Trichlorfon

H302: Harmful if swallowed [Warning Acute toxicity, oral]

H317: May cause an allergic skin reaction [Warning Sensitization, Skin]

H400: Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410: Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

P261, P264, P270, P272, P273, P280, P301+P317, P302+P352, P321, P330, P333+P317, P362+P364, P391, and P501 (click each P-code to see the statement)

H301 (29.6%): Toxic if swallowed [Danger Acute toxicity, oral]

H302+H312 (48.1%): Harmful if swallowed or in contact with skin [Warning Acute toxicity, oral; acute toxicity, dermal]

H302 (70.4%): Harmful if swallowed [Warning Acute toxicity, oral]

H312 (48.1%): Harmful in contact with skin [Warning Acute toxicity, dermal]

H317 (100%): May cause an allergic skin reaction [Warning Sensitization, Skin]

H334 (48.1%): May cause allergy or asthma symptoms or breathing difficulties if inhaled [Danger Sensitization, respiratory]

H400 (100%): Very toxic to aquatic life [Warning Hazardous to the aquatic environment, acute hazard]

H410 (100%): Very toxic to aquatic life with long lasting effects [Warning Hazardous to the aquatic environment, long-term hazard]

P233, P260, P261, P264, P270, P271, P272, P273, P280, P284, P301+P316, P301+P317, P302+P352, P304+P340, P317, P321, P330, P333+P317, P342+P316, P362+P364, P391, P403, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 81 reports by companies from 4 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

H319: Causes serious eye irritation [Warning Serious eye damage/eye irritation]

H331: Toxic if inhaled [Danger Acute toxicity, inhalation]

H340: May cause genetic defects [Danger Germ cell mutagenicity]

H360: May damage fertility or the unborn child [Danger Reproductive toxicity]

H370: Causes damage to organs [Danger Specific target organ toxicity, single exposure]

H372: Causes damage to organs through prolonged or repeated exposure [Danger Specific target organ toxicity, repeated exposure]

H373: May causes damage to organs through prolonged or repeated exposure [Warning Specific target organ toxicity, repeated exposure]

P203, P260, P261, P264, P264+P265, P270, P271, P272, P273, P280, P301+P317, P302+P352, P304+P340, P305+P351+P338, P308+P316, P316, P318, P319, P321, P330, P333+P317, P337+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

H301: Toxic if swallowed [Danger Acute toxicity, oral]

H320: Causes eye irritation [Warning Serious eye damage/eye irritation]

H361: Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

H371: May cause damage to organs [Warning Specific target organ toxicity, single exposure]

P203, P260, P261, P264, P264+P265, P270, P272, P280, P301+P316, P302+P352, P305+P351+P338, P308+P316, P318, P321, P330, P333+P317, P337+P317, P362+P364, P405, and P501 (click each P-code to see the statement)

H312: Harmful in contact with skin [Warning Acute toxicity, dermal]

H334: May cause allergy or asthma symptoms or breathing difficulties if inhaled [Danger Sensitization, respiratory]

P233, P260, P261, P264, P270, P271, P272, P273, P280, P284, P301+P317, P302+P352, P304+P340, P317, P321, P330, P333+P317, P342+P316, P362+P364, P391, P403, and P501 (click each P-code to see the statement)

Fresh air, rest. Refer for medical attention.

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

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

Induce vomiting (ONLY IN CONSCIOUS PERSONS!). Rest. Refer for medical attention .

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop.

SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. IMMEDIATELY call a hospital or poison control center even if no symptoms (such as redness or irritation) develop. IMMEDIATELY transport the victim to a hospital for treatment after washing the affected areas.

INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. IMMEDIATELY call a physician and be prepared to transport the victim to a hospital even if no symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing.

INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, administer a slurry of activated charcoal in water and simultaneously call a hospital or poison control center. IMMEDIATELY transport the victim to a hospital. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

Excerpt from ERG Guide 152 [Substances - Toxic (Combustible)]:

SMALL FIRE: Dry chemical, CO2 or water spray.

LARGE FIRE: Water spray, fog or regular foam. If it can be done safely, move undamaged containers away from the area around the fire. Dike runoff from fire control for later disposal. Avoid aiming straight or solid streams directly onto the product.

FIRE INVOLVING TANKS, RAIL TANK CARS OR HIGHWAY TANKS: Fight fire from maximum distance or use unmanned master stream devices 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 in direct contact with flames. For massive fire, use unmanned master stream devices or monitor nozzles; if this is impossible, withdraw from area and let fire burn. (ERG, 2024)

In case of fire in the surroundings, use appropriate extinguishing media.

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide.

Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary.

If material involved in fire: Extinguish fire using agent suitable for type surrounding fire. (Material itself does not burn, or burns with difficulty.)

For small fires, use dry chemical, carbon dioxide, water spray, or foam. For large fires, use water spray, fog, or foam. ... If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters. Notify local health and fire officials and pollution control agencies. From a secure, explosion-proof location, use water pray to cool exposed containers. If cooling streams are ineffective (venting sound increases in volume and pitch, tank discolors, or shows any signs of deforming), withdraw immediately to a secure position. ... The only respirators recommended for firefighting are self-contained breathing apparatuses that have full face-pieces and are operated in a pressure-demand or other positive-pressure mode.

Special hazards arising from the substance or mixture: Carbon oxides, oxides of phosphorus, hydrogen chloride gas.

Excerpt from ERG Guide 152 [Substances - Toxic (Combustible)]:

IMMEDIATE PRECAUTIONARY MEASURE: Isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids.

SPILL: Increase the immediate precautionary measure distance, in the downwind direction, as necessary.

FIRE: If tank, rail tank car or highway tank is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2024)

Personal protection: filter respirator for organic gases and particulates adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Do NOT wash away into sewer. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Then store and dispose of according to local regulations.

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided. Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal.

Environmental considerations - Land spill: Dig a pit, pond, lagoon, holding area to contain liquid or solid material. Cover solids with a plastic sheet to prevent dissolving in rain or fire fighting water. Dike surface flow using soil, sand bags, foamed polyurethane, or foamed concrete.

Environmental considerations - Water spill: Use natural barriers or oil control booms to limit spill travel. Use natural deep water pockets, excavated lagoons, or sand bag barriers to trap material at bottom. Remove trapped material with suction hoses.

As for other organophosphorus pesticides, stay upwind; keep out of low areas. Ventilate closed spaced before entering them. Wear positive-pressure breathing apparatus and special protective clothing. Do not touch spilled material; stop leak if you can do so without risk. Use water spray to reduce vapors. Small spills: Absorb with sand or other noncombustible absorbent material and place into containers for later disposal. Small dry spills: With clean shovel place material into clean dry containers and cover; move containers from spill area. Large spills: Dike far ahead of spill for later disposal. Ventilate area after cleanup is complete. It may be necessary to contain and dispose of this chemical as a hazardous waste. If material or contaminated runoff enters waterways, notify downstream users of potentially contaminated waters.

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

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber; Contaminated packaging: Dispose of as unused product.

Add a combustible solvent and burn in a furnace equipped with an afterburner and an alkali scrubber. In accordance with 40CFR165, follow recommendations for the disposal of pesticides and pesticide containers. Must be disposed properly by following package label directions or by contacting your local or federal environmental control agency, or by contacting your regional EPA office.

Trichlorofon initially hydrolyzes to the more toxic compound dichlorvos at pH 8 and 37.5 °C, but is essentially 100% hydrolyzed in approximately 24 hr to nontoxic products which can be mixed with a portion of soil rich in organic matter and buried. Recommendable methods: Incineration, hydrolysis, and landfill. Peer-review: Large amount of trichlorofon should be incinerated at high temperature in a unit with effluent gas scrubbing. (Peer-review conclusions of a IRPTC expert consultation (May 1985))

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust. Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided.

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed.

Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday.

Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands.

For more Preventive Measures (Complete) data for Trichlorfon (11 total), please visit the HSDB record page.

Excerpt from ERG Guide 152 [Substances - Toxic (Combustible)]:

ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area. Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Cover with plastic sheet to prevent spreading. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS. (ERG, 2024)

Separated from strong bases and food and feedstuffs. Keep in a well-ventilated room.

Keep container tightly closed in a dry and well-ventilated place. Storage class (TRGS 510): Non Combustible Solids.

Store in a secure poison location. ... Store in tightly closed containers in a cool, well-ventilated area away from alkaline materials. Where possible, automatically transfer material from other storage containers to process containers.

Biological Exposure Indices (BEI) [ACGIH] - Acetylcholinesterase activity in red blood cells = 70% of individual's baseline; Butylcholinesterase activity in serum or plasma = 60% of individual's baseline; Sample at end of shift; [TLVs and BEIs]

1.0 [mg/m3]

13 [mg/m3]

170 [mg/m3]

0.1 [mg/m3], inhalable fraction

8 hr Time Weighted Avg (TWA): 1 mg/cu m, Inhalable fraction

Peak Exposure Recommendation: Transient increases in workers' exposure levels may exceed 3 times the value of the TLV-TWA level for no more than 15 minutes at a time, on no more than 4 occasions spaced 1 hour apart during a workday, and under no circumstances should they exceed 5 times the value of the TLV-TWA level. In addition, the 8-hour TWA is not to be exceeded for an 8-hour work period.

A4; Not classifiable as a human carcinogen.

Biological Exposure Index (BEI): Determinant: Cholinesterase activity in red blood cells; Sampling Time: Discretionary; BEI: 70% of individual's baseline. The determinant is nonspecific, since it is also observed after exposure to other chemicals. /Acetylcholinesterase Inhibiting Pesticides/

2017 Notice of Intended Changes (NIC): These substances, with their corresponding indices, comprise those for which (1) a BEI is proposed for the first time, (2) a change in the Adopted index is proposed, (3) retention as an NIC is proposed, or (4) withdrawal of the Documentation and adopted BEI is proposed. In each case, the proposals should be considered trial indices during the period they are on the NIC. These proposals were ratified by the ACGIH Board of Directors and will remain on the NIC for approximately one year following this ratification. If the Committee neither finds nor receives any substantive data that change its scientific opinion regarding an NIC BEI, the Committee may then approve its recommendation to the ACGIH Board of Directors for adoption. If the Committee finds or receives substantive data that change its scientific opinion regarding an NIC BEI, the Committee may change its recommendation to the ACGIH Board of Directors for the matter to be either retained on or withdrawn from the NIC. Chemical: Cholinesterase Inhibiting Pesticides. /Cholinesterase Inhibiting Pesticides/

Table: Cholinesterase Inhibiting Pesticides [Table#2331]

(inhalable fraction and vapour): 0.1 mg/m

1 mg/m³ (inhalable particulate matter) [2003]

Evaporation at 20 °C is negligible; a harmful concentration of airborne particles can, however, be reached quickly when dispersed.

The substance may cause effects on the nervous system by a cholinesterase inhibiting effect. This may result in convulsions, respiratory failure and death. Cholinesterase inhibition. Exposure at high levels could cause death. The effects may be delayed. Medical observation is indicated.

Repeated or prolonged contact may cause skin sensitization. The substance may have effects on the nervous system. Cholinesterase inhibition. Cumulative effects are possible. See Acute Hazards/Symptoms.

Tolerances are established for residues of the insecticide trichlorfon (dimethyl (2,2,2-trichloro-1-hydroxyethyl) phosphonate) in or on the following food commodities:[Table#2325]

Safety glasses, all-purpose canister mask, sleeve-closed gown, gloves and long boots. (USCG, 1999)

Eye/face protection: Face shield and safety glasses. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU).

Skin protection: Handle with gloves.

Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace.

Respiratory protection: For nuisance exposures use type P95 (US) or type P1 (EU EN 143) particle respirator. For higher level protection use type OV/AG/P99 (US) or type ABEK-P2 (EU EN 143) respirator cartridges. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU).

Wear protective gloves and clothing to prevent any reasonable probability of skin contact. ... All protective clothing (suits, gloves, footwear, headgear) should be clean, available each day, and put on before work. ... Wear dust-proof chemical goggles and face shield unless full-face-piece respiratory protection is worn.

NO open flames.

PREVENT DISPERSION OF DUST! STRICT HYGIENE! AVOID EXPOSURE OF (PREGNANT) WOMEN! AVOID EXPOSURE OF ADOLESCENTS AND CHILDREN! IN ALL CASES CONSULT A DOCTOR!

Use local exhaust or breathing protection.

Protective gloves. Protective clothing.

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

Do not eat, drink, or smoke during work.

Trichlorfon is a white crystalline solid. It is a wettable powder. It can cause illness by inhalation, skin absorption and/or ingestion. It is used as a pesticide.

White solid; [Merck Index] White solid; Formulated as soluble powder and granular products; [Reference #2]

WHITE CRYSTALS.

White crystalline solid.

White crystals

White, crystalline solid

Colorless crystals

Ethyl ether-like

Weak, characteristic odor

212 °F at 0.1 mmHg (NTP, 1992)

BP: 100 °C at 0.1 mm Hg

212 °F at 0.1 mmHg

181 to 183 °F (NTP, 1992)

83-84 °C

181-183 °F

10 to 50 mg/mL at 70 °F (NTP, 1992)

In water, 1.20X10+5 mg/L at 25 °C

Soluble in benzene, ethanol; sparsely soluble in diethyl ether and petroleum ether

Solubility: 152 g/kg in benzene; 299 g/kg in dichloromethane; 200 g/kg in isopropanol; 30 g/kg in toluene

Soluble in benzene, chloroform, ether; insoluble in oils

Very soluble in methylene chloride; freely soluble in acetone, alcohol, chloroform, ether; soluble in benzene; very slightly soluble in hexane, pentane, carbon tetrachloride, diethyl ether

Solubility in water, g/100ml at 25 °C: 15.4

1.73 at 68 °F (USCG, 1999) - Denser than water; will sink

1.73 g/cu cm at 20 °C

Relative density (water = 1): 1.73

1.73 @ 20°C

7.8e-06 mmHg at 68 °F (NTP, 1992)

0.0000078 [mmHg]

7.8X10-6 mm Hg at 20 °C

Vapor pressure, Pa at 20 °C:

7.8x10-6

log Kow = 0.51

Stable under recommended storage conditions.

Stable at room temperature.

Subject to hydrolysis and dehydrochlorination. Decomposition proceeds more rapidly with heating, and above pH 6. Rapidly converted by alkalis to dichlorvos, which is then hydrolyzed.

Slowly decomposed in aqueous acidic solutions

Decomposed by alkali.

When heated to decomposition it emits very toxic fumes of /chloride and phosphorous oxides/.

Corrosive to metals

Index of refraction = 1.3439 at 20 °C/D

This chemical decomposes at higher temperatures in water and at pH <5.5. It is sensitive to prolonged exposure to moisture. It is unstable in alkaline solutions.

Alcohols and Polyols

Halogenated Organic Compounds

Sulfonates, Phosphonates, and Thiophosphonates, Organic

TRICHLORFON is incompatible with alkalis. It is corrosive to black iron and mild steel. It is corrosive to metals. It is subject to hydrolysis. (NTP, 1992)

Incompatible materials: Strong oxidizing agents.

Incompatibilities: Alkaline materials: lime, lime sulfur, etc. Corrosive to iron and steel.

IDENTIFICATION AND USE: Trichlorfon is a white, crystalline solid. It is used as anthelmintic drug and systemic insecticide. HUMAN STUDIES: Trichlorfon, an organophosphate, has a moderately potent anticholinesterase activity. 379 cases of trichlorfon poisoning were reviewed, and in some cases (3%), acute poisonings were accompanied by loss of memory and problem-solving ability, delirium, depression and anxiety, psychomotor stimulation, hallucinations, and paranoid delusions; in other cases (21%), poisoning was accompanied by a delayed type polyneuropathy. Of 15 live births in one Hungarian village in 1989-90, 11 (73%) were affected by congenital abnormalities and six were twins. Of the 11, four had Down's syndrome. The likely causes of such clusters were excluded. A case control study and environmental investigations revealed the excessive use of trichlorfon at local fish farms. Trichlorfon content was very high in fish (100 mg/kg) and several pregnant women, including all mothers of babies with Down syndrome, had consumed contaminated fish in the critical period for the congenital abnormalities observed. Trichlorfon demonstrated clastogenic, mutagenic, and DNA damaging effects in human lymphocytes in vitro. Significant and persistent increases (lasting at least 180 days after exposure) in aneuploidy in lymphocytes of individuals who attempted suicide by using trichlorfon were reported. ANIMAL STUDIES: Trichlorfon was a moderate contact allergen in the skin. When applied to the eyes of rabbits it has short lasting miotic effect and produces little or no irritation. In rats given daily oral doses of 300 mg/kg body weight technical trichlorfon for 5 days, brain edema, congestion of organs, fatty degeneration, and glycogen depletion of the liver, glycogen depletion of the heart muscle and emphysema and local inflammation in the lungs were observed. Significant cholinesterase depression was noted at 300 mg/kg in rats. The dietary level of 500 ppm (about 10.5 mg/kg/day) inhibited RBC cholinesterase activity in dogs. Trichlorfon does not have a cumulative effect. There was no significant difference in the incidence of tumors between treated and control groups in mice or hamsters. A single 80 mg/kg body weight dose administered to rats orally by gavage on day 13 of pregnancy caused an increased number of embryonic deaths, a decreased number of live fetuses and increased fetal anomalies, such as exencephaly and failure of eyelids to close; administration of 8 mg/kg body weight throughout pregnancy produced no teratogenic manifestations. Trichlorfon did not induce mutation in Drosophila melanogaster, but because of high toxicity, only low doses could be tested. Trichlorfon induces gene mutation in Salmonella typhimurium and Escherichia coli and in Saccharomyces cerevisiae. It also induces a mitotic crossing over, gene conversion, and mitotic recombination. The positive results in microorganisms indicate that trichlorfon induces mainly base-pair substitution or mutation in the absence of metabolic activation. Trichlorfon also induces a chlorophyll mutation and chromosomal damage in plants. ECOTOXICITY STUDIES: Trichlorfon is moderately toxic for fish and moderately to highly toxic for aquatic arthropods. Trichlorfon applied to ponds at the rate of 1 mg/liter water destroyed the food invertebrates for fish. Large numbers of zooplankton, rotifers, and crustacea died in the first 24 hours after treatment, whereas benthos died during the first week. The affected fauna community recovered slowly. Trichlorfon treatment deprived the fish of valuable foods, such as crustacean and bottom fauna, for as long as 1 month after treatment. No effects on numbers, breeding pairs, nesting success, or mortality of forest songbirds were seen following aerial application of trichlorfon. An observed reduction in singing and increased feeding activity may have been the result of a reduction in food organisms. Trichlorfon was teratogenic for zebrafish embryos leading to anomalies in the absorption of the yolk sac, spine bending and pericardial edemas. Immunological responses and immune gene expressions of prawn exposed to trichlorfon at 0.4 mg/L for 24 hr were perturbed, thus causing a deficiency in immunity and subsequent increased susceptibility to pathogen infections. Trichlorfon influenced fish plasma antioxidative status, caused lipid peroxidation then resulted in hepatocytes apoptosis.

Trichlorfon is a cholinesterase or acetylcholinesterase (AChE) inhibitor. A cholinesterase inhibitor (or 'anticholinesterase') suppresses the action of acetylcholinesterase. Because of its essential function, chemicals that interfere with the action of acetylcholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death. Nerve gases and many substances used in insecticides have been shown to act by binding a serine in the active site of acetylcholine esterase, inhibiting the enzyme completely. Acetylcholine esterase breaks down the neurotransmitter acetylcholine, which is released at nerve and muscle junctions, in order to allow the muscle or organ to relax. The result of acetylcholine esterase inhibition is that acetylcholine builds up and continues to act so that any nerve impulses are continually transmitted and muscle contractions do not stop. Among the most common acetylcholinesterase inhibitors are phosphorus-based compounds, which are designed to bind to the active site of the enzyme. The structural requirements are a phosphorus atom bearing two lipophilic groups, a leaving group (such as a halide or thiocyanate), and a terminal oxygen.

Cancer Classification: Likely to be Carcinogenic to Humans (High Doses); Not Likely to be Carcinogenic to Humans (Low Doses)

No data are available in humans. Inadequate evidence of carcinogenicity in animals. OVERALL EVALUATION: Group 3: The agent is not classifiable as to its carcinogenicity to humans.

A4; Not classifiable as a human carcinogen.

Trichlorfon

Group 3: Not classifiable as to its carcinogenicity to humans

Volume 30: (1983) Miscellaneous Pesticides

Volume Sup 7: Overall Evaluations of Carcinogenicity: An Updating of IARC Monographs Volumes 1 to 42, 1987; 440 pages; ISBN 92-832-1411-0 (out of print)

3, not classifiable as to its carcinogenicity to humans. (L135)

Acute exposure to cholinesterase inhibitors can cause a cholinergic crisis characterized by severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Accumulation of ACh at motor nerves causes overstimulation of nicotinic expression at the neuromuscular junction. When this occurs symptoms such as muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis can be seen. When there is an accumulation of ACh at autonomic ganglia this causes overstimulation of nicotinic expression in the sympathetic system. Symptoms associated with this are hypertension, and hypoglycemia. Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur. Certain reproductive effects in fertility, growth, and development for males and females have been linked specifically to organophosphate pesticide exposure. Most of the research on reproductive effects has been conducted on farmers working with pesticides and insecticdes in rural areas. In females menstrual cycle disturbances, longer pregnancies, spontaneous abortions, stillbirths, and some developmental effects in offspring have been linked to organophosphate pesticide exposure. Prenatal exposure has been linked to impaired fetal growth and development. Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

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

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

MAY BE ABSORBED! See Inhalation.

Redness. Pain. Pupillary constriction. Blurred vision.

Nausea. Vomiting. Weakness. Abdominal cramps. Diarrhoea. Pupillary constriction. Muscle cramps. Excessive salivation. Laboured breathing. Unconsciousness.

Symptoms of low dose exposure include excessive salivation and eye-watering. Acute dose symptoms include severe nausea/vomiting, salivation, sweating, bradycardia, hypotension, collapse, and convulsions. Increasing muscle weakness is a possibility and may result in death if respiratory muscles are involved. Hypertension, hypoglycemia, anxiety, headache, tremor and ataxia may also result.

Chemical: TRICHLORFON

Neurotoxin - Predominantly motor

Other Poison - Organophosphate

Skin Sensitizer - An agent that can induce an allergic reaction in the skin.

ACGIH Carcinogen - Not Classifiable.

FAO/WHO ADI: 0.04 mg/kg

Children

Females 13-49 yrs

Human Health Benchmarks for Pesticides - 2021 Update

LC50 (rat) = 533 mg/m3

LD50 Rat (male and female) percutaneous >5000 mg/kg/24 hr

LD50 Rat oral 250 mg/kg

LD50 Rat dermal 2000 mg/kg

LD50 Rat ip 160 mg/kg

For more Non-Human Toxicity Values (Complete) data for Trichlorfon (17 total), please visit the HSDB record page.

If the compound has been ingested, rapid gastric lavage should be performed using 5% sodium bicarbonate. For skin contact, the skin should be washed with soap and water. If the compound has entered the eyes, they should be washed with large quantities of isotonic saline or water. In serious cases, atropine and/or pralidoxime should be administered. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of '-oximes' has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally.

The aim of this study is to determine the effect of levamisole and levamisole-trichlorfon combination on isolated sheep trachea. Contraction was achieved with levamisole concentrations (10(-8)-10(-3) M) on tracheal strips of adult sheep (> 1 year of age). Pretreatment with trichlorfon (10(-7) M)-levamisole (10(-7) M) decreased the pD2 and E(max) of Ach when compared to levamisole pretreatment (p < or = 0.01). Pretreatment with levamisole (10(-7) M), decreased the E(max) (p < or = 0.01) and pD2 (p < 0.05) of bethanechol concentrations (10(-8)-10(-3) M) significantly. Pretreatment with atropine (10(-6) M) decreased the E(max) of levamisole (10(-4) M) significantly (p < 0.05). To conclude, levamisole acted mainly on the muscarinic receptors of the sheep trachea and this effect was partly inhibited by atropine. Adverse interaction was present between levamisole and trichlorfon.

In the forward mutation test system ade6 of the yeast Saccharomyces pombe, trichlorfon in combination with azinphos-methyl produced clearly synergistic effects for toxicity and mutagenicity. The addition of S9 microsomal liver fraction decreased the efficiency of single and combined treatments.

12 organophosphorus insecticides were tested for toxicity and mutagenicity in the forward mutation test system ade6 of the yeast Schizosaccharomyces pombe. EMS and MMS were selected as positive controls. 3 compounds, dichlorvos, trichlorfon and paraoxon, showed a linear dose-response relationship. Among the other compounds investigated, methyl derivatives, though in general more toxic than ethyl derivatives, did not significantly increase the mutation frequency. Trichlorfon, tested in combination with malathion, methylparathion or methylazinphos (guthion), produced clearly synergistic effects for both toxicity and mutagenicity. The addition of S9 microsomal liver fraction decreased the efficiency of both single and combined treatments only where a dose-response relationship or a synergistic effect was obtained.

Two randomized crossover studies were conducted to examine the effects of a combination of aluminum hydroxide (aluminium hydroxide) and magnesium hydroxide (Maalox TC), cimetidine, and ranitidine on the pharmacokinetics of trichlorfon (metrifonate) and its metabolite in a total of 34 healthy subjects (ages 45-75 yr) who received a single oral tablet of 50 mg trichlorfon alone, with or 90 min before a suspension of Maalox TC, or with or after pretreatment with oral tablets of 400 mg cimetidine or 150 mg ranitidine. The ratios and 90% confidence intervals (trichlorfon with comedication/trichlorfon alone) of AUC and Cmax of the drug and its metabolites fulfilled the criteria defined for showing lack of relevant interaction for all treatment comparisons in both studies. Trichlorfon was well tolerated.

For more Interactions (Complete) data for Trichlorfon (6 total), please visit the HSDB record page.

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Organophosphates and related compounds/

Basic Treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway if needed). Suction if necessary. Aggressive airway control may be needed. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... . /Organophosphates and related compounds/

LC50; Species: Gammarus fasciatus (/Scud/) mature; Conditions: static bioassay without aeration, 21 °C, pH 7.2-7.5, water hardness 40-50 mg/L as calcium carbonate and alkalinity of 30-35 mg/L; Concentration: 40 ug/L for 96 hr (95% confidence limit: 26-60 ug/L) /Technical material 98%/

LC50; Species: Procambarus (Crayfish) mature; Conditions: static bioassay without aeration, 12 °C, pH 7.2-7.5, water hardness 40-50 mg/L as calcium carbonate and alkalinity of 30-35 mg/L; Concentration: 7800 ug/L for 96 hr (95% confidence limit: 6520-9330 ug/L) /Technical material 98%/

LC50; Species: Pteronarcella badia (/Stonefly/) naiads; Conditions: static bioassay without aeration, pH 7.2-7.5, water hardness 40-50 mg/L as calcium carbonate and alkalinty of 30-35 mg/L; Concentration: 11 ug/L for 96 hr (95% confidence limit: 7.6-16 ug/L) /Technical material 98%/

LC50; Species: Pteronarcys california (/Stonefly/) second year class; Conditions: static bioassay without aeration, 16 °C, pH 7.2-7.5, water hardness 40-50 mg/L as calcium carbonate and alkalinity of 30-35 mg/L; Concentration: 35 ug/L/96 hr (95% confidence limit: 22-55 ug/L) /Technical material 98%/

For more Ecotoxicity Values (Complete) data for Trichlorfon (85 total), please visit the HSDB record page.

/BIRDS and MAMMALS/ Japanese quail /Coturnix japonica/ were given trichlorfon daily for 20 days at an oral dose of 5 mg/kg body weight. Hematological examinations were made on the 5th, 10th, 15th, and 20th day of treatment and on the 5th, 10th, 15th, and 30th day after stopping treatment. The number of erythrocytes dropped on the 5th and 10th days, and the values of the hematocrit and hemoglobin fell on the 5th day. A significant increase in erythroblast contents was found on the 5th and 10th day. No other significant changes of the above parameters were observed up to the 30th day after treatment. The numbers of leukocytes, lymphocytes, neutrophils, and monocytes sharply increased from the 5th to 15th day of treatment, and quikly dropped to normal ranges on the 10th day after stopping treatment.

/AQUATIC SPECIES/ The cardio-respiratory function, oxidative stress and fish antioxidants were analyzed in juvenile Nile tilapia exposed for 96 hr to a sublethal trichlorfon concentration of 0.5 mg/L. The exposure to TRC induced oxidative stress in the heart, as manifested by the glutathione S-transferase depletion and hydroperoxide elevation, and was the most sensitive organ when compared to the liver and gills, in which the antioxidant mechanisms against TRC exposure were sufficient to remove reactive oxygen species (ROS), preventing the increase of lipid peroxidation. TRC exposure also reduced O(2) uptake (V O(2)) and increased the critical oxygen tension (PcO(2)), reducing the species capacity to survive prolonged hypoxic conditions. The heart rate and force contraction were significantly impaired, making the heart the most sensitive organ when exposed to the TRC.

/AQUATIC SPECIES/ Trichlorfon (TCF) is one of the most used veterinary pharmaceuticals not only to fight infestations but also as a preventive measure worldwide. The high concentrations used generate concerns about environmental and human health. ...The acute toxicity of this compound to non-target organisms belonging to different trophic levels /was assessed/: Danio rerio (early life stages and adults), Daphnia magna and algae (Pseudokirchneriella subcapitata and Chlorella vulgaris), and studied the potential of the biomarkers cholinesterase (ChE), glutathione-S-transferase (GST), lactate dehydrogenase (LDH) and catalase (CAT) to assess sub-lethal effects of trichlorfon in zebrafish and daphnids. The fish embryo test followed the OECD draft guideline FET and was based on the exposure of newly fertilized eggs to 0, 2.5, 5.0, 10, 20, 40, 80 and 160 mg/L of TCF for 5 days; the fish acute test followed the OECD guideline 203 and was based on the exposure of adult fish to 0, 2.5, 5, 10, 20, 40, 60 and 80 mg/L of TCF for 4 days; Daphnia sp. immobilization assay followed the OECD guideline 202 and was based on the exposure of juvenile daphnids to 0, 0.1, 0.3, 0.5, 0.7, 0.9, 1 and 2 ug/L of TCF for 2 days and the algae growth inhibition assay followed the OECD guideline 201 and was based on the exposure of the two species to 0, 1, 3.2, 10, 32, 100 and 300 mg/L of TCF for 4 days. Biomarker levels were measured after 96 hr exposure to TCF in zebrafish early life stages and adults and after 48 hr exposure in D. magna. Tested organisms seem to have dissimilar sensitivities towards TCF exposure. D. magna (48 hr-LC(50)=0.29 ug/L) was the most sensitive organism, followed by early life stages and adults of zebrafish (96 hr-LC(50)=25.4 and 28.8 mg/L, respectively) and finally by the algae P. subcapitata (96 hr-LC(50)=274.5 mg/L) and C. vulgaris (no effect observed). As daphnids are a source of food for organisms of higher trophic levels, the impairment on its population is prone to have consequences in the entire ecosystem. The biomarker activities measured in daphnids and fish seemed to be useful tools in the assessment of trichlorfon effects, especially ChE activity which was the most sensitive biomarker tested for all organisms. Trichlorfon was teratogenic for zebrafish embryos leading to anomalies in the absorption of the yolk sac, spine bending and pericardial oedemas. The present research suggests that further work is urgently needed in order to monitor environmental concentrations of trichlorfon and to test the long term effects of environmentally realistic concentrations of this compound.

/AQUATIC SPECIES/ Trichlorfon (TRC) is the most common organophosphorous insecticide used in aquaculture practices in Southeast Asian countries. Indiscriminate use of TRC can either damage or alter the enzymatic and hormonal activities in the living organisms. In this present study, therefore, toxicogenomic analyses using real time PCR was used to characterize expression levels of various genes in Pangasianodon hypophthalmus after exposure to three concentrations, the 96 hr 1/100(LC(50)) (0.01 mg/L), the 96 hr 1/10(LC(50)) (0.1 mg/L) and the 96 hr 1/2(LC(50)) (0.5 mg/L) of TRC for 6 hr, 24 hr, 96 hr, 7 days, 14 days, 28 days and 56 days respectively. The expression kinetics of stress and other cellular toxicity representative genes such as heat shock protein70 (HSP70), growth hormone, acetylcholinesterase (AChE), trypsinogen, cytochrome P4501B (CYP1B) and cytochrome oxidase subunit 1 (COI) were investigated in liver and gills. TRC at a level of 0.1 mg/L and 0.5 mg/L induced a time and dose-dependent increase in the expression of the HSP70, COI and CYPIB while the transcript level of AChE, growth hormone and trypsinogen were significantly down-regulated. These results could permit to develop a "molecular biomarker system" which can be applied as a first-tier method of identifying contaminant exposure before effects at population level occur.

For more Ecotoxicity Excerpts (Complete) data for Trichlorfon (23 total), please visit the HSDB record page.

The substance is very toxic to aquatic organisms. This substance may be hazardous to the environment. Special attention should be given to bees and fish.

Trichlorfon's production and use as a veterinary medicine may result in its release to the environment through various waste streams; it's use as an insecticide will result in its direct release to the environment. If released to air, a vapor pressure of 7.8X10-6 mm Hg at 20 °C indicates trichlorfon will exist in both the vapor and particulate phases in the atmosphere. Vapor-phase trichlorfon will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 2.5 days. Particulate-phase trichlorfon will be removed from the atmosphere by wet and dry deposition. Photodegradation of trichlorfon is slow and can result in the formation of another insecticide, dichlorvos. If released to soil, trichlorfon is expected to have high to very high mobility based upon reported Koc values of 6-79. Volatilization from moist soil surfaces is not expected to be an important fate process based upon an estimated Henry's Law constant of 2.2X10-11 atm-cu m/mole. Trichlorfon is not expected to volatilize from dry soil surfaces based upon its vapor pressure. The dissipation half-life for trichlorfon in soil is reported as <1-27 days. If released into water, trichlorfon may adsorb to suspended solids and sediment based upon the reported Koc values. Complete degradation of trichlorfon in aquatic environments occurs in <20 days. Volatilization from water surfaces is not expected to be an important fate process based upon this compound's Henry's Law constant. An estimated BCF of 3 suggests the potential for bioconcentration in aquatic organisms is low. Trichlorfon is subject to hydrolysis with half-lives (22 °C) of 510 days (pH 4), 46 hours (pH 7), and <30 minutes (pH 9) being reported. Occupational exposure to trichlorfon may occur through inhalation and dermal contact with this compound at workplaces where trichlorfon is produced or used. Monitoring data indicate that the general population may be exposed to trichlorfon mainly via dermal contact where the pesticide is used, specifically at golf courses. Exposure can also occur through its medical administration. (SRC)

Trichlorfon is not known to occur as a natural product.

Trichlorfon's production and use as a veterinary anthelmintic medicine(1) may result in its release to the environment through various waste streams; it's use as an insecticide(1) will result in its direct release to the environment(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), Koc values of 6-79(2-3) indicate that trichlorfon is expected to have high to very high mobility in soil(SRC). Volatilization of trichlorfon from moist soil surfaces is not expected to be an important fate process(SRC) given an estimated Henry's Law constant of 2.2X10-11 atm-cu m/mole(SRC), based upon its vapor pressure, 7.8X10-6 mm Hg(4), and water solubility, 1.2X10+5 mg/L(5). Trichlorfon is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(4). Trichlorfon, at an initial concentration of 2 ppm in soil, degraded 100% in 1.5 months at pH values of 3-4.6 and in 0.5 months at pH values of 8.7-9.05(6). Half-lives in clay (pH 7.9) and calcerous (pH 8.1) soils have been determined to be 1.15 and 1.05 days, respectively(7). Persistence of trichlorfon in soils has been reported as 2 weeks or less and is degraded by ammonifying microorganisms(8). Trichlorfon degrades rapidly in aerobic soils with reported half-lives of approximately 1-27 days under non-sterile conditions(9). The dissipation half-life of trichlorfon from plants has been estimated to be 2.36-3.10 days(10).

TERRESTRIAL FATE: The reported half-life for trichlorfon in aerobic soils was reported as 3-27 days. Using standard practices for application of pesticides to golf greens, trichlorfon dissipation half-lives were found to be 1.1 and 6 days in 1996 and 1997, respectively(1). Loss of trichlorfon due to volatilization, clipping removal and leaching from the greens was minimal(1). Dissipation of trichlorfon in individual components of the greens were as follows(1):[Table#2326]

AQUATIC FATE: Based on a classification scheme(1), Koc values of 6-79(2-3) indicate that trichlorfon may adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is not expected(4) based upon an estimated Henry's Law constant of 2.2X10-11 atm-cu m/mole(SRC), derived from its vapor pressure, 7.8X10-6 mm Hg(5), and water solubility, 1.2X10+5 mg/L(6). Trichlorfon is subject to hydrolysis and decomposition proceeds more rapidly with heating, and above pH 6(7). Hydrolysis half-lives (22 °C) of trichlorfon were reported as 510 days (pH 4), 46 hours (pH 7), and <30 minutes (pH 9)(7). According to a classification scheme(8), an estimated BCF of 3(SRC), from its log Kow of 0.51(9) and a regression-derived equation(10), suggests the potential for bioconcentration in aquatic organisms is low. Complete biodegradation of trichlorfon in river water occurred within 5 days at 10 mg/L, 13 days at 20 mg/L, and 20 days at 30 mg/L(11). In screening studies carried out at 20 °C using activated sludge inoculum, the aerobic biodegradation rate of trichlorfon was determined to be 0.28/day with a half-life of 2.5 days(12). Trichlorfon underwent photochemical conversion to dichlorvos when irradiated under UV light in an aqueous solution(13).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), dichlorvos, which has a vapor pressure of 0.0158 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase dichlorvos is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals, ozone and nitrate radicals; the half-life for these reactions in air is estimated to be 11-19 hours, 70 days and 3.2 hours(SRC), calculated from respective rate constants of 2.0X10-11 to 3.5X10-11(3-5), 1.7X10-19(5) and 2.5X10-13(5) cu cm/molecule-sec. Dichlorvos absorbs light in the UV range with a maximum absorbance of 295-305 nm and was found to have a photodegradation rate constant of 2.652X10-9 L/sec, giving it a photodegradation half-life of about 7.25 hours(6).

AEROBIC: Complete biodegradation of trichlorfon in river water occurred within 5 days at 10 mg/L, 13 days at 20 mg/L, and 20 days at 30 mg/L(1). Persistence of trichlorfon in soils has been reported as 2 weeks or less and is degraded by ammonifying microorganisms(1). Trichlorfon degrades rapidly in aerobic soils with reported half-lives of approximately 1-27 days under non-sterile conditions(2). The biodegradation rate constant and half-life for trichlorfon was determined to be 0.28/day and 2.5 days, respectively, in an aerobic biodegradability test using an activated sludge inoculum incubated at 20 °C for 50 days(3). The decomposition rate of trichlorfon in river water at pH 7.39 was higher than in distilled water at pH 7.3-7.5 indicating that biodegradation aided in trichlorfon's decomposition in water(4).

The rate constant for the vapor-phase reaction of trichlorfon with photochemically-produced hydroxyl radicals has been estimated as 6.2X10-12 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 2.6 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Trichlorfon is subject to hydrolysis and decomposition proceeds more rapidly with heating, and above pH 6(2). Hydrolysis half-lives (22 °C) of trichlorfon were reported as 510 days (pH 4), 46 hours (pH 7), and <30 minutes (pH 9)(2). Trichlorfon is unstable under basic conditions and liberates hydrochloric acid in alkaline hydrolysis to form dichlorvos(3). Half-lives of 3.7 days, 6.5 hours and 63 minutes for trichlorfon have been reported in Sorensen buffers of pH 6, 7 and 8, respectively, at 37.5 °C(3). Trichlorfon slowly decomposes in aqueous acidic solutions(4). Trichlorfon was degraded to dichlorvos in water (99:1 water-ethanol) with half-lives of about 670, 67 and 17 hours at respective pH values of 6, 7 and 8(5). Photolysis of trichlorfon is slow(2). Trichlorfon underwent photochemical conversion to dichlorvos when irradiated under UV light in an aqueous solution(6).

An estimated BCF of 3 was calculated in fish for trichlorfon(SRC), using a log Kow of 0.51(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low.

The Koc of trichlorfon has been reported to be 6-79(1-6). According to a classification scheme(7), these Koc values suggests that trichlorfon is expected to have high to very high mobility in soil(SRC). In lysimeter studies designed to simulate golf course fairways and greens, trichlorfon was found to migrate quickly and was detected in the leachate after the first watering event(8).

The Henry's Law constant for trichlorfon is estimated as 2.2X10-11 atm-cu m/mole(SRC) derived from its vapor pressure, 7.8X10-6 mm Hg(1), and water solubility, 1.2X10+5 mg/L(2). This Henry's Law constant indicates that trichlorfon is expected to be essentially nonvolatile from water and moist soil surfaces(3). Trichlorfon is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1). In a study of a creeping bentgrass putting green under customary field management practices at the University of California-Riverside Turf Research Facility conducted in 1996 and 1997, the cumulative loss of trichlorfon due to volatilization was only 0.01 and 0.008% of applied mass, respectively(4).

SURFACE WATER: The highest concentration of trichlorfon in water samples taken downstream from a pesticide factory in Hunan, China was 4 ppm(1). Trichlorfon was detected at 14 of 22 sampling sites collected 1989-1990 in the Guadalquivir River Basin, Spain at mean concentrations of 0.01-2.18 ug/L(2). Trichlorfon was detected in 18 surface water samples collected from two vineyard catchments in southwestern Germany at concentrations of 6-182 ug/L after aerial application(3). Trichlorfon was detected in water samples collected Sep 2008 to Mar 2009 from 24 stream systems in southeast Australia at 0.002-0.006 ug/L(4).

SEDIMENT: Trichlorfon was not detected (detection limit 2.0 ug/kg) in sediment samples collected Sep 2008 to Mar 2009 from 24 stream systems in southeast Australia(1).

SOURCE DOMINATED: Average daily ambient concentration of trichlorfon were 1.1X10-3, 1.7X10-3 and 1.5X10-3 ng/cu m over golf courses in Boston, MA, Philadelphia, PA and Rochester, NY, respectively(1). Maximum concentrations of trichlorfon over the same golf courses were 5.1X10-2, 8.1X10-2 and 7.0X10-2 ug/cu m, respectively(1).

Trichlorfon was detected in 1 of 13,980 food samples collected by state food laboratories in 10 states (California, Florida, Indiana, Massachusetts, Michigan, New York, North Carolina, Oregon, Virginia, Wisconsin) during fiscal year 1988; it was not detected in 13,085 food samples collected during a similar study conducted in fiscal year 1989(1). In a study of grapes, 60% of trichlorfon residues were found in the skin; levels were higher in grape juice concentrate, raisins, and wine than in grapes, and trichlorfon accumulated in wine(2). Trichlorfon applied as a veterinary medicine can produce residues in meat(3). Trichlorfon was not detected (detection limit 9.35 ng/g) in 278 honey samples collected in 2003-2004 from 33 locations throughout Turkey(4).

Trichlorfon was not detected in the following food products(1-4):[Table#2328]

Trichlorfon was detected at 0.05 ppm in seeds harvested from plants treated with twice the registered rate of foliar spray application, it was not detected (detection limit 0.02 ppm) in alfalfa plants germinated from those seeds(1). Trichlorfon was not detected (detection limit not reported) in 8 tomato, 12 cucumber or 4 onion samples from Cuba, but was detected at 0.08-0.12 ug/kg in 12 pepper crop samples(2).

Trichlorfon was not detected (detection limit 0.05 mg/kg) in Australian farmed yellowtail kingfish (Seriola lalandi) or Mulloway (Argyrosomus hololepidotus); fish were collected Sept 2003 to July 2004(1).

Trichlorfon was not detected in the liver tissue of 23 food-producing animals in 1980(1). Trichlorfon was not detected (detection limit 0.2 mg/kg) in four raw wool samples(2).

Following dermal and intragastric application of trichlorfon to cows, the parent compound and dichlorvos were detected in the milk up to 22 days after application(1).

Samples of tobacco leaf collected 1976-1977 from cured commercial crops in three warehouses in Ontario, Canada did not contain trichlorfon(1). Trichlorfon was not detected in cured tobacco samples collected 1976-1978 from 33-34 farms in southern Ontario even though fields had been treated with the chemical(1). Trichlorfon was not detected (detection limit 10 ug/kg) in 118 tobacco samples from China(2). Trichlorfon is listed as an ingredient in two home use products(3).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 338 workers (131 of these are female) were potentially exposed to trichlorfon in the US(1). The NOES Survey does not include farm workers. Occupational exposure to trichlorfon may occur through inhalation and dermal contact with this compound at workplaces where trichlorfon is produced or used(SRC). During vineyard spraying operations, the operator's hands in the cab (with no air-conditioning) of a spray tractor are potentially exposed to 56.16 ug/100 sq cm trichlorfon via dermal contact with contaminated surfaces of the cab(2). In pesticide formulating plants, exposure to trichlorfon may be from spillage; there is a high potential for exposure at mixing and bagging stations(3). Trichlorfon is applied to several crops and forests via aerial or ground spraying (2,4-5) and contaminated equipment may be a potential source of dermal exposure of operators to trichlorfon(2). Crop workers may be exposed during application, however, their main exposure results from contact with treated foliage or to pesticide or pesticide-contaminated material made airborne through agitation of foliage during work activity(3-4). Incidental to treating a crop, some pesticides, such as trichlorfon, may drift onto workers in neighboring fields or in nearby suburban areas without there being any intent to treat those areas(3,5). Monitoring data indicate that the general population may be exposed to trichlorfon mainly via dermal contact where the pesticide is used, specifically at golf courses(SRC). Exposure can also occur through its medical administration(SRC).

A Chinese total diet study, conducted in 1990, found that the average daily intake of trichlorfon was 0, 0, 0 and 11.5 ug/person/day in 4 different regions(1).

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

SRP: Wastewater from contaminant suppression, cleaning of protective clothing/equipment, or contaminated sites should be contained and evaluated for subject chemical or decomposition product concentrations. Concentrations shall be lower than applicable environmental discharge or disposal criteria. Alternatively, pretreatment and/or discharge to a permitted wastewater treatment facility is acceptable only after review by the governing authority and assurance that "pass through" violations will not occur. Due consideration shall be given to remediation worker exposure (inhalation, dermal and ingestion) as well as fate during treatment, transfer and disposal. If it is not practicable to manage the chemical in this fashion, it must be evaluated in accordance with EPA 40 CFR Part 261, specifically Subpart B, in order to determine the appropriate local, state and federal requirements for disposal.

Product: Offer surplus and non-recyclable solutions to a licensed disposal company. Contact a licensed professional waste disposal service to dispose of this material. Dissolve or mix the material with a combustible solvent and burn in a chemical incinerator equipped with an afterburner and scrubber; Contaminated packaging: Dispose of as unused product.

Add a combustible solvent and burn in a furnace equipped with an afterburner and an alkali scrubber. In accordance with 40CFR165, follow recommendations for the disposal of pesticides and pesticide containers. Must be disposed properly by following package label directions or by contacting your local or federal environmental control agency, or by contacting your regional EPA office.

Trichlorofon initially hydrolyzes to the more toxic compound dichlorvos at pH 8 and 37.5 °C, but is essentially 100% hydrolyzed in approximately 24 hr to nontoxic products which can be mixed with a portion of soil rich in organic matter and buried. Recommendable methods: Incineration, hydrolysis, and landfill. Peer-review: Large amount of trichlorofon should be incinerated at high temperature in a unit with effluent gas scrubbing. (Peer-review conclusions of a IRPTC expert consultation (May 1985))

/GUIDE 131 FLAMMABLE LIQUIDS - TOXIC/ Fire or Explosion: HIGHLY FLAMMABLE: Will be easily ignited by heat, sparks or flames. Vapors may form explosive mixtures with air. Vapors may travel to source of ignition and flash back. Most vapors are heavier than air. They will spread along ground and collect in low or confined areas (sewers, basements, tanks). Vapor explosion and poison hazard indoors, outdoors or in sewers. Those substances designated with a (P) may polymerize explosively when heated or involved in a fire. Runoff to sewer may create fire or explosion hazard. Containers may explode when heated. Many liquids are lighter than water. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/

/GUIDE 131 FLAMMABLE LIQUIDS - TOXIC/ Health: TOXIC; may be fatal if inhaled, ingested or absorbed through skin. Inhalation or contact with some of these materials will irritate or burn skin and eyes. Fire will produce irritating, corrosive and/or toxic gases. Vapors may cause dizziness or suffocation. Runoff from fire control or dilution water may cause pollution. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/

/GUIDE 131 FLAMMABLE LIQUIDS - TOXIC/ Public Safety: CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number listed on the inside back cover. As an immediate precautionary measure, isolate spill or leak area for at least 50 meters (150 feet) in all directions. Keep unauthorized personnel away. Stay upwind, uphill and/or upstream. Ventilate closed spaces before entering. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/

/GUIDE 131 FLAMMABLE LIQUIDS - TOXIC/ Protective Clothing: 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. /Organophosphorus pesticide, liquid, flammable, poisonous; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, poisonous, flammable; Organophosphorus pesticide, liquid, toxic, flammable/

For more DOT Emergency Guidelines (Complete) data for Trichlorfon (16 total), please visit the HSDB record page.

UN 2784; Organophosphorus pesticides, liquid, flammable, toxic, flash point less than 23 °C

UN 2783; Organophosphorus pesticides, solid, toxic

UN 3017; Organophosphorus pesticides, liquid, toxic, flammable, flash point not less than 23 °C

UN 3018; Organophosphorus pesticides, liquid, toxic

For more Shipping Name/ Number DOT/UN/NA/IMO (Complete) data for Trichlorfon (8 total), please visit the HSDB record page.

49 403 75; Trichlorfon (agricultural insecticides, not elsewhere classified, liquid)

49 403 76; Trichlorfon (agricultural insecticides, not elsewhere classified, other than liquid)

49 403 77; Trichlorfon (insecticides, other than agricultural, not elsewhere classified)

No person may /transport,/ offer or accept a hazardous material for transportation in commerce unless that person is registered in conformance ... and the hazardous material is properly classed, described, packaged, marked, labeled, and in condition for shipment as required or authorized by ... /the hazardous materials regulations (49 CFR 171-177)./

The International Air Transport Association (IATA) Dangerous Goods Regulations are published by the IATA Dangerous Goods Board pursuant to IATA Resolutions 618 and 619 and constitute a manual of industry carrier regulations to be followed by all IATA Member airlines when transporting hazardous materials. Organophosphorus pesticide, solid, toxic; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, toxic, flammable; and Organophosphorus pesticide, liquid, toxic are included on the dangerous goods list. /Organophosphorus pesticide, solid, toxic; Organophosphorus pesticide, liquid, flammable, toxic; Organophosphorus pesticide, liquid, toxic, flammable; and Organophosphorus pesticide, liquid, toxic/

The International Maritime Dangerous Goods Code lays down basic principles for transporting hazardous chemicals. Detailed recommendations for individual substances and a number of recommendations for good practice are included in the classes dealing with such substances. A general index of technical names has also been compiled. This index should always be consulted when attempting to locate the appropriate procedures to be used when shipping any substance or article. /Organophosphorus pesticide, solid, toxic; Organophosphorus pesticide, liquid, flammable, toxic, flashpoint less than 23 °C; Organophosphorus pesticide, liquid, toxic, flammable, flashpoint not less than 23 °C; and Organophosphorus pesticide, liquid, toxic are included on the dangerous goods list. /Organophosphorus pesticide, liquid, flammable, toxic, flashpoint less than 23 °C; Organophosphorus pesticide, liquid, toxic, flammable, flashpoint not less than 23 °C; and Organophosphorus pesticide, liquid, toxic/

Do not transport with food and feedstuffs. Marine pollutant.

Symbol: Xn, N; R: 22-43-50/53; S: (2)-24-37-60-61

UN Hazard Class: 6.1; UN Pack Group: III