チオりん酸O-(4-ブロモ-2-クロロフェニル)O-エチルS-プロピル

Insecticides

Active substance -> EU Pesticides database: Not approved

Pesticides -> Organophosphate Insecticides

Pesticide (Profenofos) -> USDA PDB

Pesticide

log Kow = 4.68

4.44

Pale yellow liquid

Amber color, oily liquid

Readily miscible with most organic solvents.

In water, 28 mg/l @ 25 °C

When heated to decomposition it emits very toxic /sulfur oxides, phosphorus oxides, hydrogen bromide, & hydrogen chloride/.

... On hydrolysis DT50 (calculated) (20 °C) 93 day (pH 5), 14.6 days (pH 7), 5.7 hr (pH 9).

0.0000009 [mmHg]

9.00X10-7 mm Hg @ 25 °C

Profenofos is a pale yellow liquid with garlic-like odor. Corrosive. Used as an insecticide.

Pale yellow or amber liquid with an odor like garlic; [HSDB]

Warning

H302: Harmful if swallowed [Warning Acute toxicity, oral]

P261, P264, P270, P271, P273, P280, P301+P317, P302+P352, P304+P340, P317, P321, P330, P362+P364, P391, and P501 (click each P-code to see the statement)

Danger

H302+H312+H332 (34.8%): Harmful if swallowed, in contact with skin or if inhaled [Warning Acute toxicity, oral; acute toxicity, dermal; acute toxicity, inhalation]

P261, P262, P264, P270, P271, P272, P273, P280, P301+P317, P302+P352, P304+P340, P316, P317, P321, P330, P333+P317, P361+P364, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Regulation (EC) No 1107/2009 (amended)

Profenofos is listed in the dataset of EPA Human Health Benchmarks for Pesticides under the Safe Drinking Water Act (40 eCFR 141)

2002/2076

REACH registered substance: O-(4-bromo-2-chlorophenyl) O-ethyl S-propyl phosphorothioate (EC: 255-255-2)

A human cholinesterase inhibitor; Caused morphological changes and decrease in count and motility to mice sperm after five days of dosing; Liver function affected by acute and sub-chronic dosing in rabbits based on enzyme testing; [HSDB] Lower ratio of symptomatic human poisoning cases reported per pound of usage than other cholinesterase inhibiting pesticides; [Reference #1] 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]

Tolerances are established for combined residues of the insecticide profenofos (O-(4-bromo-2-chlorophenyl)-O-ethyl-S-propyl phosphorothioate and its metabolites converted to 4-bromo-2-chlorophenyl and calculated as profenofos in or on the following food commodities: cattle, fat; cattle, mbyp; cattle, meat; cottonseed; cottonseed hulls; eggs; goats, fat; goats, mbyp; goats, meat; hogs, fat; hogs, mbyp; hogs, meat; horses, fat; horses, mbyp; horses, meat; milk; poultry, fat; poultry, mbyp; poultry, meat; sheep, fat; sheep, mbyp; sheep, meat.

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.

Cord, detonating, flexible

UN0065

Div 1.1 Explosives (with a mass explosion hazard) (49 eCFR § 173.50)

Cord, detonating, flexible

UN0289

Div 1.4 Explosives (with no significant blast hazard) (49 eCFR § 173.50)

Acute Tox. 4 (100%)

Acute toxicity - category 4

Acute toxicity (Oral) - Category 4

Acute Tox. 4 *

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.

Tolerances are established for combined residues of the insecticide profenofos (O-(4-bromo-2-chlorophenyl)-O-ethyl-S-propyl phosphorothioate and its metabolites converted to 4-bromo-2-chlorophenyl and calculated as profenofos in or on the following food commodities: cattle, fat: 0.05 ppm; cattle, mbyp: 0.05 ppm; cattle, meat: 0.05 ppm; cottonseed: 3.0 ppm; cottonseed hulls: 6.0 ppm; eggs: 0.05 ppm; goats, fat: 0.05 ppm; goats, mbyp: 0.05 ppm; goats, meat: 0.05 ppm; hogs, fat: 0.05 ppm; hogs, mbyp: 0.05 ppm; hogs, meat: 0.05 ppm; horses, fat: 0.05 ppm; horses, mbyp: 0.05 ppm; horses, meat: 0.05 ppm; milk: 0.01 ppm; poultry, fat: 0.05 ppm; poultry, mbyp: 0.05 ppm; poultry, meat: 0.05 ppm; sheep, fat: 0.05 ppm; sheep, mbyp: 0.05 ppm; sheep, meat: 0.05 ppm.

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.

... Five OP pesticides inhibit 50% of the brain fatty acid amide hydrolysis activity (ED50) at <30 mg/kg 4 hr after ip administration to mice; while inhibition by chlorpyrifos, diazinon, and methamidophos occurs near acutely toxic levels, and profenofos and tribufos are effective at asymptomatic doses. ... Fatty acid amide hydrolysis inhibition of > or =76% in brain depresses movement of mice administered anandamide at 30 mg/kg ip, often leading to limb recumbency. Thus, OP pesticides and related inhibitors of fatty acid amide hydrolysis potentiate the cannabinoid activity of anandamide in mice.

... Mixtures of atropine with eserine, pyridinium oximes, or the bispyridinium compound SAD-128 increased the LD50 of coadministered profenofos by up to sevenfold in chicks and fourfold in mice. Atropine and the oximes were less effective as profenofos antidotes, indicating that profenofos-inhibited AChE may undergo rapid aging. Brain AChE from chicks poisoned with profenofos was not reactivated by pralidoxime methanesulfonate, although it was from chicks poisoned with the phosphoramidothiolate, methamidophos. Similarly, eel AChE, inhibited in vitro by bioactivated (-)-profenofos, the most toxic isomer, did not reactivate in contrast to that inhibited by methamidophos, nonbioactivated (-)-profenofos, and (+)-profenofos, with or without bioactivation.

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), Koc values in soil ranging from 869 to 3,162(2) indicate that profenofos is expected to have low to slight mobility in soil(SRC). Volatilization of profenofos from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.2X10-8 atm-cu m/mole(SRC), derived from its vapor pressure, 9.00X10-7 mm Hg(3), and water solubility, 28.0 mg/l(3). Profenofos is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 9.00X10-7 mm Hg(3). Profenofos metabolizes rapidly under alkaline aerobic conditions(2). In an alkaline (pH 7.8) soil, propenofos degraded with a half-life of 2 days(2). The rate of metabolism is influenced by chemical hydrolysis and aerobic metabolism in neutral and acid soils is likely to be slower(2). Profenofos also metabolizes rapidly under alkaline anaerobic conditions(2). In alkaline (pH 7.8) soil, profenofos degraded with a half-life of 3 days under anaerobic conditions(2).

AQUATIC FATE: Based on a classification scheme(1), Koc values in soil ranging from 869 to 3,162(2), indicate that profenofos 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 2.2X10-8 atm-cu m/mole(SRC), derived from its vapor pressure, 9.00X10-7 mm Hg(4), and water solubility, 28.0 mg/l(4). According to a classification scheme(5), BCF values in fish of 29 (body), 45 (head), and 682 (viscera)(6), suggests the potential for bioconcentration in aquatic organisms moderate to high(SRC). Hydrolysis half-lives of profenofos are 104-108 days, 24-62 days, and 0.33 days for pHs 5, 7, and 9, respectively(2). Profenofos is stable to photolysis in water(2). Profenofos metabolizes rapidly under alkaline aerobic conditions(2). In an alkaline (pH 7.8) soil, profenofos degraded with a half-life of 2 days(2). The rate of metabolism is influenced by chemical hydrolysis and aerobic metabolism under neutral and acid conditions is likely to be slower(2). Profenofos also metabolizes rapidly in alkaline anaerobic conditions(2). In alkaline (pH 7.8) soil, profenofos degraded with a half-life of 3 days under anaerobic conditions(2). The field dissipation half-life for profenofos averaged 9 days (range, 6.3-8 days)(7).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), profenofos, which has a vapor pressure of 9.00X10-7 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere(SRC). Vapor-phase profenofos 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 8.6 hrs(SRC), calculated from its rate constant of 4.5X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase profenofos may be removed from the air by wet and dry deposition(SRC). Profenofos is stable toward direct photolysis(4).

Between the years 1987-1989, the concn level of profenofos residues in various vegetables from Thailand was 0.11 mg/kg(1). Between the years 1985-1991, the max concn of profenofos in one of 2,464 samples of apples from the USA was 0.08 ppm(2). In Denmark, profenofos was detected in 1 of 19 samples of spring onions between the years 1995-1996(3). In Egypt in the year 1995, profenofos was detected in 1 of 62 samples of tomatoes at a mean concn of 0.72 mg/kg (range, 0.04-2 mg/kg)(4).

Profenofos 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.

Between the years 1984-1986, the mean daily intake per unit body weight (ug/kg body wt/day) of profenofos was measured for the following age groups: 6-11 mo (<0.0001), 2 yr (0.0001), 14-16 yr female (<0.0001), 14-16 yr male (<0.0001), 25-30 yr female (<0.0001), 25-30 yr male (<0.0001), 60-65 yr female (<0.0001), and 60-65 yr male (<0.0001)(1).

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.

Tolerances are established for combined residues of the insecticide profenofos (O-(4-bromo-2-chlorophenyl)-O-ethyl-S-propyl phosphorothioate and its metabolites converted to 4-bromo-2-chlorophenyl and calculated as profenofos in or on the following food commodities: cattle, fat; cattle, mbyp; cattle, meat; cottonseed; cottonseed hulls; eggs; goats, fat; goats, mbyp; goats, meat; hogs, fat; hogs, mbyp; hogs, meat; horses, fat; horses, mbyp; horses, meat; milk; poultry, fat; poultry, mbyp; poultry, meat; sheep, fat; sheep, mbyp; sheep, meat.

Metabolism of organophosphates occurs principally by oxidation, by hydrolysis via esterases and by reaction with glutathione. Demethylation and glucuronidation may also occur. Oxidation of organophosphorus pesticides may result in moderately toxic products. In general, phosphorothioates are not directly toxic but require oxidative metabolism to the proximal toxin. The glutathione transferase reactions produce products that are, in most cases, of low toxicity. Paraoxonase (PON1) is a key enzyme in the metabolism of organophosphates. PON1 can inactivate some organophosphates through hydrolysis. PON1 hydrolyzes the active metabolites in several organophosphates insecticides as well as, nerve agents such as soman, sarin, and VX. The presence of PON1 polymorphisms causes there to be different enzyme levels and catalytic efficiency of this esterase, which in turn suggests that different individuals may be more susceptible to the toxic effect of organophosphate exposure.

... The levels of profenofos in whole blood, urine, and gastric contents were 1200 ng, 350 ng, and 3.35 mg/mL, respectively.

Rats rapidly excrete 14C-profenofos after oral admin. The predominant metabolic pathway involves stepwise dealkylation & hydrolysis, followed by conjugation.

Used as insecticide and acaricide for cotton and vegetables; [Merck Index] Only used on cotton in the US; [Reference #1]

A restricted use pesticide in the US; [Reference #1]

Farming (Pesticides) [Category: Industry]

For Profenofos (USEPA/OPP Pesticide Code: 111401) 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./

Control of insects (particularly Lepidopetera) and mites.

Acaricide

USEPA/OPP Pesticide Code 111401; Trade Names: Curacron, CGA-15324, Selecron, Polycron.

Emulsifiable concentration, ultra low volume (ULV) liquid

Mixture (profenofos +) cypermethrin; deltramethrin