Isofenphos

345.39

345.39

246-814-1

3018|2902

DTXSID8032417

2929909012

88.9

4.12

1.131 g/cm³ @ Temp: 20 °C

<-12 °C

120 °C @ Press: 0.01 Torr

202.7±29.3 °C

1.528

In water, 0.0221 mg/mL at 20 °C

0-6°C

2.2 x 10 -4 Pa (20 °C)

Oral-rat LD50: 28 mg/kg; Oral-Mouse LD50: 91.3 mg/kg

Open flame is flammable; heat releases toxic phosphorus oxide, nitrogen oxide, sulfur oxide gas

Characteristic

Henry's Law constant= 4.15X10-8 atm cu-m/mol @ 20 °C

Colorless oil /Technical/

Hydrolyzed by alkali solution.

Amines, Phosphines, and Pyridines

Organothiophosphates, such as ISOFENPHOS, 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.

I

6.1(a)

3018

2

24/25-50/53-52/53-36-20/21/22-11

36/37-45-60-61-26-16

VO4395500

T,N,Xn,F

The warehouse is ventilated, low temperature and dry; stored and transported separately from food materials

Photodegradation on soil surface in the laboratory is extremely rapid. Under natural light, photodegradation is not so fast.

P210-P273-P280-P305 + P351 + P338

H225-H302 + H312 + H332-H319-H412

Excerpt from ERG Guide 152 [Substances - Toxic (Combustible)]: Combustible material: may burn but does not ignite readily. Containers may explode when heated. Runoff may pollute waterways. Substance may be transported in a molten form. (ERG, 2016)

|Danger|H301: Toxic if swallowed [Danger Acute toxicity, oral]|P264, P270, P273, P280, P301+P310, P302+P352, P312, P321, P322, P330, P361, P363, P391, P405, and P501|H301+H311 (92.68%): Toxic if swallowed or in contact with skin [Danger Acute toxicity, oral; acute toxicity, dermal]|P260, P264, P270, P271, P273, P280, P284, P301+P310, P302+P352, P304+P340, P310, P312, P320, P321, P322, P330, P361, P363, P391, P403+P233, P405, and P501|Aggregated GHS information provided by 41 companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H300: Fatal if swallowed [Danger Acute toxicity, oral]|P201, P202, P260, P262, P264, P270, P271, P280, P281, P284, P301+P310, P302+P350, P304+P340, P305+P351+P338, P307+P311, P308+P313, P310, P314, P320, P321, P322, P330, P332+P313, P337+P313, P361, P363, P403+P233, P405, and P501

Excerpt from ERG Guide 152 [Substances - Toxic (Combustible)]: SMALL FIRE: Dry chemical, CO2 or water spray. LARGE FIRE: Water spray, fog or regular foam. Move containers from fire area if you can do it without risk. Dike fire-control water for later disposal; do not scatter the material. Use water spray or fog; do not use straight streams. FIRE INVOLVING TANKS OR CAR/TRAILER LOADS: Fight fire from maximum distance or use unmanned hose holders or monitor nozzles. Do not get water inside containers. Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire. For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn. (ERG, 2016)

Excerpt from ERG Guide 152 [Substances - Toxic (Combustible)]: As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

Excerpt from ERG Guide 152 [Substances - Toxic (Combustible)]: ELIMINATE all ignition sources (no smoking, flares, sparks or flames in immediate area). Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Cover with plastic sheet to prevent spreading. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS. (ERG, 2016)

Excerpt from ERG Guide 152 [Substances - Toxic (Combustible)]: Wear positive pressure self-contained breathing apparatus (SCBA). Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection. Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible. (ERG, 2016)

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./|The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials.|The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article.

SEDIMENT: In Florida, isofenphos was not detected (limits of detection ranging from 1.2 to 36 mg/kg, dry weight) in 68 sediment samples taken from lakes, estuaries, streams and outflows(1).

URBAN/SUBURBAN: The concn of isofenphos in ambient air from Kitakyushu, Japan was 10 ng/cu m in July 1991 and 0.73 ng/cu m in April 1992(1).

The concentration of isofenphos was 210 and 380 ng/g in house dust from two New Jersey homes in 1991(1); isofenfos was not detected in indoor air in these homes(1).

most toxic

LD50 Rat oral 28 mg/kg|LD50 Rat skin 188 mg/kg|LD50 Mouse oral 91,300 ug/kg (91.3 mg)|LD50 Rabbit skin 162 mg/kg|For more Non-Human Toxicity Values (Complete) data for ISOFENPHOS (7 total), please visit the HSDB record page.

Isofenphos' former(1) production may have resulted in its release to the environment through various waste streams; its former use as an insecticide on crops and turf grass(2) resulted in its direct release to the environment(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), Koc values from 633 to 1,474 on four soils(2) indicate that isofenphos is expected to have low mobility in soil(SRC). Volatilization of isofenphos from moist soil surfaces is not expected to be an important fate process(SRC) given a Henry's Law constant of 4.15X10-8 atm-cu m/mole(3). Isofenphos is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 3.00X10-6 mm Hg(4). Isophenophos degrades on soil exposed to light with a half-life of 72 days(2). In a week-long incubation study using 6 soils with a history of isofenphos use and 19 soils with no previous use, an increased rate of mineralization in the soils with previous use history (35.9 +/- 2.4% of the parent mineralized to CO2) was found compared with the nonhistory soils (2.4+/-1.0%)(2). In a 4-week incubation study, 62.8% of the parent was recovered from a soil with no history of use and only 12.9% from a soil that was previously treated with isofenphos(2). Mineralization of the aromatic ring was evident(2). Isofenphos oxygen analog (also called isofenphos oxon) was identified as degradation product(2).|TERRESTRIAL FATE: In turf plots in Georgia and Minnesota and soil plots in Georgia and California, isofenphos dissipated from the upper 6 inches of soil with first-order half-lives of 7 to 81 days and DT50s (the time in which 50% of the pesticide dissipates from the surface of the soil) ranging from 10 to 63 days(1). In California, a rapid initial dissipation (half-life = 7 days) was followed by a plateau and a secondary dissipation half-life of >63 days(1). When both isofenphos and the structurally-similar oxon analog are considered together, the dissipation half-lives range from 21 to 170 days(1). The studies only tracked isofenphos and the formation of its oxygen analog, but did not evaluate the formation of other degradates (including volatiles) or incorporation/ binding within the soil(1). The pesticide use history was unknown in the Georgia turf and soil plots(1). Isofenphos use was not reported in the previous 5 years on the other sites(1). Supplemental field studies covering 23 sites reported dissipation half-lives ranging from less than 2 weeks to more than 1 year, depending on factors such as formulation, location, and number of applications(1). Isofenphos and its oxygen analog were not detected below 12 inches in the Georgia and Minnesota turf studies or below 6 inches in the Georgia bareground study(1). Isofenphos was detected to 18 inches and the oxygen analog to 30 inches in the California bareground study(1). The soils in the California study had a much lower organic matter content (<0.5%) than did the other three sites(1). The results suggest that while isofenphos is not highly mobile through the soil profile, under certain conditions it may move into the subsurface(1).|AQUATIC FATE: Based on a classification scheme(1), Koc values from 633 to 1,474 on four soils(2) indicate that isofenphos is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(SRC) based upon a Henry's Law constant of 4.15X10-8 atm-cu m/mole(3). According to a classification scheme(4), BCF values in fish tissues of 94.5 (fillet), 469 (viscera), and 277 (whole body)(2), suggests bioconcentration in aquatic organisms is high(SRC). Isophenphos is stable to hydrolysis at pHs 5 and 7 and degrades slowly at pH 9 with a half-life of 131 days(2). Isophenophos is stable to photolysis in water(2). Using non- sterilized, filtered river water at pH 7.3, isofenphos degraded in 97 and 175 days at 22 and 6 °C, respectively(5). In seawater at pH 8.1, isofenphos degraded in 118 and 224 days at 22 and 6 °C, respectively(5). In filtered estuarine water (pH 7.8, salinity 20 g/l) from the Ebre River, Spain, the degradation half-life for isofenphos ranged from 9.8-11.9 days(6).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), isofenphos, which has a vapor pressure of 3.00X10-6 mm Hg at 25 °C(2), will exist in both the vapor and particulate phases in the ambient atmosphere(SRC). Vapor-phase isofenphos 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 1.4 hrs(SRC), calculated from its rate constant of 2.75X10-10 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase isofenphos may be removed from the air by wet and dry deposition(SRC).

Photodegradation on soil surface in the laboratory is extremely rapid. Under natural light, photodegradation is not so fast.|The rate constant for the vapor-phase reaction of isofenphos with photochemically-produced hydroxyl radicals has been estimated as 2.75X10-10 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 1.4 hrs at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Isophenphos is stable to hydrolysis at pHs 5 and 7 and degrades slowly at pH 9 with a half-life of 131 days(2). At pH 6.1, isophenphos degraded in ultrapure water in 174 and 265 days at 22 and 6 °C, respectively(3). Isophenophos is stable to photolysis in water but degrades on soil exposed to light with a half-life of 72 days(2). In the presence of photosensitizers found in both river and seawater, photolysis half-lives in these waters were 21 and 19 days, respectively(3).

131.83|BCFs of 94.5 (fillet), 469 (viscera), and 277 (whole body) in fish tissues were measured for isofenphos(1). According to a classification scheme(2), these BCF values suggests the potential for bioconcentration in aquatic organisms is high(SRC).

602.56 L/kg|The Koc of isofenphos ranged from 633 to 1,474 on four soils(1). According to a classification scheme(2), these Koc values suggest that isofenphos is expected to have low mobility in soil(SRC).

The Henry's Law constant for isofenphos is 4.15X10-8 atm-cu m/mole(1). This Henry's Law constant indicates that isofenphos is expected to be essentially nonvolatile from water surfaces(2). Isofenphos is not expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 3.00X10-6 mm Hg(3).

GROUNDWATER: Between the years 1986-87, isofenphos was detected in 2 of 19 groundwater samples from wells in Massachusetts at a range of concns from 1.17 to 2.12 ug/l(1). Isofenphos was not detected in 78 groundwater samples from wells in New York between 1986-87(1). STORET shows no detections of isofenphos (limits of detection ranging from 0.04 to 0.5 ug/l) in 1,040 ground-water monitoring samples taken between August 1989 and September 1996 in Florida(2). No sample depths (depth to ground water) were reported(2). No specific link was established between the well samples and specific isofenphos use areas(2).|SURFACE WATER: The concn of isofenphos in surface water from a golf course putting green was 1,200 ppb(1); the putting green had been treated with 450 mg/sq m of isofenphos(1). No concentration was reported for one stream sample in Illinois. Isofenphos was not found above the limit of detection/quantification (0.03 to 0.5 ug/l) in 237 New York water samples (231 stream, 4 canal, and 2 lake samples)(2).

In Canada between 1992-1994, isofenphos was found in 1 of 105 broccoli (fresh) samples and 1 of 211 cauliflower (fresh) samples at concns <0.05 ppm(1). In Canada between 1989-1991, isofenphos was found in 1 of 1,044 samples of potato (fresh) and 2 of 187 samples of broccoli (fresh) at concns of 0.05 ppm(2).

Occupational exposure to isofenphos may occur through inhalation of dust and dermal contact with this compound at workplaces where isofenphos is produced or used. The general population may be exposed to isofenphos in areas were it is used as a pesticide. (SRC)

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. (See all compounds classified as Insecticides.)

Elimination is very quick; almost 95% is excreted within 24 hr, in urine & feces.|... Dermal absorption in man was 3.6 + or - 3.6% of applied dose for 24-hr exposure and 3.6 + or - 0.5% for 72-hr exposure. Skin wash recovery data show that isofenphos evaporates from the skin during the absorption process; the surface dose is minimal (< 1%) by 24 hr. Skin stripping showed no residual isofenphos in stratum corneum. ... Skin surface recovery in vivo with soap and water was 61.4 + or - 10.4% for the first dosing time (15 min). Time-recovery response declined with time to 0.5 + or - 0.2% at 24 hr. In vitro absorption utilizing flow-through diffusion methodology with human cadaver skin and human plasma receptor fluid gave 2.5 + or - 2.0% dose absorbed, an amount similar to in vivo studies. An additional 6.5 + or - 24% was recovered in the skin amples (total of 9%). Skin surface wash at 24 hr recovered 79.7 + or - 2.2% and skin content was 6.5 + or - 2.4% (total dose accountability of 88.7 + or - 4.6%). Neither in vitro absorption nor in vitro evaporation studies predicted the potential skin evaporation of isofenphos. Published dermal studies in the rat had predicted isofenphos absorption at 47% of applied dose (12-fold greater than actual in man).

The rate of metabolism of [14C]isofenphos (IFP) to isofenphos oxon (IFP-oxon), des N-isofenphos (d-N-IFP), and des N-isofenphos oxon (d-N-IFP-oxon) by rat, guinea pig, monkey, dog, and human liver microsomal p450 enzymes was studied to obtain Vmax and Km values for Michaelis-Menten kinetics. The monkey had the highest Vmax value for the conversion of IFP to IFP-oxon (desulfuration), 162 nmol isofenphos hr-1 per 1.3 nanomoles p450, followed by guinea pig (98), rat (66), dog (43), and human (14). The Km values for the desulfuration of isofenphos were 19.2, 7.4, 14.1, 23.3, and 18.4 microM, respectively, for the monkey, guinea pig, rat, dog, and human. The Vmax values for the dealkylation process (conversion of IFP to d-N-IFP) were 64.6, 17.2, 9.7, and 7.3 nmol isofenphos hr-1 per 1.3 nanomoles P-450 for the monkey, rat, dog, and human, respectively. For the dealkylation process, monkey had the highest Km value, 16.3 microM IFP, followed by human (11.2), rat (9.9), and dog (9.3). The rate of metabolism of IFP-oxon and d-N-IFP to d-N-IFP-oxon were separately studied. The Vmax and Km values obtained in this study for animal and human liver p450 enzymes will be used to develop a PB-PK/PB-PD model to predict the fate and toxicity of isofenphos in animals and man.

0.31 Days

A preparation of liver mixed-function oxidases and brain NTE was used to rapidly detect activations of OPs. The compounds (0.1 mM or less) to be tested were incubated with microsomes isolated from livers of phenobarbital-treated chick embryos (P-450 content averaged 1.81 + or - 0.27 nmol/mg protein, means + or - SD, N = 5) and NTE (average of 13.8 nmol/min/mg protein) from untreated chick embryo brains. The NTE was separated by calcium precipitation and its activity assayed as usual. The low inhibitions of NTE of compounds that were not neurotoxic (parathion, Diazinon) did not increase in the presence of NADPH; inhibitions of NTE of compounds that required activation (leptophos, S,S,S-tri-n-butyl phosphorotrithioate, and tri-o-cresyl phosphate) greatly increased with NADPH. Both the recently identified neuropathic OP isofenphos (IFP) and its oxon required activation to inhibit NTE (inhibitions of 20 and 80%, respectively).|The degenerative process of the myofibers of the diaphragm of rats intoxicated with the organophosphate isofenphos, a compound that inhibits esterases, was studied at different intervals of intoxication. Early disorganization of the intermyofibrillar network and of the myofilaments, as well as dilatation of organelles, were observed by use of transmission electron microscopy. These changes precede macrophage invasion of the muscle fibers. Early expression of ubiquitin was observed in segments of muscle fibers by immunohistochemistry. Bands of polyubiquitin complexes in muscle homogenates were observed by immunoblotting. These bands disappeared in later stages of intoxication. A 42.5-kDa band corresponds to actin, as observed by immunoblotting using antisarcometric actin. This indicates relatively large amounts of polyubiquitin complex associated with sarcomeric actin in muscle fibers in early stages of intoxication.|Adult male Wistar rats were given oral organophosphate compounds dissolved in glycerol formal: dichlorvos, isofenphos, metamidophos, and diazinon. Half of the animals also received pralidoxime mesylate (20 mg/kg, intraperitoneal). Control animals received only the solvent. Twenty-four hours after treatment, the diaphragm muscle was collected for histological counts of necrotic muscle fibers in transverse sections.|The cytotoxicity of isophenphos, an organophosphorus insecticide that has the potential to cause delayed polyneuropathy, was evaluated in GBK and V79 cells. A 72 hr time course following isophenphos exposure indicated a dose-dependent growth inhibition as determined by cell counts. The administration of isophenphos (20 g/ml) to GBK cells cultured at high densities indicated a decrease in the activities of LDH isoenzymes. Analysis of V79 cells revealed a decrease of LDH3, the only LDH isoenzyme detected in these cells.

Excerpt from ERG Guide 152 [Substances - Toxic (Combustible)]: Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin. Contact with molten substance may cause severe burns to skin and eyes. Avoid any skin contact. Effects of contact or inhalation may be delayed. Fire may produce irritating, corrosive and/or toxic gases. Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution. (ERG, 2016)

Excerpt from ERG Guide 152 [Substances - Toxic (Combustible)]: Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves. Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Do not use mouth-to-mouth method if victim ingested or inhaled the substance; give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. For minor skin contact, avoid spreading material on unaffected skin. Keep victim calm and warm. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. (ERG, 2016)

Basic treatment: Establish a patent airway. Suction if necessary. Aggressive airway control may be needed. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... . /Organophosphates and related compounds/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious or has severe pulmonary edema. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. Administer atropine. Correct hypoxia before giving atropine ... . Administer pralidoxime chloride (2 PAM). USE UNDER DIRECT PHYSICIAN ORDERS ONLY ... . Treat seizures with adequate atropinization and correction of hypoxia. Rarely is diazepam necessary ... . For hypotension with signs of hypovolemia, administer fluid cautiously and consider vasopressors for hypotension with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Organophosphates and related compounds/

... A unique case of attempted suicide /was reported/ by intramuscular injection of the organophosphate isofenphos which resulted in a muscarinic and nicotinic syndrome lasting 15 days and requiring prolonged mechanical ventilation and hospitalization. The patient, who demonstrated no signs of delayed polyneuropathy on hospital day 25, subsequently died of pneumonia. Toxicological investigations showed isofenphos plasma decay and confirmed the intramuscular route of poisoning. It appears that continuous isofenphos absorption resulted in the prolonged intoxication observed in this patient.|Late progressive polyneuropathy followed by pyramidal findings in a 20-year old agricultural laborer who ingested Isofenphos solution during his work, is presented. The patient was confined to a wheelchair within 6 weeks, regained walking ability within 6 months, and a 23 months' follow up revealed slight additional clinical improvement with minimal progression of the pyramidal signs. The neuropathic clinical manifestations, the EMG and the nerve conduction studies were compatible with a pathology of a distal, mainly axonal, mainly motor neuropathy.|The organophosphate pesticide, isofenphos, is associated with human myeloid leukemia. In this study we describe metabolic changes in K562 myeloid blast cells from exposure to varying concentrations of isofenphos using the stable [1,2-13C(2)]glucose isotope as the single tracer and biological mass spectrometry. Isofenphos (1, 10, 100 microg/ml/72 hr) treated K562 cells showed increases of 10.7, 33.8 and 39.7% in lactate production as well as a 14.2% increase (1 microg/ml/72 hr) in 13C incorporation into nucleic acid ribose from glucose. Concomitantly, we observed a decrease in glucose oxidation and the synthesis of glutamate, palmitate and stearate from glucose. Our results demonstrate that this organophosphate pesticide exerts a leukemogenic effect by the recruitment of glucose carbons for nucleic acid synthesis thus promoting proliferation simultaneous with poor differentiation. The imbalanced metabolic phenotype with a severe defect in glucose oxidation, lipid and amino acid synthesis concurrent with de novo synthesis of nucleic acids in response to isofenphos treatment conforms to the invasive proliferating phenotype observed in TGF-beta treated lung epithelial carcinoma cells.

Amaze

USEPA/OPP Pesticide Code 109401; Trade Names: Amaze, Oftanol, BAY 92114, SRA 12869, Pryfon 6.|Granules, emulsifiable concentrate, wettable powder, powder for deep seed treatment|Mixtures (isofenphos +): thiram; fenamiphos; phoxin; carbonfuran; disulfoton

The acute biocidal effects of organophosphorus pesticides are a central feature of modern agricultural chemistry, and also define the concerns of regulatory toxicology. Less well known, but more complex and idiosyncratic, is the potential for some agents to produce a delayed and progressive polyneuropathy--Organophosphorus Induced Delayed Neurotox-icity (OPIDN). On three occasions during the past ten years, the National Institute for Occupational Safety and Health (NIOSH) had been asked to evaluate human delayed neurotoxicity from three commercially available pesticides. These were leptophos, fenthion, and isofenphos. In each case, human disease was either observed or suggested by specialized toxicity testing. The reasons that federally recommended screening measures failed to identify a potential for human neurotoxicity were not accidental, but stem from a systematic approach that focuses on a traditional definition of acute lethal toxicity. The oral single dose study on one species appears to be insufficient for recognizing the delayed neurotoxic hazard of many representatives of this chemical class. The recent addition of a recommended biochemical assay--neurotoxic esterase (NTE)--to federal guidelines potentially improves sensitivity, but it is purely adjunctive and does not amend underlying ambiguities in selecting the dose and route of administration. It is also quite probable that human neurotoxicity may be a potential hazard from exposure to more than the handful of organophosphorus pesticides that have been described in the literature.

AOAC Method 987.01. Isofenphos Technical in Pesticide Formulations by Gas Chromatographic Method .|FDA Method 232.1. Organophosphorous Residues General Method for Nonfatty Foods. Analysis by GC/FPD. Detection limit unspecified.|FDA Method 232.3. Organophosphorous Residues General Methods for Non-Fatty foods. Analysis by GC/FPD. Detection limit unspecified.|FDA Method 232.4. Organophosphorous Residues General Methods for Nonfatty Foods. Analysis by GC/ECD. Detection limit unspecified.

Agrochemicals -> Insecticides