Sulprofos

322.45

322.45

252-545-0

1248

3018

DTXSID8032675

Colorless oil; tan liquid /technical grade/

101

5.48

Liquid

1.20 g/cm³ @ Temp: 20 °C

-15 °C

155-158 °C @ Press: 0.1 Torr

197.8±29.3 °C

1.583

Low

APPROX 4°C

Vapour pressure, Pa at 20°C:

LD50 orally in rats: 227 mg/kg (Bull, Ivie)

Phosphorus odor|Mercaptan-like odor

Henry's Law constant = 8.6X10-7 atm-cu m/mol @ 25 °C /Estimated/

170.03 Ų [M+H]+

Hydroxyl radical reaction rate constant = 1.1X10-10 cu cm/molecule-sec @ 25 °C /Estimated/

No rapid reaction with air. No rapid reaction with water.

Esters, Sulfate Esters, Phosphate Esters, Thiophosphate Esters, and Borate Esters

Organothiophosphates 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.

III

6.1(b)

3018

3

21-23/25-50/53

36/37-45-60-61

TE4165000

T,N

Separated from food and feedstuffs. Keep in a well-ventilated room. Store in an area without drain or sewer access. Provision to contain effluent from fire extinguishing. Well closed.

Hydrolyzed in basic conditions and is stable in acid or neutral conditions.

P260-P273-P280-P284-P301 + P310-P310

H301 + H311-H330-H410

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

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)|Liquid formulations containing organic solvents may be flammable. Gives off irritating or toxic fumes (or gases) in a fire.

|Danger|H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]|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 104 companies from 2 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H301: Toxic if swallowed [Danger Acute toxicity, oral]|P260, P264, P270, P280, P301+P310, P302+P352, P307+P311, P312, P314, P321, P322, P330, P361, P363, P405, and P501

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)

Skin: Wear appropriate personal protective clothing to prevent skin contact. Eyes: No recommendation is made specifying the need for eye protection. Wash skin: The worker should immediately wash the skin when it becomes contaminated. Remove: Work clothing that becomes wet or significantly contaminated should be removed and replaced. Change: No recommendation is made specifying the need for the worker to change clothing after the work shift. (NIOSH, 2016)|Wear appropriate personal protective clothing to prevent skin contact.|/Wear/ protective gloves, protective clothing, /and/ face shield, or eye protection in combination with breathing protection. /from table/|(See protection codes)

If material on fire or involved in fire: Use water in flooding quantities as fog. Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.) /Organophosphorus pesticides, solid, toxic/|If material on fire or involved in fire: Do not extinguish fire unless flow can be stopped. 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, dry chemical or carbon dioxide. /Organophosphorus pesticides, liquid, flammable, toxic; Organophosphorus pesticides, liquid, toxic/

Environmental considerations: Air spill: Apply water spray or mist to knock down vapors. /Organophosphorus pesticides, liquid, flammable, toxic; Organophosphorus pesticides, liquid, toxic; Organophosphorus pesticides, solid, toxic/|Environmental considerations: Water spill: Use natural barriers or oil spill control booms to limit spill travel. Remove trapped material with suction hoses. /Organophosphorus pesticides, liquid, flammable, toxic; Organophosphorus pesticides, liquid, toxic; Organophosphorus pesticides, solid, toxic/|Environmental considerations: Land spill: Dig a pit, pond, lagoon, holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete. Absorb bulk liquid with fly ash, cement powder, or commercial sorbents. /Organophosphorus pesticides, liquid, flammable, toxic; Organophosphorus pesticides, liquid, toxic; Organophosphorus pesticides, solid, toxic/

SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers. Contaminated clothing should not be taken home at end of shift, but should remain at employee's place of work for cleaning.|SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.|The worker should immediately wash the skin when it becomes contaminated.|Work clothing that becomes wet or significantly contaminated should be removed and replaced.|For more Preventive Measures (Complete) data for SULPROFOS (13 total), please visit the HSDB record page.

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.

Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 1 mg/cu m

Personal protection: complete protective clothing including self-contained breathing apparatus. Do NOT let this chemical enter the environment. Collect leaking liquid in sealable containers. Absorb remaining liquid in sand or inert absorbent. Then store and dispose of according to local regulations. Do NOT wash away into sewer.

Separated from food and feedstuffs. Keep in a well-ventilated room. Store in an area without drain or sewer access. Provision to contain effluent from fire extinguishing. Well closed.

A harmful contamination of the air will not or will only very slowly be reached on evaporation of this substance at 20 °C.

Cholinesterase inhibition. The substance may cause effects on the nervous system. This may result in convulsions and respiratory failure. The effects may be delayed. Medical observation is indicated. Exposure could cause death.

Cholinesterase inhibition. Cumulative effects are possible. See Acute Hazards/Symptoms.

AVOID ALL CONTACT! FIRST AID: USE PERSONAL PROTECTION. IN ALL CASES CONSULT A DOCTOR!

Use ventilation, local exhaust or breathing protection.

Protective gloves. Protective clothing.

Wear face shield or eye protection in combination with breathing protection.

A combination of sulprofos and malathion caused a fivefold potentiation of acute oral toxicity in rats, based on oral LD50s. Similarly, a simultaneous dosing of sulprofos and azinphos-ethyl yielded a threefold potentiation of toxicity.|In long term therapy, adrenocorticoids antagonize the antiglaucoma effects of anticholinesterases (incr ocular pressure). ... Anticholinergics antagonize the miotic (antiglaucoma) & other muscarinic effects of anticholinesterases on the autonomic & central nervous systems. Tricyclic antidepressants (anticholinergic effects) antagonize the antiglaucoma (miotic) effects of anticholinesterases in glaucoma. ... Antihistamines with anticholinergic effects antagonize the miotic (antiglaucoma) & CNS effects of anticholinesterases. Anticholinesterases potentiate tranquilizing & behavioral changes induced by antihistamines. The actions of anticholinesterase agents on autonomic effector cells, & to some extent those on CNS, are antagonized by atropine, an antidote of choice. Barbiturates are potentiated by anticholinesterases. ... Dexpanthenol potentiates the effects of anticholinesterases. Fluorophosphate insecticides potentiate the effects of other anticholinesterases. /Anticholinesterases/|Barbiturates are potentiated by anticholinesterases. Although barbiturates may be used cautiously in treating convulsions, extreme care is essential in handling poisonings due to anticholinesterases, particularly organophosphorus pesticides. Echothiophate, a cholinesterase inhibitor used as miotic, potentiates other such inhibitors... used for other purposes (additive effects) or possibly synergistic. Those exposed to organophosphate insecticides must take strict precautions. ...Organophosphorus insecticides: additive anticholinesterase effects. Hazardous. Patients on anticholinesterases (even topical, such as eye drops) should avoid areas where organophosphorus insecticides... recently... used. /Anticholinesterase/|Anticholinesterase (organophosphorus) insecticides antagonize polarizing muscle relaxants. Phenothiazines /and thioxanthenes/: ...May enhance toxic effects of organophosphorus insecticides. /Insecticides, organophosphorus/

LD50 Rat (male) oral 304 mg/kg|LD50 Rat (female) oral 176 mg/kg|LD50 Rat (male) percutaneous 5,491 mg/kg|LD50 Rat (female) percutaneous 1,064 mg/kg|For more Non-Human Toxicity Values (Complete) data for SULPROFOS (8 total), please visit the HSDB record page.

Sulprofos's former production and use as a pesticide(1), resulted in its direct release to the environment(SRC). All registrations for sulprofos have been cancelled. The last tolerance for sulprofos (cottonseed) was cancelled in 1999(2).

TERRESTRIAL FATE: Based on a classification scheme(1), Koc values of 12,000(2) and 13,500(3), measured in soil, indicate that sulprofos is expected to have no mobility in soil(SRC). Volatilization of sulprofos from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 8.6X10-7 atm-cu m/mole derived from its vapor pressure, 6.3X10-7 mm Hg(4), and water solubility, 0.31 mg/l(4). Sulprofos is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(4). The half-life of sulprofos in soils ranges from several days to several weeks depending upon soil type, and the major metabolites are sulprofos sulfoxide and sulprofos sulfone(4). Hydrolysis in moist soils may occur based on hydrolysis half-lives in water (22 °C) of 26, 151, and 51 days at pH 4, 7, and 9, respectively(4).|AQUATIC FATE: Based on a classification scheme(1), Koc values of 12,000(2), and 13,500(3) measured in soil, indicate that sulprofos is expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(4) based upon an estimated Henry's Law constant of 8.6X10-7 atm-cu m/mole derived from its vapor pressure, 6.3X10-7 mm Hg(5), and water solubility, 0.31 mg/L(5). According to a classification scheme(6), an estimated BCF of 3300(SRC), from a log Kow of 5.48(5) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is very high(SRC). The hydrolysis half lives of sulprofos at 22 °C are 26 days at pH 4, 151 days at pH 7 and 51 days at pH 9(5). Sulprofos is also expected to undergo biodegradation in aquatic environments based on shake-flask tests containing estuarine water only or estuarine water and sediment(8). First order rate constants were 0.00817 1/hr in sediment/water slurries and 0.00148 1/hr in water, respectively(8); corresponding to half-lives of 3.5 days and 19.5 days, respetively.|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), sulprofos, which has a vapor pressure of 6.3X10-7 mm Hg at 20 °C(2), is expected to exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase sulprofos 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 4 hours(SRC), calculated from its rate constant of 1.1X10-10 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase sulprofos may be removed from the air by wet and dry deposition(SRC). Sulprofos is also susceptible to direct photolysis; for thin films in sunlight, 50% decomposition was observed in <2 days(2).

The rate constant for the vapor-phase reaction of sulprofos with photochemically-produced hydroxyl radicals has been estimated as 1.1X10-10 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 4 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). The hydrolysis half lives of sulprofos at 22 °C are 26 days at pH 4, 151 days at pH 7 and 51 days at pH 9(2). It also photodegrades in water and on soil surfaces; for thin films in sunlight, 50% decomposition occurs in <2 days(2). Sulprofos was degraded roughly 82%, 90%, and 92% on cotton foliage, glass plates, and in dilute aqueous solution when exposed to sunlight for 2 days(3).

An estimated BCF of 3,300 was calculated for sulprofos(SRC), using a log Kow of 5.48(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is very high(SRC).

1.20e+04 L/kg|Experimental Koc values for sulprofos are 12,000(1) and 13,500(2). According to a classification scheme(2), these estimated Koc values suggest that sulprofos is expected to be immobile in soil(SRC).

The Henry's Law constant for sulprofos is estimated as 8.6X10-7 atm-cu m/mole(SRC) derived from its vapor pressure, 6.3X10-7 mm Hg(1), and water solubility, 0.31 mg/l at 20 °C(1). This Henry's Law constant indicates that sulprofos is expected to be essentially nonvolatile from water surfaces(2). Sulprofos's estimated Henry's Law constant indicates that volatilization from moist soil surfaces is not expected to be an important environmental fate process(SRC). Sulprofos is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

GROUNDWATER: According to the California well inventory database, none of the 34 wells sampled in Del Norte and Siskiyou counties in California between 7/1/94 and 6/30/95 had detectable levels of sulprofos(1). After a review of the literature, sulprofos was reported in groundwater from normal agricultural use in only 1 unspecified state(2). The number of detections and the state were not reported. According to EPA's Pesticides in Groundwater Database, sulprofos was not found in groundwater samples from California (n=2) in 1987-1988, Indiana (n=161) in 1987-1988, and Hawaii (n=8) in 1986; of the 59 wells sampled in Iowa in 1985-1987, only one contained sulprofos at 1.3 -1.4 ug/L(3).

Sulprofos was not found on any of the 81 commodities (6970 produce samples) in a 1989 pesticide screening program in San Antonio, TX(2). The detection limit was 0.75 ppm.

Since sulprofos is no longer registered or used as a pesticide in the United States(1), the potential for occupational exposure and general population exposure is considered low.(SRC).

Sulprofos is rapidly and nearly completely absorbed following oral exposure. In rats, more than 98% of an oral dose of sulprofos was eliminated within 48-72 hr after dosing. Rats that received one 11 mg/kg dose or ten 10 mg/kg doses of sulprofos during 15 days also excreted >96% of the dose (or last dose) within 24 hr. The primary route of excretion was through the urine, and <11% was excreted in the feces. ...Tissues and organs retained 92% within 24 hr.|Pigs rapidly excreted an oral dose of sulprofos. More than 95% of the dose was excreted in urine by 24 hours. ...Maximum blood levels occurred 4 hours posttreatment, at which time tissue levels were <0.01 ppm, except for 0.27- and 0.53-ppm levels in liver and kidney, respectively. Traces of sulprofos and its sulfoxide were found in the omental fat. All tissue residues were <0.05 ppm of sulprofos equivalents at 48 hours posttreatment.|A lactating Jersey cow was treated orally with the insecticide O-ethyl O-(4-(methylthio)phenyl-14-C) S-propyl phosphorodithioate (BAY NTN 9306) at 0.12 mg/kg as a single oral dose. The administered radiocarbon was essentially quantiatively excreted during a 6-day post-treatment period; about 90% of the dose appeared in urine, about 0.1% in milk and the rest in feces. Ten days after the 1st treatment, the animal was treated again with the radiochemical at 0.62 mg/kg. Twelve hours later, when radiocarbon residues in the blood were maximal, the cow was sacrificed, and tissue and digestive tract content samples were analyzed for metabolites.

After absorption, sulprofos was metabolized rapidly and excreted primarily in the urine. The metabolism involved oxidation of the methylthio sulfur to sulfoxide and sulfone derivates and hydrolysis of the phosphorus O-phenyl ester to phenolic metabolites (rat, cow).|Sulprofos is involved in a series of oxidation reactions that may result in replacing the thiono sulfur with oxygen and/or the addition of first one and then two oxygen atoms to the thioether sulfur. The phosphorus-O-phenyl ester of sulprofos and any of these materials may be hydrolyzed to the free phenols, which are then conjugated and eliminated, usually in the urine. The oxidation of the thioether sulfur to its sulfoxide is catalyzed by microsomal flavin-contain monooxygenase. The major sulprofos metabolites are phenol, phenol sulfoxide, phenol sulfone, and their conjugates. Sulprofos sulfoxide, sulprofos sulfone, O-analog and O-analog sulfone were also identified in pigs, goats and cows but not in the rat or hen.|...Metabolism of this insecticide by the cow involved oxidation of the methylthio sulfur to sulfoxide and sulfone derivatives and hydrolysis of the phosphorus O-phenyl ester to give phenolic metabolites that were excreted primarily in the urine in conjugated form. The low residues secreted into milk were also primarily conjugated phenols.

The characteristic pharmacological effects of the anti-ChE agents are due primarily to the prevention of hydrolysis of ACh by AChE at sites of cholinergic transmission. Transmitter thus accumulates, and the response to ACh that is liberated by cholinergic impulses or that is spontaneously released from the nerve ending is enhanced. With most of the organophosphorus agents ... virtually all the acute effects of moderate doses are attributable to this action. /Anticholinesterase agents/|The cardiovascular actions of anticholinesterase agents are complex, since they reflect both ganglionic and postganglionic effects of accumulated ACh on the heart and blood vessels. The predominant effect on the heart from the peripheral action of accumulated ACh is bradycardia, resulting in a fall in cardiac output. Higher doses usually cause a fall in blood pressure, often as a consequence of effects of anticholinesterase agents on the medullary vasomotor centers of the CNS. /Anticholinesterase agents/

Exposure Routes: inhalation, ingestion Symptoms: Nausea, vomiting, abdominal cramps, diarrhea, salivation; headache, dizziness, lassitude (weakness, exhaustion); rhinorrhea (discharge of thin mucus), chest tightness; blurred vision, miosis; cardiac irregularities; muscle fasciculation; dyspnea (breathing difficulty) Target Organs: respiratory system, central nervous system, cardiovascular system, blood cholinesterase (NIOSH, 2016)

Eye: If this chemical contacts the eyes, immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Contact lenses should not be worn when working with this chemical. Skin: If this chemical contacts the skin, immediately wash the contaminated skin with soap and water. If this chemical penetrates the clothing, immediately remove the clothing, wash the skin with soap and water, and get medical attention promptly. Breathing: If a person breathes large amounts of this chemical, move the exposed person to fresh air at once. If breathing has stopped, perform mouth-to-mouth resuscitation. Keep the affected person warm and at rest. Get medical attention as soon as possible. Swallow: If this chemical has been swallowed, get medical attention immediately. (NIOSH, 2016)|(See procedures)

Fresh air, rest. Refer immediately for medical attention.

Remove contaminated clothes. Rinse and then wash skin with water and soap. Refer for medical attention .

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Airway protection. Insure that a clear airway exists. Intubate the patients and aspirate the secretions with a large-bore suction device if necessary. Administer oxygen by mechanically assisted pulmonary ventilation if respiration is depressed. Improve tissue oxygenation as much as possible before administering atropine, so as to minimize the risk of ventricular fibrillation. In severe poisonings, it may be necessary to support pulmonary ventilation mechanically for several days. /Organophosphate pesticides/|Atropine sulfate. Administer atropine sulfate intravenously, or intramuscularly if intravenous injection is not possible. Remember that atropine can be administered through an endotracheal tube if initial IV access if difficult to obtain. Depending on the severity of poisoning, doses of atropine ranging from very low to ...high ...may be required, or even continuous infusion. The objective of atropine antidotal therapy is to antagonize the effects of excessive concentrations of acetylcholine at end-organs having muscarinic receptors. Atropine does not reactivate the cholinesterase enzyme or accelerate disposition of organophosphate. Recrudescence of poisoning may occur if tissue concentrations of organophosphate remain high when the effect of atropine wears off. Atropine is effective against muscarinic manifestations, but it is ineffective against nicotinic actions, specifically muscle weakness and twitching, and respiratory depression. Despite the limitations, atropine is often a life-saving agent in organophosphate poisonings. Favorable response to a test dose of atropine... can help differentiate poisoning by anticholinesterase agents from other conditions. However, lack of response, with no evidence of atropinization (atropine refractoriness) is typical of more severe poisonings. The adjunctive use of nebulized atropine has been reported to improve respiratory distress, decrease bronchial secretions, and increase oxygenation. ...Do not administer atropine or pralidoxime prophylactically to workers exposed to organophosphate pesticides. Prophylactic dosage with either atropine or pralidoxime may mask early signs and symptoms of organophosphate poisoning and thus allow the worker to continue exposure and possibly progress to more severe poisoning. Atropine itself may enhance the health hazards of the agricultural work setting: impaired heat loss due to reduced sweating and impaired ability to operate mechanical equipment due to blurred vision. This can be caused by mydriasis, one of the effects of atropine. /Organophosphate pesticides/|Glycopyrolate has been studied as an alternative to atropine and found to have similar outcomes using continuous infusion. Ampules of... glycopyrolate were added to ...saline and this infusion was titrated to the desired effects of dry mucous membranes and heart rate above 60 beats/min. During this study, atropine was used as a bolus for a heart rate less than 60 beats/min. The other apparent advantage to this regimen was a decreased number of respiratory infections. This may represent an alternative when there is a concern for respiratory infection due to excessive and difficult to control secretions, and in the presence of altered level of consciousness where the distinction between atropine toxicity or relapse of organophosphate poisoning is unclear. /Organophosphate pesticides/|Pralidoxime. Before administration of pralidoxime, draw a blood sample (heparinized) for cholinesterase analysis (since pralidoxime tends to reverse the cholinesterase depression). Administration pralidoxime (Protopam, 2-PAM), a cholinesterase reactivator, in cases of severe poisoning by organophosphate pesticides in which respiratory depression, muscle weakness, and/or twitching are severe. When administered early (usually less than 48 hours after poisoning) pralidoxime relieves the nicotinic as well as the muscarinic effects of poisoning. Pralidoxime works by reactivating the cholinesterase and also by slowing the "aging" process of phosphorylated cholinesterase to a non-reactivatable form. ... Dosage of pralidoxime may be repeated in 1-2 hours, then at 10-12 hour intervals if needed. In very severe poisonings, dosage rates may be doubled. Repeated doses of pralidoxime are usually required. In cases that involve continuing absorption of organophosphate (as after ingestion of large amounts), or continuing transfer of highly lipophilic organophosphate from fat into blood, it may be necessary to continue administration of pralidoxime for several days beyond the 48 hour post-exposure interval usually cited as the limit of its effectiveness. ... Blood pressure should be monitored during administration because of the occasional occurrence of hypertensive crisis. Administration should be slowed or stopped if blood pressure rises to hazardous levels. Be prepared to assist pulmonary ventilation mechanically if respiration is depressed during or after pralidoxime administration. If intravenous injection is not possible, pralidoxime may be given by deep intramuscular injection. /Organophosphate pesticides/|For more Antidote and Emergency Treatment (Complete) data for SULPROFOS (18 total), please visit the HSDB record page.

/HUMAN EXPOSURE STUDIES/ A follow-up study of 232 people three years after a history of organophosphorus pesticide poisoning disclosed only one person with slight residual blurring of vision that might have been related to the earlier poisoning, though at the time of poisoning over one third of the people had blurring, which lasted only a day or two after exposure was discontinued. The possible exceptional case had findings suggestive of basilar artery insufficiency, rather than effects of poisoning. /Organophosphorus pesticides/|/SIGNS AND SYMPTOMS/ Signs and symptoms of acute intoxication by organophosphorus insecticides include muscarinic, nicotinic, and central nervous system (CNS) manifestations. Symptoms may develop rapidly, or there may be a delay of several hours after exposure before they become evident. The delay tends to be longer in the case of more lipophilic compounds, which also require metabolic activation. Symptoms may increase in severity for more than one day and may last for several days. In severe cases, respiratory failure is a dominant effect. /Organophosphorus insecticides/|/SIGNS AND SYMPTOMS/ The clinical picture of organophosphorus intoxication results from accumulation of ACh at nerve endings. ...The symptoms can be summarized in three groups as follows: (a) Muscarinic manifestations- increased bronchial secretion, excessive sweating, salivation, and lachrymation; pinpoint pupils, bronchoconstriction, abdominal cramps (vomiting and diarrhea); and bradycardia. (b) Nicotinic manifestations- fasciculation of fine muscles and, in more severe cases, of diaphragm and respiratory muscles; and tachycardia. (c) Central nervous system manifestations- headache, dizziness, restlessness, and anxiety; mental confusion, convulsions, and coma; and depression of the respiratory centre. All these symptoms can occur in different combinations and can vary in time of onset, sequence, and duration, depending on the chemical, dose, and route of exposure. Mild poisoning might include muscarinic and nicotinic signs only. Severe cases always show central nervous system involvement; the clinical picture is dominated by respiratory failure, sometimes leading to pulmonary edema, due to the combination of the above-mentioned symptoms. /Organophosphorus insecticides/|/SIGNS AND SYMPTOMS/ /After skin exposure,/ localized sweating and fasciculation at the site of contact, with systemic effects occuring following absorption. /Organophosphorus pesticides/|For more Human Toxicity Excerpts (Complete) data for SULPROFOS (10 total), please visit the HSDB record page.

BAY NTN 9306

The substance can be absorbed into the body by inhalation of its aerosol, through the skin and by ingestion.|inhalation, ingestion

nausea, vomiting, abdominal cramps, diarrhea, salivation; headache, dizziness, lassitude (weakness, exhaustion); rhinorrhea (discharge of thin nasal mucus), chest tightness; blurred vision, miosis; cardiac irreg; muscle fasciculation; dyspnea (breathing difficulty)

Pupillary constriction, muscle cramp, excessive salivation. Headache. Sweating. Dizziness. Nausea. Diarrhoea. Vomiting. Laboured breathing. Unconsciousness. Symptoms may be delayed.

MAY BE ABSORBED! Further see Inhalation.

Blurred vision.

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

200,000 pounds in 1989, 794,000 pounds in 1982|For 1989-1991, 894,000 lbs of sulprofos were applied to cotton crops annually in 11 states. Heaviest usage was in Mississippi followed by Texas.|In 1992, 637,000 acres of cotton crops were treated with 852,000 lbs of sulprofos in 11 states. Heaviest usage was in Mississippi followed by Texas and Louisiana.

Emulsifiable concentrate; Ultra-low volume liquid|Trade names: Bolstar; Helothion

During the reregistration process, EPA approved the registrants' request for voluntary cancellation of sulprofos registrations (61 FR 65218, December 11, 1996) (FRL-5573-6). No active registrations exist for sulprofos.|Sulprofos is a selective organophosphate used to control foliar lepidopterous, dipterous and hemipterous insects. ... It is particularly efficacious in beet and armyworm control. /Former use/

Method: EPA-OSW 8141B, Organophosphorus Compounds by Gas Chromatography/Flame Photometric Detector: Capillary Column Technique; Analyte: sulprofos; Matrix: water, soil, and waste samples; Detection Level: 3.5 ug/L.|Method: EPA-OSW 8141B, Organophosphorus Compounds by Gas Chromatography/Nitrogen Phosphorus Detector Detector: Capillary Column Technique; Analyte: sulprofos; Matrix: water, soil, and waste samples; Detection Level: not reported.|Method: NIOSH 5600, Organophosphorus Pesticides; Procedure: Gas Chromatography, Photometric Detection; Analyte: sulprofos; Matrix: air; Estimated Level of Detection: 0.06 ug/sample.|Method: OSHA PV2037; Procedure: Gas Chromatography/Flame Photometric Detection; Analyte: sulprofos; Matrix: air; Detection Level: 35 ug/cu m.|For more Analytic Laboratory Methods (Complete) data for SULPROFOS (7 total), please visit the HSDB record page.

Agrochemicals -> Insecticides|Pharmaceuticals