FONOFOS
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
 -IDENTIFICATION
SYNONYMS
FONOFOS O-AETHYL-S-PHENYL-AETHYL-DITHIOPHOSPHONAT (German) DIFONATE DIFONATUL DYFONAT DYFONATE DYPHONATE O-ETHYL-S-PHENYL ETHYLPHOSPHONODITHIOATE O-ETHYL S-PHENYL ETHYLDITHIOPHOSPHONATE O-ETHYL S-PHENYL ETHYLPHOPHONOTHIOLOTHIONATE ETHYLPHOSPHONODITHIOIC ACID O-ETHYL S-PHENYL ESTER FONOPHOS N 2790 OMS 410 PHOSPHONODITHIOIC ACID, ETHYL-, O-ETHYL S-PHENYL ESTER STAUFFER N 2790
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; HSDB , 1990)
USES/FORMS/SOURCES
It is used as an insecticide (HSDB). It is sold as 10% and 20% granules (Dyfonate as 50 and 100 g/kg), and as an emulsifiable concentrate of 4 lb/gallon (HSDB). Fonofos is an ORGANOPHOSPHORUS insecticide and is a potent cholinesterase inhibitor. It has been lethal to animals in small amounts by any exposure route, including ocular (Clayton & Clayton, 1982). The ACGIH has established a Biological Exposure Index (BEI) for organophosphate cholinesterase inhibitors. Refer to the BIOMONITORING section for more information.
FONOFOS, also called DYFONATE(R), is O-ethyl S-phenyl ethylphosphonothiolothionate (ACGIH, 1986). It is a light yellow liquid with a pungent mercaptan-like odor (HSDB). It is only slightly soluble in water (13 ppm at 20 degrees C), but is miscible with acetone (HSDB) and most organic solvents (ACGIH, 1986).
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- USES: Fonofos is an organophosphorus compound used as an insecticide.
- 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 fonofos, 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 fonofos. 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 fonofos, 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 fonofos. 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.
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
- Fonofos is particularly dangerous because it lacks any irritant properties in experimental animal studies, yet has been lethal when applied in small amounts to the skin or eyes (Clayton & Clayton, 1982).
- Fonofos had no effect in rats at a dose of 10 ppm in the diet for 2 years (Clayton & Clayton, 1982). It inhibited plasma, red blood cell, and brain cholinesterase in dogs at doses of 0.4 to 6 mg/kg in a 90-day study. In a 2-year study at the same doses, there were nervous behavior, tremors, liver damage, gastrointestinal effects, and increased nasal, salivary and lacrimal secretions, in addition to cholinesterase inhibition (Clayton & Clayton, 1982). No effects were seen in the latter study at a dose of 0.2 mg/kg/day. Rats exposed to fonofos for 2 years had inhibition of cholinesterase and concomitant behavioral effects at dietary doses of 31.6 and 100 ppm, but not at 10 ppm (Clayton & Clayton, 1982).
-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, 1978). The rate of hydrolysis depends on both the specific organophosphate compound involved and the increase in pH caused by the detoxicant used (EPA, 1978; 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, 1975a). 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, 1975a). 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, 1978). 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, 1975a). 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, 1978). 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
MAXIMUM TOLERATED EXPOSURE
- Fonofos is not included in the World Health Organization (WHO) classification and is believed to be obsolete as a pesticide (World Health Organization, 2006).
A 32-year-old woman who had ingested 300 mL of fonofos with suicidal intent became progressively comatose and finally suffered respiratory arrest. Tracheal intubation, mechanical ventilation, vigorous gastric lavage and intravenous administration of atropine and obidoxime brought about complete clinical recovery within 24 hours of ingestion of this potentially fatal dose of Fonofos (Quadri & Malacrida, 1990).
In rats, 31.6 parts per million of fonofos in the diet for 13 weeks caused no effects; 100 ppm in the diet produced moderate cholinesterase inhibition (Sittig, 1985; Clayton & Clayton, 1993). Although local irritation was negligible, eye instillation of 0.1 mL of technical fonofos was fatal in rabbits (ACGIH, 1991). In dogs, a No-Effect Level of 8 parts per million (0.2 milligrams/kilogram) was noted in a 14-week feeding study and in a 106 week feeding study (ACGIH, 1991). In rats fed fonofos in the diet for 105 weeks, a No-Effect Level of 10 parts per million was noted (ACGIH, 1991). At 31.6 and 100 parts per million in a two-year feeding study, tremors, nervous behavior, and cholinesterase inhibition were noted, but no effects were noted at 10 parts per million (Clayton & Clayton, 1993). In dogs, a 90-day feeding study at 0.4 to 0.6 milligrams/kilogram of fonofos caused moderate toxic signs and decreased cholinesterase activity (Clayton & Clayton, 1993). In two-year feeding studies at 0.4 to 6.0 milligrams/kilogram, some hepatic toxicity and typical cholinesterase poisoning signs were seen in addition to cholinesterase inhibition (Clayton & Clayton, 1993). The maximum acceptable toxicant concentration (MATC) of fonofos for the fathead minnow is estimated to be between 16 to 33 micrograms/liter The corresponding chronic value (geometric means of MATC values) would be 23 micrograms/liter. Acute toxicity tests gave a 96-hour LC50 value of 1090 micrograms fonofos/liter. The acute-chronic ratio (96 hour LC50/chronic value) is 47 for fonofos (EPA, 1982).
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). Children tend to be more sensitive to organophosphates than adults (Zwiener & Ginsburg, 1988).
Three workers at a pesticide-formulating plant developed symptoms of organophosphate poisoning associated with each worker wearing a uniform that was contaminated with 76 percent parathion and then laundered. The uniform had been laundered three times before the third worker wore it and he still developed nausea, vomiting, and red cell cholinesterase activity of 75 percent of normal (Clifford & Nies, 1989).
- Carcinogenicity Ratings for CAS944-22-9 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: Fonophos EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: Fonofos 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: Fonofos 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 CAS944-22-9 (U.S. Environmental Protection Agency, 2011):
Oral: Slope Factor: RfD: 2x10(-3) mg/kg-day
Inhalation: Drinking Water:
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS944-22-9 (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 CAS944-22-9 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS944-22-9 (National Institute for Occupational Safety and Health, 2007):
Listed as: Fonofos REL: IDLH: Not Listed
- OSHA PEL Values for CAS944-22-9 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS944-22-9 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS944-22-9 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS944-22-9 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS944-22-9 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS944-22-9 (U.S. Environmental Protection Agency, 2010):
Listed as: Fonofos Reportable Quantity, in pounds: 500 Threshold Planning Quantity, in pounds: Note(s): Not Listed
- EPA SARA Title III, Community Right-to-Know for CAS944-22-9 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS944-22-9 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS944-22-9 (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 CAS944-22-9 (NFPA, 2002):
-HANDLING AND STORAGE
SUMMARY
Storage Conditions: Fonofos should be stored in its sealed original containers, in well-aired, fresh and dry storehouses or in shaded and well-aired places. It is recommended that the product's temperature not exceed 25 to 30 degrees C. Keep fonofos away from sources of heat, free flames or spark-generating equipment. Fonofos should be inaccessible to unauthorized persons, children, and domestic animals (HSDB , 1990).
-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.
- Wear full protective clothing when working in the vicinity of spills or leaks or when fighting fires (AAR, 1987).
- Protective clothing should include goggles, since great care should be taken to avoid eye contact (ACGIH, 1986).
- Any contaminated clothing should be discarded as hazardous waste. Repeated laundering may not remove organophosphate from clothing (Clifford & Nies, 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.
- 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% 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 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 944-22-9.
-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.
When heated to decomposition, fonofos can emit highly toxic fumes of oxides of phosphorus and sulfur (Sax & Lewis, 1989). Wear positive pressure breathing apparatus and special protective clothing (EPA, 1985). Dike fire control water for later disposal; do not scatter the material (EPA, 1985).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS944-22-9 (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 CAS944-22-9 (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).
DUST/VAPOR HAZARD
- When heated to decomposition, fonofos releases toxic and irritating fumes of oxides of phosphorus and sulfur (Sax & Lewis, 1989).
REACTIVITY HAZARD
- When heated to decomposition, fonofos can emit highly 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).
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 CAS944-22-9 (AIHA, 2006):
- DOE TEEL Values for CAS944-22-9 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Fonofos TEEL-0 (units = mg/m3): 0.1 TEEL-1 (units = mg/m3): 0.3 TEEL-2 (units = mg/m3): 1.3 TEEL-3 (units = mg/m3): 200 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 CAS944-22-9 (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 CAS944-22-9 (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.
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, 1978) EPA, 1975a). 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). Alternatively, the material can be inactivated with strong detergent (Ford, 1989). 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. 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. Water spray may be used to reduce or knock down vapors (AAR, 1987). BIOREMEDIATION: The fungus, Phanerochaete chrysosporium, was used to biodegrade 3 organophosphate insecticides. The degredation levels after 18 days of incubation in a nitrogen limited culture was chlorpyrifos (27.5%), fonofos (12.2%), and terbufos (26.6%) (Bumpus et al, 1993).
Isolate and ventilate the area. Keep sources of fire away. Wear rubber or neoprene gloves and overshoes and an approved respirator. Get fire-fighting equipment ready. 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 (Ford, 1989; EPA, 1975). 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). 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, 1975). 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 (Ford, 1989; EPA, 1975). 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. Water spray may be used to reduce or knock down vapors (AAR, 1987). 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
- Fonofos does not occur naturally. It is produced commercially and used as an insecticide. It may be released to the envrionment during use and/or production (HSDB, 2003).
ENVIRONMENTAL FATE AND KINETICS
OTHER Fonofos is immobile in sandy loam and silt loam soils. It is mobile in quartz sand. It decomposes in aerobic soils by microbes in 4 to 8 weeks. Fonofos is non-volatile from soil but volatile from water. It degrades in aerobic soils with a half-life of 3 to 16 weeks. Fonofos is moderately persistent (EPA, 1988). The half-life of fonofos in soil under a broad range of conditions is 30 to 45 days which avoids any long-term environmental problems (HSDB , 1990). Fonofos persists in soil for approximately 56 days (HSDB , 1990). Fonofos was incorporated into soil at a rate of 5.6 and 11.2 kg/ha as granular or EC. Four months after application, 33 to 35 percent of granular and 38 to 41 percent of EC application (both 5.6 kg/ha) remained in soil. No fonofos metabolites were detected in soil (HSDB , 1990). In a study of fonofos and four other insecticides applied as a commercial granular formulation to furrows of an organic soil, it was shown that lateral or vertical movement was not significant in any insecticide-water combination. Also, unretained water did not contain significant concentrations of insecticides (Chapman et al, 1984). Volatilization losses of fonofos from non-tilled soil were 2 to 4 times greater than the losses from conventionally-tilled fields. As much as one half of the pesticide applied was volatilized during the 26 days of the study. The maximum volatilization rates were measured at midday, indicating that soil dryness was not an important factor in the rate (Whang et al, 1993).
ENVIRONMENTAL TOXICITY
- Fonofos is a soil insecticide useful in controlling soil insects such as corn rootworms (Diabrotica species), wireworms (Elateridae), garden symphylan (Scutigerella Immaculata), root maggots (Hylemya species), crickets (Gryllidae) and others. It has generally been safe to plants except when placed directly in contact with the seeds of small seeded crops (HSDB , 1990).
- Fonofos is not absorbed by foliage and is not translocated in the plant body. It is a cholinesterase inhibitor and accumulates in carrots (EPA, 1988).
Four months after soil application, potatoes, beets, and rutabagas had little or no detectable residue at either a 5.6 or 11.2 kg/ha application rate. Wheat had 0.01 to 0.07 ppm fonofos but little or none in mature plants or grain. Carrots, at the 5.6 kg/ha application rate, had 0.35 and 0.04 ppm fonofos and dyfoxon, respectively (HSDB , 1990).
- A laboratory study determined the acute and chronic toxicity of fonofos to standard fresh-water aquatic organisms. Fonofos was acutely toxic to bluegil, Daphnia, and midge at 5.3, 2.7, and 39 mcg/L, respectively (Fairchild et al, 1992).
- Fonofos is moderately to highly toxic to birds and highly toxic to freshwater fish and salt water organisms (EPA, 1988).
- Fonofos was applied to sweet corn fields at a recommended application rate of 1.0 kg active ingredients/ha. Honey bees were placed in these fields and the effect on the fonofos on mortality rate monitored. Fonofos residues in dead bees and in pollen from hives were low and could not be the cause of death. The probable cause of death in the bees was aerial application of other insecticides, notably carbofuran (Kevan, 1992).
- Simulated avian field studies indicate granular treatments of fonofos may result in some mortality, as well as brain AChE inhibition, but that effects are not likely to diminish wildlife resources (EPA, 1988).
One study showed that ingestion of fewer than five granules of fonofos could be lethal to sparrow-sized birds. Study results suggested that the hazards associated with granular insecticides may be more dependent on which species (cf. size and feeding behavior) inhabit a treated area than on the actual application rate (Hill & Camardese, 1984).
- Direct exposure of fonofos to wildlife should be avoided (HSDB , 1990).
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
- 246.33 (Budavari, 1996; EPA, 1985)
DESCRIPTION/PHYSICAL STATE
- Fonofos is a light, yellow-colored liquid with a pungent, mercaptan-like or aromatic odor (Budavari, 1996; EPA, 1985; Sittig, 1991; ACGIH, 1991; Clayton & Clayton, 1982; EPA, 1988; HSDB , 1999).
VAPOR PRESSURE
- 2.1x10(-4) mmHg (at 25 degrees C) (EPA, 1985)
SPECIFIC GRAVITY
- NORMAL TEMPERATURE AND PRESSURE
DENSITY
- NORMAL TEMPERATURE AND PRESSURE
- OTHER TEMPERATURE AND/OR PRESSURE
BOILING POINT
- 130 degrees C; 266 degrees F (Budavari, 1996; EPA, 1985; HSDB , 1997)
FLASH POINT
- > 200 degrees F (Tagliabue closed cap) (Clayton & Clayton, 1993)
SOLUBILITY
Fonofos is practically insoluble in water (Budavari, 1996). 13 ppm (at 20 degrees C) (ACGIH, 1991; Clayton & Clayton, 1993) 13 ppm (at 22 degrees C) (HSDB , 1999)
Fonofos is miscible with organic solvents (Budavari, 1996). Fonofos is miscible with acetone, ethanol, kerosene, 4-methylpentan-2-one, and xylene (HSDB , 1999).
OTHER/PHYSICAL
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