化合物详情

Pesticide Ecotoxicity Data from EPA: 38

USDA APHIS Chemical Effects: collection=usda_chemeffect&query_type=synonym&query='^22224-92-6$'

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), fenamiphos, which has a vapor pressure of 9.0X10-6 mm Hg at 20 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase fenamiphos 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 5 hours(SRC), calculated from its rate constant of 7.8X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase fenamiphos may be removed from the air by wet or dry deposition(SRC). When exposed to natural sunlight on soil, fenamiphos photodegrades with a half-life of 3.23 hrs(4), indicati...

Leaching of fenamiphos was studied using two soil columns, one containing a sandy loam soil (organic carbon 1.1%; pH 7.4) and the other a clay loam soil (organic carbon 2.8%; pH 7.6)(1). Retention was greater in the clay loam soil, resulting in a greater conversion of fenamiphos to its thiooxidized forms(1). Results of column leaching studies indicate that fenamiphos was relatively mobile with 16.2 to 63.8% of applied radioactivity found in leachate(2). The major metabolites, fenamiphos sulfoxide and fenamiphos sulfone, were more mobile than the parent(2). The greatest mobility of fenamiphos and its metabolites was in soil with the lowest cation exchange capacity and lowest percentage of organic matter (sand soil for Indiana) whereas the lowest mobility of fenamiphos and its metabolites...

ANAEROBIC: Fenamiphos, applied at a rate of 13.3 ppm to a Howe sandy loam soil, was incubated for 6 days under aerobic conditions followed by 60 days incubation under anaerobic conditions(1). Fenamiphos declined from 36.3% of the applied amount on day zero of anaerobic incubation (following the 6-day aerobic incubation) to 21.8% after 60 days of anaerobic incubation with a half-life of 87.9 days(1). The major metabolite was fenamiphos sulfoxide(1). Other reported metabolites were fenamiphos sulfone, 4-(methylthio)-m-cresol (MTMC), 4-(methylsulfonyl)-m-cresol (MTMC-sulfone), and 3-methyl-4-(methylsulfonyl)-anisole(1).

Fenamiphos does not bioaccumulate in fish (species non-specified) to any appreciable extent and any residues taken up by fish are quickly depurated when fish are no longer exposed to the residues(1). After 28 days of exposure, the avg measured BCF were 21 and 61 for fillet and whole fish, respectively(1). The maximum BCF measured for fenamiphos residues were 89 for whole fish and 24 for fillet tissue(1). During the 14-day depuration period, more than 95% of the accumulated 14C-fenamiphos residues depurated(1). According to a classification scheme(2), BCFs ranging from 21 to 89(1) suggest that for bioconcentration in aquatic organisms is moderate(SRC). A BCF for fenamiphos of 468 was measured in earthworms(3).

The Henry's Law constant for fenamiphos is estimated as 9.0X10-9 atm-cu m/mole(SRC) derived from its vapor pressure, 9.0X10-6 mm Hg(1), and water solubility, 400 mg/L(1). This Henry's Law constant indicates that fenamiphos is expected to be essentially nonvolatile from moist soil and water surfaces(2). Fenamiphos is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1). When applied at a rate of 12 lbs of active ingredient/acre to a sandy loam soil, <0.1% of the fenamiphos volatilized after 7 days indicating that fenamiphos does not volatilize rapidly from soil(3).

The rate constant for the vapor-phase reaction of fenamiphos with photochemically-produced hydroxyl radicals has been estimated as 7.8X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 5 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Fenamiphos was found to be stable in acidic and neutral buffer solutions at 5 and 22 °C while dissipation was rapid at 50 °C(2). The hydrolysis half-lives for fenamiphos at 32 °C and pH 4.1, 7.1, and 9.1 were 228, 5310, and 37 hrs, respectively(2). When exposed to natural sunlight, fenamiphos photodegrades on soil with a half-life of 3.23 hrs(3). The radioactive components identified from the exposed soil samples were fenamiphos sulfoxide and...

RAIN/SNOW/FOG: Fenamiphos was not detected (detection limit not reported) in rain water samples from Achaia Perfecture, Greece, sampled Mar to Sept 2006; four sites were sampled, Patras and Rio (urban), and Aigio and Sympolitia (rural)(1).

Fenamiphos was not detected (detection limit 0.025 mg/kg) in 17 store-bought egg samples(1).

Fenamiphos was not detected (detection limit 0.025 mg/kg) in 20 milk samples(1).

The substance is very toxic to aquatic organisms. Avoid release to the environment in circumstances different to normal use.

RURAL/REMOTE: Fenamiphos was not detected (detection limit 0.0093 ug/cu m) in 92 rural community samples taken from 1986 to 2000 in California(1).

Fenamiphos was not detected (detection limit 0.025 mg/kg) in 17 fish samples. However, fenamiphos sulfone, a degradation product of fenamiphos was detected in fish at 0.057 mg/kg(1).

Fenamiphos' former production may have resulted in its release to the environment through various waste streams; its former use as an nematicide(1) may have resulted in its direct release to the environment(SRC). Fenamiphos use was cancelled for extremely vulnerable soils (excessively drained and predominantly sand or loamy sand)) and shallow water tables as of May 31, 2005. A five year phase out for other products began May 31, 2003 and was to be completed by May 31, 2008. An amendment to this ruling gave exception to Nemacur 10% turf and ornamental nematicide and Nemacur 3 Emulsifiable Systemic Insecticide-Nematicide which would be phased out by Nov 30, 2008(2).

Occupational exposure to fenamiphos may occur through inhalation and dermal contact with this compound at workplaces where fenamiphos was produced or used. Monitoring data indicate that the general population may be exposed to fenamiphos via ingestion of drinking water, and dermal contact with products containing fenamiphos(SRC). However, fenamiphos use in the US was cancelled for extremely vulnerable soils and shallow water tables as of May 31, 2005(1). A five year phase out for other products began May 31, 2003 and was to be completed by May 31, 2008. An amendment to this ruling gave exception to Nemacur 10% turf and ornamental nematicide and Nemacur 3 Emulsifiable Systemic Insecticide-Nematicide which would be phased out by Nov 30, 2008(1). This indicates that exposure, both occupati...

Fenamiphos' former US production may have resulted in its release to the environment through various waste streams; its former US use as an nematicide may have resulted in its direct release to the environment. In the US, fenamiphos use was to be completely phased out by Nov 30, 2008. If released to air, a vapor pressure of 9.0X10-6 mm Hg at 20 °C indicates fenamiphos will exist in both the vapor and particulate phases in the atmosphere. Vapor-phase fenamiphos 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 5 hours. Particulate-phase fenamiphos will be removed from the atmosphere by wet or dry deposition. When exposed to natural sunlight on soil, fenamiphos photodegrades with a half...

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.

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.

Male mice were treated orally with the organophosphorus insecticides fenamiphos and dichlorvos at 10 and 150 mg/kg respectively. The insecticides produced signs of toxicosis characteristic of cholinesterase inhibition and induced death in all treated mice. Pretreatment of mice with diphenhydramine HCl (20 and 30 mg/kg subcutaneously 15 min. before either insecticide significantly (P < 0.05) reduced the incidence of toxic manifestations (excessive salivation, Straub tail, and whole body tremor), delayed the onset of death and increased the percentage of survivors. Doses of diphenhydramine less than 20 mg/kg were not so effective. The data indicated a protective property of diphenhydramine against organophosphorus insecticide-induced toxicosis.

respiratory system, central nervous system, cardiovascular system, blood cholinesterase

LC50 (rat) = 91 mg/m3/4h

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...

ACGIH Carcinogen - Not Classifiable.

inhalation, skin absorption, ingestion, skin and/or eye contact

Fenamiphos 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...

Oral Chronic Reference Dose Reference: IRIS Current

Oral RfD: 0.00025 mg/kg/day (UF: 100, MF: 1)

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

Fraction of Contaminant Absorbed Dermally from Soil: 0.1

A4; Not classifiable as a human carcinogen.

Fraction of Contaminant Absorbed Dermally from Soil: 0.1

Reference: Smith, C.D. and Nowell, L.H., 2024. Health-Based Screening Levels for evaluating water-quality data (3rd ed.). DOI:10.5066/F71C1TWP