FENSULFOTHION
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
 -IDENTIFICATION
SYNONYMS
FENSULFOTHION AGRICUR B 25141 BAY 25141 BAYER 25141 BAYER S767 CHEMAGRO 25141 DACONIT DASANIT DESANIT O,O-DIAETHYL-O-4-METHYLSULFINYL-PHENYL- MONOTHIOPHOSPHAT (German) O,O-DIAETHYL-O-(4-METHYLSULFINYL-PHENYL)- THIONOPHOSPHAT (German) p,O-DIETHYL O-p-(METHYLSULFINYL-PHENYL)- PHOSPHOROTHIOATE O,O-DIETHYL O-(p-(METHYLSULFINYL)PHENYL) PHOSPHOROTHIOATE O,O-DIETHYL O-(4-(METHYLSULFINYL)PHENYL) PHOSPHOROTHIOATE O,O-DIETHYL O-p-(METHYLSULFINYL)PHENYL THIOPHOSPHATE DIETHYL p-METHYLSULFINYLPHENYL THIOPHOSPHATE DMSP OMS 37 PHENOL, p-(METHYLSULFINYL)-, O-ESTER with O, O-DIETHYL PHOSPHOROTHIOATE PHOSPHOROTHIOIC ACID, O,O-DIETHYL O-(p- (METHYLSULFINYL)PHENYL) ESTER PHOSPHOROTHIOIC ACID, O,O-DIETHYL O-(4- (METHYLSULFINYL)PHENYL) ESTER S 767 TERRACUR P VUAGT VUAGT 108 VUAGT 96
IDENTIFIERS
Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.
SYNONYM REFERENCE
- (RTECS , 1990; Budavari, 1989; HSDB , 1990; Sittig, 1985; EPA, 1985)
USES/FORMS/SOURCES
Fensulfothion is used as a nematocide, insecticide, and mosquito larvicide (ACGIH, 1986; Sax & Lewis, 1989; Budavari, 1989; EPA, 1985; Sittig, 1985; Sax & Lewis, 1987; EPA, 1988; HSDB , 1993). Some formulations may be restricted to use by certified applicators in the USA (EPA, 1988; HSDB , 1993). The ACGIH has established a Biological Exposure Index (BEI) for organophosphates (see BIOMONITORING section).
Fensulfothion is an organophosphate compound. It occurs as a brown liquid or yellow oil (HSDB , 1993). It is soluble in most organic solvents, except aliphatic hydrocarbons, and is sparingly soluble in water (HSDB , 1993). The effects of many of the organophosphates are similar. This review is based on the properties of organophosphates in general, with effects attributed specifically to fensulfothion noted.
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- USES: Fensulfothion is an organophosphorus compound used as a nematocide, insecticide, and mosquito larvicide.
- TOXICOLOGY: Organophosphates competitively inhibit pseudocholinesterase and acetylcholinesterase, preventing hydrolysis and inactivation of acetylcholine. Acetylcholine accumulates at nerve junctions, causing malfunction of the sympathetic, parasympathetic, and peripheral nervous systems and some of the CNS. Clinical signs of cholinergic excess develop.
- EPIDEMIOLOGY: Exposure is common, but serious toxicity is unusual in the US. Common source of severe poisoning in developing countries.
The following are signs and symptoms from organophosphates in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for fensulfothion, but could potentially occur in individual cases. MILD TO MODERATE POISONING: MUSCARINIC EFFECTS: Can include bradycardia, salivation, lacrimation, diaphoresis, vomiting, diarrhea, urination, and miosis. NICOTINIC EFFECTS: Tachycardia, hypertension, mydriasis, and muscle cramps. SEVERE POISONING: MUSCARINIC EFFECTS: Bronchorrhea, bronchospasm, acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia also develop. DELAYED EFFECTS: Intermediate syndrome is characterized by paralysis of respiratory, cranial motor, neck flexor, and proximal limb muscles 1 to 4 days after apparent recovery from cholinergic toxicity, and prior to development of delayed peripheral neuropathy. Manifestations can include inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, respiratory paralysis. Recovery begins 5 to 15 days after onset. Distal sensory-motor polyneuropathy may rarely develop 6 to 21 days following exposure to some organophosphate compounds, however, it has not yet been reported in humans after exposure to fensulfothion. Characterized by burning or tingling followed by weakness beginning in the legs which then spreads proximally. In severe cases may result in spasticity or flaccidity. Recovery requires months and may not be complete. CHILDREN: May have different predominant signs and symptoms than adults (more likely CNS depression, stupor, coma, flaccidity, dyspnea, and seizures). Children may also have fewer muscarinic and nicotinic signs of intoxication (ie, secretions, bradycardia, fasciculations and miosis) as compared to adults. INHALATION EXPOSURE: Organophosphate vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic and central effects if exposed to significant concentrations.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
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.
ACUTE CLINICAL EFFECTS
TOXICOLOGY: Organophosphates competitively inhibit pseudocholinesterase and acetylcholinesterase, preventing hydrolysis and inactivation of acetylcholine. Acetylcholine accumulates at nerve junctions, causing malfunction of the sympathetic, parasympathetic, and peripheral nervous systems and some of the CNS. Clinical signs of cholinergic excess can develop. EPIDEMIOLOGY: Exposure to organophosphates is common, but serious toxicity is unusual in the US. This particular organophosphate is considered obsolete by the WHO; exposure is rare. The following are signs and symptoms from organophosphates in general, which are due to the anticholinesterase activity of this class of compounds. All of these effects may not be documented for fensulfothion, but could potentially occur in individual cases. EXPOSURE MILD TO MODERATE POISONING: MUSCARINIC EFFECTS: Can include bradycardia, salivation, lacrimation, diaphoresis, vomiting, diarrhea, urination, and miosis. NICOTINIC EFFECTS: Tachycardia, hypertension, mydriasis, and muscle cramps. SEVERE POISONING: MUSCARINIC EFFECTS: Bronchorrhea, bronchospasm, and acute lung injury. NICOTINIC EFFECTS: Muscle fasciculations, weakness, and respiratory failure. CENTRAL EFFECTS: CNS depression, agitation, confusion, delirium, coma, and seizures. Hypotension, ventricular dysrhythmias, metabolic acidosis, pancreatitis, and hyperglycemia can also develop. DELAYED EFFECTS: Intermediate syndrome is characterized by paralysis of respiratory, cranial motor, neck flexor, and proximal limb muscles 1 to 4 days after apparent recovery from cholinergic toxicity, and prior to the development of delayed peripheral neuropathy. Manifestations can include the inability to lift the neck or sit up, ophthalmoparesis, slow eye movements, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, and respiratory paralysis. Recovery begins 5 to 15 days after onset. Distal sensory-motor polyneuropathy may rarely develop 6 to 21 days following exposure to some organophosphate compounds, however, it has not yet been reported in humans after exposure to fensulfothion. Characterized by burning or tingling followed by weakness beginning in the legs which then spreads proximally. In severe cases, it may result in spasticity or flaccidity. Recovery requires months and may not be complete. CHILDREN: May have different predominant signs and symptoms than adults (more likely CNS depression, stupor, coma, flaccidity, dyspnea, and seizures). Children may also have fewer muscarinic and nicotinic signs of intoxication (ie, secretions, bradycardia, fasciculations and miosis) as compared to adults. INHALATION EXPOSURE: Organophosphate vapors rapidly produce mucous membrane and upper airway irritation and bronchospasm, followed by systemic muscarinic, nicotinic and central effects if exposed to significant concentrations.
- Fensulfothion is a very toxic substance. It can cause typical anticholinesterase poisoning (ACGIH, 1986; EPA, 1985; Sittig, 1985; Sax & Lewis, 1987; EPA, 1988; HSDB , 1993). It is not well absorbed through the skin in humans, but is well absorbed following ingestion or inhalation of the aerosolized material (ACGIH, 1986; Sax & Lewis, 1989; EPA, 1985; HSDB , 1993). It is irritating to the skin with direct contact (ACGIH, 1986; HSDB , 1993).
- Application of a 5% granular formulation of fensulfothion to the forearm skin of human volunteers for two hours, twice daily for 3 days, failed to produce decreased cholinesterase activity (ACGIH, 1986). Dermal irritation did occur (ACGIH, 1986).
- One member of a family died and 4 others developed anticholinesterase poisoning when they stayed in a house that had been fumigated with approximately 12,000 mg of fensulfothion (applied to an area of about 10 square meters in two rooms) (HSDB , 1993). Symptoms began after the first night, and a daughter died 6 days after the spraying (HSDB , 1993).
- An elderly male accidently ingested an unknown amount of fensulfothion and became comatose, as well as having other signs of anticholinesterase poisoning (HSDB , 1993). It required 69 days of hospitalization for nearly full recovery; some neurological sequelae (confusion and vagueness) persisted (HSDB , 1993).
- The hallmark of organophosphate poisoning is inhibition of plasma pseudocholinesterase and erythrocyte acetylcholinesterase (Namba, 1972).
- Death from organophosphate poisoning occurs primarily from respiratory arrest arising from failure of the respiratory center, paralysis of respiratory muscles, intense bronchoconstriction, or all three (HSDB). In severe cases when the patient has been unconscious for some time, brain damage can occur from lack of oxygen (ILO, 1983).
- Some symptoms of acute organophosphate poisoning, based upon experience with parathion, can persist for days to months. These include fatigue, ocular symptoms, EEG abnormalities, gastrointestinal complaints, excessive dreams, and intolerance to exposure to organophosphates (ILO, 1983).
- Delayed effects may be most pronounced with highly lipid-soluble organophosphates, such as fenthion, or the phosphorothioates, such as chlorpyrifos. After an initial period of apparent recovery, clinical effects may recur for up to several weeks after acute exposure (Minton & Murray, 1988).
- Some organophosphates can induce delayed neurological effects of a combined sensory-motor peripheral polyneuropathy. Sensation of numbness or tingling in the extremities may appear several weeks after acute exposure. It is not clear if all organophosphates have this activity (Cherniack, 1986; Wadia et al, 1987). For example, coumaphos induced delayed neurological effects in the standard hen assay (HSDB , 1993; Abou-Donia et al, 1982), but these delayed effects have not been reported in coumaphos-exposed humans.
METABOLIC ACIDOSIS: Metabolic acidosis has occurred in several cases of severe poisoning (Hui, 1983; Meller et al, 1981; Moore & James, 1981).
BRADYCARDIA: Bradycardia can occur following moderate to severe poisoning (Ganendran, 1974a). MYOCARDITIS: Occurrence of a protracted toxic myocarditis has been suspected (Wren et al, 1981; Kiss & Fazekas, 1982). TACHYCARDIA: Tachycardia is also common (Zwiener & Ginsburg, 1988), and a heart rate of greater than 100 beats/min was reported in 49% of patients in one study (Bardin et al, 1987). HYPERTENSION: Hypertension can occur as a nicotinic effect of organophosphate poisoning (Lund & Monteagudo, 1986). DYSRHYTHMIA: Cardiac dysrhythmias and conduction defects have been reported in patients with severe organophosphate poisoning (Wren et al, 1981; Kiss & Fazekas, 1982). EKG abnormalities may include: sinus bradycardia, A-V dissociation, idioventricular rhythms, multiform premature ventricular extrasystoles, polymorphic ventricular tachycardia, prolongation of the PR, QRS, and QT intervals, and "Torsade de Pointes" polymorphous ventricular dysrhythmias (Brill et al, 1984; Ludomirsky et al, 1982). HYPOTENSION: Hypotension can occur following moderate to severe poisoning (Ganendran, 1974a), with one studying reporting hypotension (systolic blood pressure less than 90 mmHg) in 20% of patients (Bardin et al, 1987).
DIAPHORESIS: Profuse sweating commonly occurs (Ganendran, 1974a; Bardin et al, 1987). Pallor may be noted (Done, 1979). DERMAL SENSITIZATION: Some organophosphate compounds may cause dermal sensitization following skin exposure (Milby et al, 1964). In general, organophosphates can react with proteins and are potential haptens for allergic reactions.
HYPERGLYCEMIA: Hyperglycemia may occur in severe poisonings (Namba, 1972) and it has been reported in about 22% of children with organophosphate or carbamate poisoning (Zwiener & Ginsburg, 1988), possibly resulting from acute pancreatitis (Weizman & Sofer, 1992). GLYCOSURIA: Glycosuria without ketosis may occur in severe poisonings (Namba, 1972).
Nausea, vomiting, diarrhea, abdominal cramping, and hypersalivation are common (Hayes, 1982b). FETAL INCONTINENCE: Fetal incontinence has occurred in severe poisonings (Hayes, 1965). ACUTE PANCREATITIS: Acute pancreatitis marked by elevated amylase and trypsin levels has occurred following organophosphate poisoning (Weizman & Sofer, 1992).
MIOSIS: Intense miosis (pinpoint pupils) is a typical muscarinic manifestation, and is useful diagnostically, but is not invariably present (pupils may be normal or dilated). Miosis occurred in 50/61 patients (82%) in one study (Bardin et al, 1987). MYDRIASIS: In cases of severe poisoning, individuals may exhibit mydriasis (dilatation of the pupils) (Dixon, 1957). LACRIMATION: Lacrimation and blurred vision are commonly present; blurred vision may persist for several months (Milby, 1971; Whorton & Obrinsky, 1983). RHINORRHEA: Rhinorrhea occurs initially in patients with vapor exposure (Daniels & LePard, 1991). SALIVATION: In one study, more than 50% of patients developed the muscarinic effects of excessive salivation (Bardin et al, 1987).
PROTHROMBIN TIME ABNORMALITY: Alterations in prothrombin time (both shortened and prolonged) and either increased or decreased levels of factor VII have been described, although clinically significant bleeding or hypercoagulability are rare (Von Kaulla & Holmes, 1961).
Central nervous system effects are often the earliest manifestations of poisoning and can include: giddiness, ataxia, uneasiness, restlessness, mental confusion, anxiety and tremulousness (Grob & Garlick, 1950). SEIZURE: Seizures may be an early symptom after significant exposure (Joy, 1982), and children may be more susceptible than adults to this effect (Zwiener & Ginsburg, 1988). CLOUDED CONSCIOUSNESS: Confusion and stupor can result from exposure, with more than 50% of patients in one study reporting a disturbed level of consciousness (Bardin et al, 1987). COMA: Coma can occur following severe poisonings, and these are rarely followed by generalized convulsions (Grob & Garlick, 1950). MUSCLE WEAKNESS: Muscle weakness, fatigability, and fasciculations occur commonly (Hayes, 1982b), with fasciculations present in 33/61 patients (54%) in one study (Bardin et al, 1987). PARALYSIS: Muscle paralysis can occasionally result following exposure (Done, 1979), and type II neurological effects involving paralysis can appear from 12 to 72 hours following exposure. The paralysis is unresponsive to atropine and may be due to excess acetylcholine at nicotinic receptors (Wadia et al, 1987). Paralytic signs include: inability to lift the neck or sit up, ophthalmoparesis, slow eye movement, facial weakness, difficulty swallowing, limb weakness (primarily proximal), areflexia, respiratory paralysis and death (Wadia et al, 1987). NEUROPATHY, DELAYED: Delayed neurotoxicity, including delayed peripheral neuropathy, appears to be a rare complication (Wadia et al, 1987). Typically, it appears 6 to 21 days after acute exposure and can involve progressive distal weakness and ataxia in the lower limbs. Flaccid paralysis, spasticity, ataxia, or quadriplegia may ensue (Cherniack, 1988). Recovery requires weeks to months, and the recovery may never be complete (Done, 1979). REDUCED COGNITION: Persons with other signs of organophosphate poisoning have shown reduced cognitive efficiency and slowness of thought related to the degree of cholinesterase inhibition and may be marked by impaired memory, even in the absence of other overt clinical signs (Levin & Rodnitzky, 1976).
PSYCHOSIS: Psychosis and a variety of other personality and behavioral disorders have been described from exposure to organophosphates (Joubert & Joubert, 1988; Conyers & Goldsmith, 1971; Dille & Smith, 1964). Additionally, organophosphates may exacerbate psychotic symptoms in persons with pre-existing schizophrenic tendencies. However, it is not clear if these symptoms can be induced by organophosphates in the absence of pre-existing abnormality (Levin & Rodnitzky, 1976). ANXIETY: Anxiety and/or irritability have frequently occurred in persons exposed to organophosphates (Levin & Rodnitzky, 1976). CONFUSION: Acute or chronic exposure to organophosphates may impair concentration and induce confusion and drowsiness (Levin & Rodnitzky, 1976). DEPRESSION: Depression has occurred in cases of acute organophosphate poisoning, and the severity may be correlated with the level of cholinesterase inhibition. The occurrence of depression is consistent with the theory of affective disorders being the result of cholinergic predominance in the central nervous system (Levin & Rodnitzky, 1976).
Increased bronchial secretions, bronchospasm, chest tightness, heartburn, and dyspnea have occurred in severe and moderately severe organophosphate poisonings (Hayes, 1965). HYPOVENTILATION: Hypoventilation has occurred following exposure, and was reported in 20% of patients in one study (Bardin et al, 1987). ACUTE LUNG INJURY: Noncardiogenic pulmonary edema is a manifestation of severe organophosphate poisoning (Chhabra & Sepaha, 1970), and has been seen in methyl parathion poisoning (Fazekas, 1971). BRONCHOSPASM: Bronchospasm may be a pharmacologic effect from the muscarinic activity of organophosphates (Lund & Monteagudo, 1986). TACHYPNEA: Tachypnea may occur following exposure. In one study, 39% of patients had a respiratory rate greater than 30 breaths per minute (Bardin et al, 1987). RESPIRATORY FAILURE: Acute respiratory insufficiency, due to any combination of depression of the respiratory center, respiratory paralysis, bronchospasm or increased bronchial secretions, is the main cause of death in many acute organophosphate poisonings (Lerman & Gutman, 1988; Anon, 1984). PNEUMONITIS: Aspiration of commercial organophosphate preparations which contain hydrocarbon solvents may cause potentially fatal chemical pneumonitis (Lund & Monteagudo, 1986).
CHRONIC CLINICAL EFFECTS
- At the time of this review, no studies of chronic exposure to fensulfothion were found in humans or experimental animals.
- In general, chronic exposure to organophosphates can lead to cumulative depression of cholinesterase levels until a critical lack of activity causes symptoms of organophosphate poisoning to appear, in a pattern similar to that of acute poisoning (Coye et al, 1986). The level of chronic exposure which can be tolerated depends on the rate of uptake and degradation of the organophosphate in the body in relation to its potency in inhibiting acetylcholinesterase, and the rate of the individual's replenishment of acetylcholinesterase activity.
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
- PREHOSPITAL DECONTAMINATION/NOT RECOMMENDED
Universal precaution should be followed by all individuals (i.e., first responders, emergency medical, and emergency department personnel) caring for the patient to avoid contamination. Nitrile gloves are suggested. Avoid direct contact with contaminated clothing, objects or body fluids. Vomiting containing organophosphates should be placed in a closed impervious containers for proper disposal.
- DECONTAMINATION OF SPILLS/SUMMARY
A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978a). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978a; EPA, 1975a). NOTE: Do NOT use a MIXTURE of BLEACH and ALKALI for DECONTAMINATING ACEPHATE ORGANOPHOSPHATES such as ORTHENE(R). This can cause release of toxic acetyl chloride, acetylene, and phosgene gas. Spills of acephate organophosphates should be decontaminated by absorption and scrubbing with concentrated detergent (Ford JE, 1989).
Treatment of the spilled material with alkaline substances such as sodium carbonate (soda ash), sodium bicarbonate (baking soda), calcium hydroxide (slaked or hydrated lime), calcium hydroxide (lime or lime water, when in dilute solutions), and calcium carbonate (limestone) may be used for detoxification (EPA, 1975aa). Chlorine-active compounds such as sodium hypochlorite (household bleach) or calcium hypochlorite (bleaching powder, chlorinated lime) may also be used to detoxify organophosphate spills (EPA, 1975aa). While ammonia compounds have also been suggested as alternate detoxicants for organophosphate spills, UNDER NO CIRCUMSTANCES SHOULD AMMONIA EVER BE COMBINED WITH A CHLORINE-ACTIVE COMPOUND (BLEACH) AS HIGHLY IRRITATING CHLORAMINE GAS MAY BE EVOLVED
- SMALL SPILL DECONTAMINATION
3 cups of Arm & Hammer washing soda (sodium carbonate) or Arm & Hammer baking soda (sodium bicarbonate) may be combined with one-half cup of household bleach and added to a plastic bucket of water. The washing soda is more alkaline and may be more efficacious, if available. Wear rubber gloves, and use a respirator certified effective against toxic vapors. Several washes may be required for decontamination (EPA, 1978a). Spilled liquid may first be adsorbed with soil, sweeping compound, sawdust, or dry sand and then both the adsorbed material and the floor decontaminated with one of the above solutions (EPA, 1975aa). NOTE: Do NOT use a COMBINATION of BLEACH and ALKALI to DECONTAMINATE ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). Spills involving acephate organophosphates should be decontaminated by the following procedure: Isolate and ventilate the area; keep sources of fire away; wear rubber or neoprene gloves and overshoes; get fire-fighting equipment ready; contain any liquid spill around the edge and absorb with Zorb-All(R) or similar material; dispose of absorbed or dry material in disposable containers; scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R) or similar product; re-absorb scrubbing liquid and dispose as above; dispose of cleaning materials and contaminated clothing; wash gloves, overshoes and shovel with concentrated detergent. Call the National Pesticide Telecommunications Network for further assistance at 1-800-858-7378 or on the web at http://nptn.orst.edu.
- LARGE SPILL DECONTAMINATION
Sprinkle or spray the area with a mixture of one gallon of sodium hypochlorite (bleach) mixed with one gallon of water. Then spread calcium hydroxide (hydrated or slaked lime) liberally over the area and allow to stand for at least one hour (Pesticide User's Guide, 1976). Wear rubber gloves, and use a respirator certified effective against toxic vapors. Several washes may be required for decontamination (EPA, 1978a). Other decontamination methods may be recommended by manufacturers of specific agents. Check containers, labels, or product literature for possible instructions regarding spill decontamination. NOTE: Do NOT USE a COMBINATION of BLEACH and ALKALI to DECONTAMINATE ACEPHATE or ACETYL ORGANOPHOSPHATE COMPOUNDS such as ORTHENE(R). Spills involving acephate organophosphates should be decontaminated by the following procedure: Isolate and ventilate the area; keep sources of fire away; wear rubber or neoprene gloves and overshoes; get fire-fighting equipment ready; contain any liquid spill around the edge and absorb with Zorb-All(R) or similar material; dispose of absorbed or dry material in disposable containers; scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R) or similar product; re-absorb scrubbing liquid and dispose as above; dispose of cleaning materials and contaminated clothing; wash gloves, overshoes and shovel with concentrated detergent.
FURTHER CONTACT INFORMATION For further information contact the National Pesticide Telecommunications Network at 1- 800-858-7378 or contact on the web at http://nptn.orst.edu. Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required. For small pesticide spills or for further information call the pesticide manufacturer or the National Pesticide Information Center (NPIC) at 1-800-858-7378. The National Response Center (NRC) is the federal point of contact for reporting of spills and can be reached at 1-800-424-8802. For those without 800 access, contact 202-267-2675. CHEMTREC can provide technical and hazardous materials information and can be reached at 1-800-424-9300 in the US; or 703-527-3887 outside the US.
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
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 warm and quiet. Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed. Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
One member of a family died and 4 others developed anticholinesterase poisoning when they stayed in a house that had been fumigated with approximately 12,000 milligrams of fensulfothion (applied to an area of about 10 square meters in two rooms) (HSDB , 1997).
MAXIMUM TOLERATED EXPOSURE
- Fensulfothion is not included in the World Health Organization (WHO) classification and is believed to be obsolete as pesticide (World Health Organization, 2006).
An elderly man accidentally ingested an unknown amount of fensulfothion and became comatose as well as having other sign of anticholinesterase poisoning (HSDB , 1997). Note that CHILDREN MAY EXHIBIT DIFFERENT PREDOMINANT SIGNS of organophosphate poisoning from adults. In a study on 25 children poisoned by organophosphate or carbamate compounds, the major symptoms in most of them were CNS depression, stupor, flaccidity, dyspnea, and coma. Other classical signs of organophosphate poisoning, such as miosis, fasciculations, bradycardia, excessive salivation and lacrimation, and gastrointestinal symptoms, were infrequent (Sofer et al, 1989).
- Carcinogenicity Ratings for CAS115-90-2 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Fensulfothion EPA (U.S. Environmental Protection Agency, 2011): Not Listed IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Fensulfothion MAK (DFG, 2002): Not Listed NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS115-90-2 (U.S. Environmental Protection Agency, 2011):
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS115-90-2 (American Conference of Governmental Industrial Hygienists, 2010):
Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
- AIHA WEEL Values for CAS115-90-2 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS115-90-2 (National Institute for Occupational Safety and Health, 2007):
Listed as: Fensulfothion REL: IDLH: Not Listed
- OSHA PEL Values for CAS115-90-2 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS115-90-2 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS115-90-2 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS115-90-2 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS115-90-2 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS115-90-2 (U.S. Environmental Protection Agency, 2010):
Listed as: Fensulfothion Reportable Quantity, in pounds: 500 Threshold Planning Quantity, in pounds: Note(s): d
- EPA SARA Title III, Community Right-to-Know for CAS115-90-2 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS115-90-2 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS115-90-2 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):
- ICAO International Shipping Name (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS115-90-2 (NFPA, 2002):
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
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.
- When using the granulated product, wear protective gloves, goggles, and the appropriate certified respirator (HSDB , 1990).
- Wear full protective clothing when working in the vicinity of spills or leaks or when fighting fires (AAR, 1987).
- First responders, emergency medical, and emergency department personnel should take proper precautions (wear rubber gowns, rubber aprons, rubber gloves, etc) when treating patients with organophosphate poisoning to avoid contamination. Emesis containing organophosphates should be placed in closed impervious containers for proper disposal.
- DECONTAMINATION: Remove contaminated clothing. Wash the skin, including the hair, beneath the nails, groin, and umbilical area, three times.
A single washing with soap and water can remove up to 80 to 92 percent of an organophosphate on the skin if done immediately (Fredriksson, 1961). If delayed, the same procedure may remove only 50 to 70 percent. Following a soap and water wash, a second wash with 95 percent ethanol will leave only about a 5 to 10 percent organophosphate residue (Fredriksson, 1961). The best results of skin decontamination are achieved with a thorough soap and water wash, followed by a 95 percent ethanol wash, followed by a second soap and water wash (Fredriksson, 1961). Tincture of green soap contains 30 percent ethanol, and thus has been recommended for dermal decontamination of organophosphate exposures.
- LEATHER: Leather absorbs organophosphates and is extremely difficult to decontaminate. Rescuers should not wear leather items that are not completely covered by rubber or impervious plastic. Contaminated leather items may need to be disposed of by incineration.
RESPIRATORY PROTECTION
- Wear a self-contained positive pressure breathing apparatus when working in the vicinity of spills or leaks or when fighting fires (AAR, 1987).
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 115-90-2.
-PHYSICAL HAZARDS
FIRE HAZARD
Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures. POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004) 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.
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS115-90-2 (NFPA, 2002):
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
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.
- TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
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.
- NFPA Extinguishing Methods for CAS115-90-2 (NFPA, 2002):
- Choose an extinguishing agent suitable for fires in surrounding material (AAR, 1987).
- Water may be used in flooding quantities as fog (AAR, 1987).
When heated to decomposition, fensulfothion releases very toxic fumes of oxides of carbon, phosphorus, and sulfur (Sax & Lewis, 1989).
EXPLOSION HAZARD
- Storage Requirements: Store material in the original, sealed containers in well-ventilated, dry storehouses in areas away from heat sources and spark-generating equipment. Storage areas must be located away from inhabited buildings, animal shelters, or food stores (HSDB , 1990).
DUST/VAPOR HAZARD
- When heated to decomposition, fensulfothion releases very toxic fumes of oxides of carbon, phosphorus, and sulfur (Sax & Lewis, 1989).
REACTIVITY HAZARD
- When heated to decomposition, fensulfothion releases very toxic fumes of oxides of phosphorus and sulfur (Lewis, 1996).
- Most organophosphate pesticides degrade relatively rapidly in the environment; a notable exception is LEPTOPHOS, which is lipophilic (Abou-Donia, 1983).
- All organophosphate esters undergo hydrolysis in water; generally the water-soluble products of hydrolysis are less toxic than the parent compound (Minton & Murray, 1988).
- Fensulfothion is subject to hydrolysis by alkali and more resistant to acids than to bases (HSDB , 1997).
- Readily oxidizes to form sulfone and isomerizes to S-ethyl isomer (HSDB , 1997).
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
Increase, in the downwind direction, as necessary, the isolation distance of at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids in all directions.
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
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.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. 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. Keep unauthorized personnel away. Stay upwind. Keep out of low areas.
- Downwind evacuation should be considered if this material is involved in a fire or if a large discharge has occurred (AAR, 1987).
- AIHA ERPG Values for CAS115-90-2 (AIHA, 2006):
- DOE TEEL Values for CAS115-90-2 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Fensulfothion TEEL-0 (units = mg/m3): 0.01 TEEL-1 (units = mg/m3): 0.03 TEEL-2 (units = mg/m3): 2 TEEL-3 (units = mg/m3): 12.5 Definitions: TEEL-0: The threshold concentration below which most people will experience no adverse health effects. TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure. TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape. TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.
- AEGL Values for CAS115-90-2 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
- NIOSH IDLH Values for CAS115-90-2 (National Institute for Occupational Safety and Health, 2007):
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004) 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.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 152 (ERG, 2004) 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.
Isolate and ventilate the area. Keep sources of fire away and ready the fire-fighting equipment. Wear rubber or neoprene gloves and overshoes and an approved respirator during the clean-up procedures (Ford, 1989). First responders, emergency medical, and emergency department personnel should take proper precautions (wear rubber gowns, rubber aprons, rubber gloves, etc) when treating patients with organophosphate poisoning to avoid contamination. Emesis containing organophosphates should be placed in closed impervious containers for proper disposal. In Situ Amelioration: Isolate and contain spills to limit spread. Construct a clay or bentonite swale to divert uncontaminated portion of watershed around contaminated portion. Keep material out of water sources and sewers (HSDB , 1990). Decontamination Of Spills: A variety of methods have been described for organophosphate spill decontamination, most of which depend on changing the pH to promote hydrolysis to inactive phosphate diester compounds (EPA, 1978). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1975a; EPA, 1978). Decontamination Of Spills: Treatment of the spilled material with alkaline substances such as sodium carbonate (soda ash), sodium bicarbonate (baking soda), calcium hydroxide (slaked or hydrated lime), calcium hydroxide (lime or lime water, when in dilute solutions), and calcium carbonate (limestone) may be used for detoxification (EPA, 1975). Decontamination Of Spills: Alternatively, the material can be inactivated with strong detergent (Ford, 1989). Decontamination Of Spills: While ammonia compounds have also been suggested as alternate detoxicants for organophosphate spills, UNDER NO CIRCUMSTANCES SHOULD AMMONIA EVER BE COMBINED WITH A CHLORINE-ACTIVE COMPOUND (BLEACH) AS HIGHLY IRRITATING CHLORAMINE GAS MAY BE EVOLVED. Decontamination Of Spills: Other decontamination methods may be recommended by manufacturers of specific agents. Check containers, labels, or product literature for possible instructions regarding decontamination of spills. Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required. Alternate disposal may be by high temperature incineration (HSDB , 1990). For density stratification and impoundment, remove product from bottom layer by pumping through manifold or by polyethylene rope collection (HSDB , 1990). Treatment is required for concentrated product fractions. Contaminated soil may be packaged for disposal. Water spray may be used to reduce or knock down vapors (AAR, 1987).
Isolate and ventilate the area. Keep sources of fire away and ready the fire-fighting equipment. Wear rubber or neoprene gloves and overshoes and an approved respirator during the clean-up procedures (Ford, 1989). Contain any liquid spill around the edge and absorb with Zorb-All (R), soil, sweeping compound, sawdust, dry sand or similar material. Dispose of absorbed or dry material in disposible containers (EPA, 1975; Ford, 1989). Containers should be sealed to prevent further decontamination. Decontamination Of The Spill Area: Method A: Three (3) cups of Arm & Hammer washing soda (sodium carbonate) or Arm & Hammer baking soda (sodium bicarbonate) may be combined with one-half cup of household bleach and added to a plastic bucket of water. The washing soda is more alkaline and may be more effective, if available. Wear rubber gloves, and to be safe, use a respirator certified effective against toxic vapors. Several washes may be required for decontamination (EPA, 1978). Decontamination Of The Spill Area: Scrub the spilled area with concentrated detergent such as TIDE(R), ALL(R), or similar material. Re-absorb scrubbing liquid and dispose as above (Ford, 1989). Several washes may be required for decontamination (EPA, 1978).
Isolate and ventilate the area. Keep sources of fire away. Wear rubber or neoprene gloves and overshoes and approved personal protection equipment. Get fire-fighting equipment ready (Ford, 1989). Water spray may be used to reduce or knock down vapors (AAR, 1987). Treatment of the spilled material with alkaline substances such as sodium carbonate (soda ash), sodium bicarbonate (baking soda), calcium hydroxide (slaked or hydrated lime, lime or lime water when in dilute solutions), and calcium carbonate (crushed limestone) may be used for detoxification (EPA, 1975a). In general, it would be preferable to detoxify spilled material before absorbing for disposal whenever possible. Contain any liquid spill around the edge and absorb with Zorb-All (R), soil, sweeping compound, sawdust, dry sand or similar material. Dispose of absorbed or dry material in disposible containers (EPA, 1975; Ford, 1989). Containers should be sealed to prevent further decontamination. After the bulk of the material has been removed, further decontaminate spoiled surfaces with alkaline treatment as described above, or with concentrated alkaline detergent. Absorb and dispose of waste water as described above. Sprinkle or spray the area with a mixture of one gallon of sodium hypochlorite (bleach) mixed with one gallon of water. Then spread calcium hydroxide (hydrated or slaked lime) liberally over the area and allow to stand for at least one hour (Pesticide User's Guide, 1976). Wear rubber gloves, and to be safe, use a respirator certified effective against toxic vapors. Several washes may be required for decontamination (EPA, 1978). Other decontamination methods may be recommended by manufacturers of specific agents. Check containers, labels, or product literature for possible instructions regarding spill decontamination. Absorb and dispose of waste water as described above. Disposal of large quantities or contamination of large areas may be regulated by various governmental agencies and reporting may be required. Consult the local Emergency Response Committee for guidance.
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- Release of fensulfothion into the environment is possible as a result of its manufacture and use as a pesticide (HSDB , 1990).
- Removal of Fensulfothion may be possible by rainfall washout.
ENVIRONMENTAL FATE AND KINETICS
OTHER SOIL FATE Fensulfothion degrades rapidly in a sandy loam soil to the moderately persistent metabolite fensulfothion sulfone (Chisholm, 1974); In laboratory studies, the initial half-life of the agent in a sandy loam soil (organic matter 2.9 percent) and in an organic soil (organic matter 48.7 percent) was less than one week and one week, respectively, but was more than 24 weeks in the same soil which had been sterilized by autoclaving (Miles, 1979).
Based on available data, microbial degradation appears to be a major transformation process for fensulfothion in soil; chemical hydrolysis in moist soils may also contribute to its transformation (Ahmed & Morrison, 1972).
AQUATIC FATE The persistence of fensulfothion in both sterile and non-sterile natural water at 20 degrees C was approximately the same with a half-life of about 16 weeks (Miles, 1981); Volatilization and bioconcentration are not expected to be significant processes in water (Miles, 1981). The hydrolysis half-life of fensulfothion in pure water at 25 degrees c has been measures to be 58 to 87 days over a pH range of 4.5 to 8.0 (Miles, 1981).
ATMOSPHERIC FATE Vapor-phase fensulfothion will react rapidly with photochemically produced hydroxyl radicals with a resultant estimated half-life of 7.03 days at 25 degrees C, but will not react with ozone (HSDB , 1990).
ENVIRONMENTAL TOXICITY
- Published Values (HSDB , 1990)
1. LD50 (ORAL) MALLARD: 0.749 mg/kg 2. LD50 (ORAL) SHARP-TAILED GROUSE: 0.5-1.0 mg/kg 3. LD50 (ORAL) CALIFORNIA QUAIL: 1.68 mg/kg 4. LD50 (ORAL) PHEASANT: 1.34 mg/kg 5. LD50 (ORAL) CALIFORNIA QUAIL: 1.19 mg/kg 6. LC50 BOBWHITE: 35 ppm in 5-day diet 7. LC50 JAPANESE QUAIL: 83 ppm in 5-day diet 8. LC50 RING-NECKED PHEASANT: 148 ppm in 5-day diet 9. LC50 MALLARD DUCK: 43 ppm in 5-day diet 10. LC50 MALLARD DUCK: 41 ppm in 5-day diet 11. LC50 GAMMARUS FASCIATUS: 0.1 mg at 15 deg C 12. LC50 RAINBOW TROUT: 8.8 mg/L/96h 13. LC50 GOLDEN ORFE: 6.8 mg/L/96h 14. LC50 CARP: 12.8 mg/L/24h 15. LC50 CARP: 5.7 mg/L/48h
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
- 308.35 (Hayes & Laws, 1991; HSDB , 1997)
DESCRIPTION/PHYSICAL STATE
- This compound is a yellow or brown, oily liquid (HSDB , 1997).
SPECIFIC GRAVITY
- OTHER TEMPERATURE AND/OR PRESSURE
BOILING POINT
- 138-141 degrees C; 280-286 degrees F (at 0.01 mmHg) (Budavari, 1989)
SOLUBILITY
1.54 g/L (at 25 degrees C) (HSDB , 1997) slightly soluble in water (Hayes & Laws, 1991; Lewis, 1996)
OCTANOL/WATER PARTITION COEFFICIENT
- Kow = 2.229 (Bowman & Sans, 1983)
OTHER/PHYSICAL
-REFERENCES
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