of mixed type inhibition. This kinetic behavior could arise as a result of competitive interactions of parathion and chlorpyrifos with multiple forms of microsomal cytochrome p450.

Paraoxon (diethyl-p-nitrophenylphosphate) is the toxic, but non-mutagenic metabolite of the organophosphorus ester (OP) insecticide parathion. Although this agent has been used as a deacetylase inhibitor in many studies, we discovered a mutagenic synergy with paraoxon and plant-activated m-phenylenediamine or with direct-acting 2-acetoxyacetylaminofluorene in Salmonella typhimurium cells. In the present study, mammalian-activated m-phenylenediamine, o-phenylenediamine, p-phenylenediamine, benzidine, 2,3-diaminophenazine or 2-aminofluorene, as well as plant-activated benzidine or 2-aminofluorene expressed an elevated mutagenic potency when assayed with S. typhimurium strain YG1024 in the presence of paraoxon. Under non-toxic conditions, paraoxon amplified the S. typhimurium mutant yield induced by these aromatic amines between 1.9-fold and 8.4-fold. Spectrophotometric analysis demonstrated that the rate of degradation of 2-acetoxyacetylaminofluorene was not significantly different in phosphate buffer with or without paraoxon or with S. typhimurium cytosol with or without paraoxon. Also paraoxon-mediated mutagenic synergy does not appear to be due to a direct reaction with aromatic amines. Mutagenic synergy between aromatic amines and OP oxon products may be a cause of concern because people are chronically exposed to environmental and dietary aromatic amines, and a significant segment of the US population tested positive for OP insecticide residues.

For more Interactions (Complete) data for PARAOXON (7 total), please visit the HSDB record page.

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. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 48(SRC), determined from a water solubility of 3,640 mg/l at 20 °C(2) and a regression-derived equation(3), indicates that paraoxon is expected to have very high mobility in soil(SRC). Volatilization of paraoxon from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 6.4X10-10 atm-cu m/mole(SRC), using a fragment constant estimation method(4). Paraoxon is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 1.1X10-6 mm Hg at 25 °C(5). In mixed cultures, parathion was oxidized to paraoxon followed by enzymatic hydrolysis of paraoxon to p-nitrophenol and diethylphosphoric acid(6).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 48(SRC), determined from a water solubility of 3,640 mg/l(2) and a regression-derived equation(3), indicates that paraoxon is not expected to adsorb to suspended solids and sediment in water(SRC). Paraoxon is not expected to volatilize from water surfaces(3,SRC) based upon an estimated Henry's Law constant of 6.4X10-10 atm-cu m/mole(SRC), developed using a fragment constant estimation method(4). According to a classification scheme(5), an estimated BCF of 19(3,SRC), from a log Kow of 1.98(6), suggests the potential for bioconcentration in aquatic organisms is low(SRC). In mixed cultures, parathion was oxidized to paraoxon followed by enzymatic hydrolysis of paraoxon to p-nitrophenol and diethylphosphoric acid(7). All organophosphates were hydrolyzed by parathion hydrolase at rates 40 to 1,005 times faster than chemical hydrolysis(7). Hydrolysis half-lives of 173, 144, and 2.9 days were measured at pH values of 5.0, 7.4, and 9.0, respectively, at 20 °C(8).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), paraoxon, which has a vapor pressure of 1.1X10-6 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase paraoxon 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 9.9 hours(3,SRC). Particulate-phase paraoxon may be physically removed from the air by wet and dry deposition(SRC).

22 out of 25 samples of cow's milk, collected in Portugal from March to June 1991, had detectable levels of paraoxon at concns ranging from 1.5 to 8.7 ppb, average 3.6 ppb(1). In general, among the six groups of commercialized milk samples analyzed the paraoxon concn was higher in skim milk than in other milks, except in one group where fat milk had the highest level(1).

Paraoxon is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. 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. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.

Paraoxon was detected on spinach sprayed with parathion at rates of 1 and 0.5 lb/acre; paraoxon concns decreased from 0.252 to 0.082 ppm fresh weight 14 days after application at the rate of 1 lb/acre and 0.186 to 0.021 ppm fresh weight at the application rate of 0.5 lb/acre(1). Paraoxon was detected on lettuce sprayed with parathion at rates of 1 and 0.5 lb/acre; total paraoxon concns decreased from 0.026 to 0.019 ppm fresh weight 7 days after application at the rate of 1 lb/acre and 0.031 to 0.015 ppm fresh weight at the application rate of 0.5 lb/acre(2).

Symptoms of low dose exposure include excessive salivation and eye-watering. Acute dose symptoms include 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. Hypertension, hypoglycemia, anxiety, headache, tremor and ataxia may also result.

Workers handling & applying pesticides must undergo an annual medical examination at the beginning of each agricultural season. Contraindications /meaning further clinical evaluations/ for work with /organophosphorus pesticides/ are organic diseases of the central nervous system, mental disorders & epilepsy, pronounced endocrine & vegetative disorders, pulmonary tuberculosis, bronchial asthma, chronic respiratory diseases, cardiovascular diseases & circulatory disorders, gastrointestinal diseases (peptic ulcer), gastroenterocolitis, diseases of liver & kidneys, eye diseases (chronic conjunctivitis & keratitis). The blood cholinesterase activity must be determined before work starts. In the event of prolonged work periods, this activity should be determined at intervals of 3-4 days. Persons exhibiting a fall in cholinesterase activity of 25% or more must be transferred to other work where they are not exposed to organophosphorus pesticides until this activity is completely restored. Persons with initial signs of indisposition should /be protected from exposure from/ pesticides. /Organophosphorus pesticides/

... Surveillance of workers could be carried out through measurement of blood or urinary levels of the cmpd to which they are exposed, or through measurement of a metabolite. /Organic phosphorus pesticides/

Freundlich constants ranging from 0.02 to 20.5 were measured in eight soils; the highest value occurred in Pellic vertisol, 0.77% organic matter, 62.0% clay, 16% smectite(1). Adsorption coefficients of 53.7, 42.9, and 81.7 were measured on Na-montmorillonite, Ca-montmorillonite, and Fe-montmorillonite, respectively(2). The Koc of paraoxon is estimated as approximately 48(SRC), using a water solubility of 3,640 mg/l at 20 °C(3) and a regression-derived equation(4,SRC). According to a classification scheme(5), this estimated Koc value suggests that paraoxon is expected to have very high mobility in soil(SRC).

P041; As stipulated in 40 CFR 261.33, when paraoxon, as a commercial chemical product or manufacturing chemical intermediate or an off-specification commercial chemical product or a manufacturing chemical intermediate, becomes a waste, it must be managed according to federal and/or state hazardous waste regulations. Also defined as a hazardous waste is any container or inner liner used to hold this waste or any residue, contaminated soil, water, or other debris resulting from the cleanup of a spill, into water or on dry land, of this waste. Generators of small quantities of this waste may qualify for partial exclusion from hazardous waste regulations (40 CFR 261.5(e)).

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 100 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

S - Sensory organs

QS - Sensory organs

Direct inhibitors, such as paraoxon, are capable of reacting directly with the cholinesterase enzymes thereby inactivating them.

Parathion is converted in the body in part to paraoxon, a strong inhibitor of the enzyme acetyl cholinesterase. Upon inhibition of this enzyme in the tissues, acetylcholine, the substance responsible for transmission of nerve impulses in much of the nervous system, accumulates, producing an initial overstimulation and subsequent blockage of nerve stimuli.

The main feature of the toxic mechanism of organophosphorus pesticides is inhibition of the esterase enzyme activity, in particular of cholinesterase, which plays an important physiological part. Organophosphorus pesticides can also indirectly interact with the biochemical receptors of acetylcholine. /Organophosphorus pesticides/

Hydrolysis and covalent binding to nonessential esterases are two biochemical processes which can prevent paraoxon from reacting with essential enzyme, acetylcholinesterase. Both processes have been proposed as the primary route of paraoxon detoxification in vivo. These experiments were designed to assess the relative contribution of each pathway to the disappearance of paraoxon in the rabbit. In vitro, paraoxon disappeared from whole rabbit blood with a half-life of 17.7 sec. Hydrolysis by paraoxonase accounted entirely for this disappearance and covalent binding contributed essentially nothing. In vivo, following an iv injection of 0.15 mg/kg paraoxon, serum paraoxonase hydrolyzed as much as 41% of the injected dose within the first 30 sec. Pretreatment of rabbits with an ip injection of tri-o-tolyl phosphate eliminated more than 95% of the paraoxon binding sites. However, pretreatment with tri-o-tolyl phosphate had no significant effect on the half-life or volume of distribution of paraoxon, indicating that covalent binding sites did not contribute significantly to the clearance of paraoxon from whole rabbits under these conditions. Hydrolysis of paraoxon by tissue paraoxonases, in addition to that catalyzed by paraoxonase in the blood, could account for its rapid metabolism. These findings demonstrate that paraoxonase has a major role in the disappearance of paraoxon in the rabbit. This suggests that susceptibility of people to chronic paraoxon poisoning may vary, according to their inherited level and type of serum paraoxonase.

THE MAJOR URINARY METABOLITES /FOLLOWING ORAL DOSE OF (14)CARBON-PARAOXON TO MALE ALBINO RATS/ ... WERE DIETHYL PHOSPHATE (ABOUT 60%) AND DE-ETHYL-PARAOXON (6-7%).

... THE DEALKYLATION OF PARAOXON TO DE-ETHYL-PARAOXON OBSERVED IN THE METABOLISM OF BOTH PARAOXON AND PARATHION IN VIVO HAS BEEN SHOWN TO BE CATALYZED BY CYTOCHROME P450 DEPENDENT MONO-OXYGENATION.

YIELDS 4-AMINOPHENYL DIETHYL PHOSPHATE IN RAT, GUINEA PIG, CHICKEN & SPARROW. /FROM TABLE/

YIELDS PARA-NITROPHENYL IN PIG; IN RAT & GUINEA PIG; IN MAN & IN SHEEP. /FROM TABLE/

For more Metabolism/Metabolites (Complete) data for PARAOXON (11 total), please visit the HSDB record page.

Paraoxon is a known human metabolite of parathion.

Drugs that inhibit cholinesterases. The neurotransmitter ACETYLCHOLINE is rapidly hydrolyzed, and thereby inactivated, by cholinesterases. When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. Cholinesterase inhibitors are widely used clinically for their potentiation of cholinergic inputs to the gastrointestinal tract and urinary bladder, the eye, and skeletal muscles; they are also used for their effects on the heart and the central nervous system.

Pesticides designed to control insects that are harmful to man. The insects may be directly harmful, as those acting as disease vectors, or indirectly harmful, as destroyers of crops, food products, or textile fabrics.

... SLICES OF RABBIT SKIN HYDROLYZE PARAOXON AT A CONCN OF 7.7X10-3 MOL TO THE EXTENT OF 20% IN 1 HR PER G OF TISSUE. SINCE ABSORPTION OF PARAOXON ... IS SLOW.

On the basis of radioautographic studies in man and animals, it appears that skin absorption is transepidermal. The rate of dermal absorption /of paraoxon/ in the rabbit is 0.059 ug/min/cu m. The animals exhibit about a tenfold individual variation in permeability of the skin.

FEMALE RATS ... EXCRETED A HIGHER PERCENTAGE (63%) OF (14)C IN THE URINE THAN MALES (53%) PER DAY AFTER AN ORAL DOSE OF (14)C-PARAOXON ...

Effect of pregnancy & lactation on distribution of parathion & paraoxon in mice was examined. Pregnant mice treated with 5 mg/kg of parathion demonstrated higher concn of both parathion & paraoxon in blood & brain than controls which correlated with the enhanced cholinesterase inhibition in pregnant animals.

For more Absorption, Distribution and Excretion (Complete) data for PARAOXON (10 total), please visit the HSDB record page.

Used as insecticide; [Merck Index] A metabolite of the pesticide parathion (formed by microbial degradation, chemical oxidation, irradiation, and conversion in air promoted by sunlight); Formerly used to treat glaucoma; [HSDB]

Not registered for use as pesticide in the US; [HSDB]

Farming (Pesticides) [Category: Industry]

MEDICATION

ACTION: Insecticide. Not registered for use in the U.S.

PREPARED BY ACTION OF DIETHYL CHLOROPHOSPHATE ON SODIUM PARA-NITROPHENOLATE OR BY NITRATION OF DIETHYL PHENYL PHOSPHATE: SCHRADER, BIOS FINAL REPT 714: 52 (1947); ANGEW CHEM 62: 471 (1950); SWISS PATENT NUMBER 257,649 (1949); FAGERLIND ET AL, SVENSK FARM TID 56, 303, CA 46, 9259.