2,4-D

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.

STCC NUMBER

49 411 26

DESIGNATIONS

BEILSTEIN REFERENCE NUMBER:4-06-00-00908
IMO CLASSIFICATION:3.2 - Phenoxy pesticides, liquid, flammable, toxic, not otherwise specified, flashpoint less than 23 deg C
IMO CLASSIFICATION:6.1 - Phenoxy pesticides, solid, toxic, not otherwise specified; phenoxy pesticides, liquid, toxic, flammable, not otherwise specified, flashpoint between 23 deg C and 61 deg C; phenoxy pesticides, liquid, toxic, not otherwise specified

MOLECULAR FORMULA

C8-H6-Cl2-O3
OCH2COOH

ERG GUIDE NUMBER

151-SUBSTANCES - TOXIC (NON-COMBUSTIBLE)

SYNONYM REFERENCE

(EPA, 1990; EXTOXNET, 2002; HSDB, 2004; Lewis, 2000; RTECS, 2004)

USES/FORMS/SOURCES

USES

2,4-D (2,4-dichlorophenoxyacetic acid) is an organic phenoxy herbicide that is one of the most extensively used herbicides in the world. It is a systemic herbicide and plant growth regulator. 2,4-D is used to selectively limit broadleaf weeds by post-emergent control on annual mustard, Canada thistle, dandelion, lambsquarters, ragweed, and other weeds. Some formulations are used for pine release or water hyacinth control and prevention of seed formation. It is used on asparagus, barley, corn, grasses, hay, millet, oats, rice, rye, sorghum, soybeans, sugarcane, wheat, and orchard crops. 2,4-D is applied on fallow land, pasture, rangeland, turf, and noncrop areas in agriculture, forestry, and lawn and garden care. It is also used as a defoliant to control woody plants along roads, railways, and right-of-ways (ACGIH, 2001; Bingham et al, 2001a; EPA, 1990; (EPA, 2002); Harbison, 1998a; Lewis, 2001a; NPTN , 2002; NTP , 2001).
2,4-D was first registered as a herbicide in 1948. Today, it is registered in the U.S. as a General Use Pesticide (GUP) and allowed for use on more than 65 crops. There are over 1500 registered products that contain 2,4-D as an active ingredient. They include many crop herbicides, forestry products, non-cropland herbicides, aquatic weed control products, orchard weed control products, lawn care products, and wheat, corn and other monocot (grass family) crop herbicides (Bingham et al, 2001a; EPA, 1990; EXTOXNET, 2002; NPTN , 2002).
Its role in agriculture as a plant growth regulator will increase latex output of aged rubber trees and control fruit drop and ripening in citrus orchards and tomato crops (EPA, 1990; (EPA, 2002); NPTN , 2002).
In forestry it is used on rangelands for brush control; conifer release; general, noxious, and poisonous weed control; range, nursery stand, and wildlife habitat improvement; range, recreation, timber, and fire-break management; and for aquatic weed control (EPA, 1990; (EPA, 2002); NPTN , 2002; USDA , 2002).
2,4-D is a major means of accomplishing aquatic vegetation management in lakes and ponds which do not provide water for domestic or irrigation purposes. It is used for control of water hyacinth (Eichhornia crassipes), alligatorweed (Alternanthera philoxeroides), Eurasian watermilfoil (Myriophyllum spicatum), and other aquatic plants (EPA, 1990; (USACE, 2002)) .
2,4-D mimics the plant hormone auxin. It is absorbed through the plant leaves, stems, and roots. It behaves systemically, stimulating nucleic acid and protein synthesis, which influences enzyme activity, respiration, and cell division. It causes rapid cell division and abnormal growth leading to plant poisoning (NPTN , 2002; USDA , 2002).
2,4-D was a component of the military defoliant Agent Orange, used extensively in Vietnam, composing 50% of the product. Controversies associated with Agent Orange were thought to be associated with TCDD (dioxin) contamination of the 2,4,5-T component of Agent Orange. TCDD has been found to be highly toxic to laboratory animals. The numerous studies on persons exposed to Agent Orange will not be included in this review(ACGIH, 2001; EXTOXNET, 2002).

FORMS

2,4-D is a white powder or a crystalline solid with a slight phenolic odor. Yellow powders of 2,4-D are a result of phenolic impurities. Granular or liquid forms may be brown in color. It is commercially available as the acid, which is the parent compound, or in various derivatives or formulations of its inorganic salts (sodium, dimethylamine, diethanolamine, or triethanolamine salts) or ester derivatives. Formulations may be granular, amine and ester liquids, or dust aerosol spray (foam). The acids and salts of 2,4-D are in the form of colorless crystals, while the isopropyl ester is a colorless liquid (Ashford, 1994; Bingham et al, 2001a; EXTOXNET, 2002; Hartley & Kidd, 1990a; OHM/TADS, 2002).
It is often formulated as an emulsion or aqueous solution, or it exists as a dry, granular compound (EXTOXNET, 2002; Harbison, 1998a; Hathaway et al, 1996a; ILO, 1998).
It can be applied as a foliar spray in an aqueous solution for orchard applications or in higher concentrations for weed control. Many 2,4-D formulations contain the more water-soluble amine salts or the ester derivatives that readily dissolve in organic solvent. Other means of application include ground and aerial spray equipment, knapsack sprayers, pressure and hose-end applicators, lawn spreaders, cut surface treatments, basal bark spray, and injection (EPA, 1990; Bingham et al, 2001a; USDA , 2002).
The chlorinated phenoxyacid derivative 2,4-D and its congener, 2,4,5-T (2,4,5-trichlorophenoxyacetic acid) are frequently found together in commercial herbicide preparations. Dioxin (2,3,7,8-tetrachlorodibenzodioxin), a potent teratogen, is a contaminant in some preparations of 2,4-D and 2,4,5-T (Baselt, 2000a).
Technical grade 2,4-D will generally be 90% to 99% pure. There are also technical esters and formulated product grades (Harbison, 1998a; HSDB, 2004).
Technical grade 2,4-D is available in the U.S. as the free acid with 98% purity, as salts of dimethylamine, mixed ethanolamine and isopropanolamine, lithium, and sodium, as esters of isopropyl, n-butyl, sec-butyl, iso-octyl, and 2-butoxyethyl alcohols, and as an ester of butoxypolypropylene glycol (HSDB, 2004).

SOURCES

2,4-D is not known to occur naturally. It is prepared by adding 2,4-dichlorophenol and monochloroacetic acid in aqueous sodium hydroxide. It can also be produced by the chlorination of molten phenoxyacetic acid or from combining dichlorophenol, sodium, and ethyl chloroacetate with subsequent hydrolysis of the ester (Ashford, 1994; Budavari, 2000; Howard, 1991a).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

2,4-D is poisonous by ingestion, inhalation, dermal, and intravenous routes. Target organs include the CNS, skin, liver, and kidneys.

Acute exposure to 2,4-D is considered to be of slight to moderate toxicity to humans. It may be irritating to eyes, skin, and mucous membranes. Prolonged inhalation causes coughing, burning sensation in the throat and chest, nausea, vomiting, dizziness, incoordination, weakness and mild CNS depression. Seizures, coma, respiratory depression, acute lung injury, and ventricular fibrillation have been reported. Hepatic and renal toxicity has been reported.

Accidental ingestion is associated with gastritis, CNS depression, hyperthermia, dysphagia, possible respiratory muscle paralysis, and transient liver and kidney injury. High dose exposure can lead to convulsions or coma.

The free acid (2,4-D parent compound) has a somewhat higher toxicity than the sodium salt, the amine salts or the esters. The toxicity of 2,4-D may be influenced by organic carrier solvents used in commercial herbicide formulations.

Chronic exposure may result in weakness, fatigue, headache, vertigo, anorexia, nausea, eye and nasal irritation, skin irritation, bradycardia, and hypertension. Chronic exposure has also been reported to cause liver, kidney, and CNS damage. Peripheral neuropathy has also been reported.

Evidence suggests that high doses may cause reproductive effects in animals.

2,4-D is classified in Group 2B (possibly carcinogenic to humans) by the IARC. The EPA lists it as a group D carcinogen (not classifiable to human carcinogenicity). A possible relationship between 2,4-D and non-Hodgkins lymphoma has been suggested.

POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin.
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

2,4-D is toxic by all routes of exposure, although substantial dermal or inhalational exposure is usually necessary in order for systemic effects to occur(Hathaway et al, 1996; Bradberry et al, 2000). Oral exposure may occur from accidental ingestion, although many cases of intentional ingestion have been reported in the literature.

Acute exposure to 2,4-D is considered to be of slight to moderate toxicity to humans. It may be irritating to eyes, skin, and mucous membranes. Prolonged inhalation causes coughing, burning sensation in the throat and chest, nausea, vomiting, dizziness, incoordination, weakness and mild CNS depression. Seizures, coma, respiratory depression, acute lung injury, cardiac dysrhythmias including ventricular fibrillation, rhabdomyolysis and metabolic acidosis have been reported. Hepatic and renal toxicity have also been reported (Bradberry et al, 2000; ACGIH, 2001a).

Accidental ingestion is associated with gastritis, CNS depression, hyperthermia, dysphagia, possible respiratory muscle paralysis, and transient liver and kidney injury. High dose exposure can cause vomiting, diarrhea and lead to convulsions or coma (Bradberry et al, 2000; ACGIH, 2001a).

Chronic exposure may result in weakness, fatigue, headache, vertigo, anorexia, nausea, eye and nasal irritation, skin irritation, bradycardia, and hypertension. Chronic exposure has also been reported to cause liver, kidney, and CNS damage. Peripheral neuropathy has also been reported (ACGIH, 2001a).

The free acid (2,4-D parent compound) has a somewhat higher toxicity than the sodium salt, the amine salts or the esters. The toxicity of 2,4-D may be influenced by organic carrier solvents used in commercial herbicide formulations (HSDB, 2004).

The free acid form of 2,4-D is not absorbed to a great extent through the skin. In one study, only 4.46% of a dose applied in acetone to the back of the hand was recovered in the urine of human volunteers after 144 hours. The free acid of 2,4-D was absorbed to a greater extent than the dimethylamine salt; only 1.76% of the latter was recovered after application in water (Harris & Solomon, 1992).

One fatality has been reported due to ingestion of U 46 D-Fluid, a commercial product containing 500 g of 2,4-D per liter (Keller et al, 1994). It induced violent convulsions with no other significant findings in one fatal suicidal ingestion (Hathaway et al, 1991). In another fatal case, neurological findings included coma, loss of reflexes, hypotonia, and pendular motion of the eyes (ACGIH, 2001a).

In a review of 66 cases of acute 2,4-D poisonings, the following effects were noted. From ingestion: gastrointestinal effects and occasional GI hemorrhage, hypotension, hyperventilation or hypoventilation with respiratory failure, fever, hypertonia, paralysis, hyperreflexia or loss of tendon reflexes, fasciculation, ataxia, hallucinations, nystagmus, limb muscle weakness or myotonia and rhabdomyolysis, miosis, metabolic acidosis, renal failure, convulsions, and coma. One-third of the cases were fatal. Inhalation and dermal exposure can produce systemic effects, but no fatalities have been reported (Bradberry et al, 2000).

Reversible immunosuppression was seen in a group of ten Italian farmers recently exposed to 2,4-D; recovery was apparent when they were retested 50 to 70 days after exposure (Faustini et al, 1996).

The effects of acute 2,4-D poisoning may LAST FOR YEARS (Kaskevich & Soboleva, 1978).

Cytochrome P450 3A4 is involved in metabolism of 2,4-D in humans (Mehmood et al, 1996).

ANIMAL STUDIES

2,4-D has not shown systemic toxicity in animal studies so long as renal clearance was sufficient (Garabrant & Philbert, 2002). Locomotor effects were seen in rats at a high single dose of 250 or 600 mg/kg (Paulino et al, 1996; Mattsson et al, 1997). 2,4-D administered at high doses increased the levels of serotonin and dopamine in the brains of rats (Bortolozzi et al, 1998). Damage to the thymus and spleen occurred after a single oral administration in rats (Kaioumova et al, 2001a).
2,4-D was absorbed from soil at a rate similar to that from an acetone vehicle in monkeys; 24-hour percent accumulation in human skin in vitro was independent of concentration for soil loads of 5 to 40 mg/cm(2). In 8-hour studies, percutaneous absorption from soil was 0.03% for 40 mg/cm(2) soil load, compared with 3.2% in acetone vehicle. Dermal absorption from soil had an 8-hour lag time (Wester et al, 1996).

CHRONIC CLINICAL EFFECTS

Increased risk of mortality from amyotrophic lateral sclerosis was seen in a cohort of Dow Chemical employees involved in manufacturing 2,4-D) (relative risk = 3.45) (Burns et al, 2001).

Chronic exposure to 2,4-D can cause CNS effects (HSDB, 2004).

The estimated half-life for 2,4-D after dermal absorption in humans was 39.5 +/- 8.1 hours (Harris & Solomon, 1992). Thus, there is a possibility of cumulative toxicity with repeated exposure.

ANIMAL STUDIES

2,4-D had no effects by the oral route in dogs at 10 mg/kg/day for 90 days, or in rats at 400 mg/kg/day for 30 days (ACGIH, 2001a).
In subchronic feeding studies on dogs, the free acid, dimethylamine salt, and 2-ethylhexyl ester of 2,4-D had comparable toxicity on an acid-equivalent basis; the NOAEL for all three forms was 1.0 mg/kg/day (Charles et al, 1996a).
In a 1-year feeding study on dogs with the free acid form of 2,4-D, the NOAEL was 1.0 mg/kg/day; pathological changes were similar to those seen in a subchronic study and were not progressive. No immunotoxic effects were seen (Charles et al, 1996a).
In a chronic dietary study in dogs, the no observed adverse effect dose was 75 ppm. The liver and kidney were the target organs (Charles & Leeming, 1998b).
Retinal degeneration was observed in female Wistar rats administered a high dose of 150 mg/kg/day for 12 months (Mattsson et al, 1997).

-MEDICAL TREATMENT

LIFE SUPPORT

Support respiratory and cardiovascular function.

SUMMARY

FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (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.

FIRST AID

FIRST AID

If exposure occurs, follow these first aid measures (National Institute for Occupational Safety and Health, 2007; Chemsoft(R) , 2000):

EYE EXPOSURE - If this chemical contacts the eyes, immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Primary eye protection (spectacles or goggles), as defined by the Occupational Safety and Health Administration (OSHA), should be used when working with this chemical. Face shields should only be worn over primary eye protection.

Contact lens use is not recommended when working with this chemical. If contact lenses are worn, then appropriate eye and face protection devices must be used. OSHA emphasizes that dusty and/or chemical environments may represent an additional hazard to contact lens wearers.

DERMAL EXPOSURE - If this chemical contacts the skin, promptly wash the contaminated skin with soap and water. If this chemical penetrates the clothing, promptly remove the clothing and wash the skin with soap and water. Get medical attention promptly.
INHALATION EXPOSURE - If a person breathes large amounts of this chemical, move the exposed person to fresh air at once. If breathing has stopped, perform artifical respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible.
ORAL EXPOSURE - If this chemical has been swallowed, get medical attention immediately.

TARGET ORGANS - Skin, CNS, liver, and kidneys .

INHALATION EXPOSURE

INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.
If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.

DERMAL EXPOSURE

DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
Treat dermal irritation or burns with standard topical therapy. Patients developing dermal hypersensitivity reactions may require treatment with systemic or topical corticosteroids or antihistamines.

EYE EXPOSURE

DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.

ORAL EXPOSURE

Because of the potential for gastrointestinal tract irritation, CNS depression, and seizures, DO NOT induce emesis.
PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION

Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).

In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).

ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
ACUTE LUNG INJURY: Maintain ventilation and oxygenation and evaluate with frequent arterial blood gases and/or pulse oximetry monitoring. Early use of PEEP and mechanical ventilation may be needed.
SEIZURES: Administer a benzodiazepine; DIAZEPAM (ADULT: 5 to 10 mg IV initially; repeat every 5 to 20 minutes as needed. CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed) or LORAZEPAM (ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist. CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue).

Consider phenobarbital or propofol if seizures recur after diazepam 30 mg (adults) or 10 mg (children greater than 5 years).
Monitor for hypotension, dysrhythmias, respiratory depression, and need for endotracheal intubation. Evaluate for hypoglycemia, electrolyte disturbances, and hypoxia.

SUPPORTIVE CARE - Be prepared to treat respiratory depression, hypotension, and metabolic acidosis. Maintain adequate urine flow with intravenous fluids if victim is dehydrated. Monitor patient closely for cardiac arrhythmias and hyperthermia.

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

GENERAL/SUMMARY

The minimum lethal human dose to this agent has not been delineated.
The mean lethal dose in man is 28 g (estimated) (Baselt, 1997; Baselt, 2000).

ACUTE

Suicide data provide some information of minimum lethal exposure in humans. Reported levels of 2,4-D ingested in these cases ranged from at least 6500 mg to 50,000. Concentrations of 2,4-D measured in the blood and urine of another victim were 520 mg/L and 670 mg/L, respectively. Another victim had a blood level of 72 mg/100 mL, possibly the highest ever recorded (Hathaway et al, 1996; Hayes, 1982; Smith & Lewis, 1987).
In humans, fatalities have been reported after ingestion of amounts of 2,4-D acid ranging from 80 mg/kg to 1.2 to 1.8 g/kg (IARC, 1977; (McGuigan, 1986).

MAXIMUM TOLERATED EXPOSURE

GENERAL/SUMMARY

The maximum tolerated human exposure to this agent has not been delineated.
Ill effects were not reported in volunteers who ingested a one-time 5 mg/kg dose of 2,4-D (HSDB , 2002).
2,4-D is one of the group of chlorophenoxy herbicides that are considered possible human carcinogens by the IARC. The classification is based on limited evidence of carcinogenicity in humans for chlorophenoxy herbicides and inadequate evidence of carcinogenicity in experimental animals for 2,4-D ((IARC, 1987)).

Evidence used included cohort studies of workers exposed to 2,4-D in occupational scenarios which have shown an increased risk of cancers at all sites combined, soft tissue sarcoma, and bronchial or lung cancer. In addition, a statistically significant association between human exposure to phenoxy herbicides and the occurrence of soft-tissue sarcoma and malignant lymphoma (Hodgkin's and non-Hodgkin's) has been identified in population-based case control studies. A matched case-control study performed with cases of malignant lymphoma provided similar results (HSDB , 2002; (IARC, 1987)).
Results of epidemiological studies on the association between development of non-Hodgkin's lymphoma and exposure to chlorophenoxy herbicides, including 2,4-D, are not consistent (Bingham et al, 2001).

An acceptable daily intake for occupationally exposed individuals was set forth by the WHO at 0.3 mg/kg (Baselt, 1997).

ACUTE

A nonfatal case of accidental ingestion of 7.2 g of 2,4-D lead to gastritis, hyperthermia, and respiratory muscle paralysis (Baselt, 1997; Baselt, 2000).
Therapeutic administration of a total of 16.3 g of 2,4-D led to stupor, incoordination, weak reflexes, and loss of bladder control. A single dose of 3.6 grams of 2,4-D acid administered intravenously over a 2 hour period caused stupor, hyporeflexia, muscle twitching, and urinary incontinence (EXTOXNET, 2002; Hathaway et al, 1996).
Accidental inhalation exposure to 2,4-D was described for a man working with a 40% aqueous solution of 2,4-D. General weakness, excessive perspiration, oliguria, and vomiting were followed by CNS and peripheral nervous system effects such as dizziness, reflex changes, and unsteady gait. Transitory albuminuria was found in laboratory testing. After two and a half weeks, nervous system effects worsened and hemorrhagic enterocolitis developed. All symptoms except hyporeflexia had subsided by 5 months (HSDB , 2002).
Accidental exposure while applying 2,4-D as a spray from two solutions containing 235 g/L and 410 g/L reported the effects of polyneuritis (HSDB , 2002).
Aggressive behavior, confusion, coma, profound diaphoresis, and hyperthermia were reported in a 39-year-old male who intentionally ingested a large but unknown amount of 10% 2,4-D acid and 20% mecoprop. Marked myotonia and muscle weakness persisted for 2 months (Hayes, 1982) Prescott et al, 1979).

CHRONIC

A five- to ten-year exposure period at levels above 10 mg/m(3) was studied in an evaluation of worker exposure in a manufacturing environment. Workers complained of weakness, rapid fatigue, headache, and vertigo. Liver damage, slowed heartbeat and low blood pressure were also found (Sittig, 1991).

OCCUPATIONAL

CARCINOGENICITY-

ACGIH: A4, Not Classifiable as a Human Carcinogen (ACGIH, 2001).
USEPA: Carcinogenicity Assessment for Lifetime Exposure is not available at this time (IRIS , 2002).
IARC: Group 2B, chlorophenoxy herbicides, including 2,4-D, are possibly carcinogenic to humans ((IARC, 1987); NTP , 2001).

Carcinogenicity Ratings for CAS94-75-7 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: 2,4-D
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): A4 ; Listed as: 2,4-D

A4 :Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

EPA (U.S. Environmental Protection Agency, 2011): Not Assessed under the IRIS program. ; Listed as: 2,4-Dichlorophenoxyacetic acid (2,4-D)
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: 2,4-D
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 IRIS

EPA Risk Assessment Values for CAS94-75-7 (U.S. Environmental Protection Agency, 2011):

Oral:

Slope Factor:
RfD: 1x10(-2) mg/kg-day

Inhalation:

Unit Risk:
RfC:

Drinking Water:

Unit Risk:

TOXICITY VALUES

References: Lewis, 2000 NTP, 2001 RTECS, 2002
- LD50- (ORAL)CHICKEN:
- LD50- (ORAL)DOG:
- LD50- (INTRAPERITONEAL)GUINEA_PIG:
- LD50- (ORAL)GUINEA_PIG:
- LD50- (ORAL)HAMSTER:
- LD50- (INTRAPERITONEAL)MOUSE:
- LD50- (INTRAVENOUS)MOUSE:
- LD50- (ORAL)MOUSE:
- LD50- (SKIN)MOUSE:
- LD50- (INTRAPERITONEAL)RABBIT:
- LD50- (INTRAVENOUS)RABBIT:
- LD50- (SKIN)RABBIT:
- LD50- (INTRAPERITONEAL)RAT:
- LD50- (ORAL)RAT:
- LD50- (SKIN)RAT:
- LDLo- (INTRAPERITONEAL)GUINEA_PIG:
- LDLo- (ORAL)HUMAN:
- LDLo- (INTRAPERITONEAL)MOUSE:
- LDLo- (INTRAPERITONEAL)RABBIT:
- LDLo- (INTRAVENOUS)RABBIT:
- LDLo- (ORAL)RABBIT:
- LDLo- (INTRAPERITONEAL)RAT:
- TDLo- (INTRAVENOUS)DOG:
- TDLo- (ORAL)DOG:
- TDLo- (ORAL)HAMSTER:
- TDLo- (ORAL)HUMAN:
- TDLo- (ORAL)MOUSE:
- TDLo- (SUBCUTANEOUS)MOUSE:
- TDLo- (INTRAPERITONEAL)RAT:
- TDLo- (ORAL)RAT:

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS94-75-7 (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.

Under Study

2,4-D

TLV:

TLV-TWA:
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: Not Listed
Codes: Not Listed
Definitions: Not Listed

TLV Basis - Critical Effect(s):
Molecular Weight:

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

Adopted Value

2,4-D

TLV:

TLV-TWA: 10 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: A4
Codes: Not Listed
Definitions:

A4: Not Classifiable as a Human Carcinogen: Agents which cause concern that they could be carcinogenic for humans but which cannot be assessed conclusively because of a lack of data. In vitro or animal studies do not provide indications of carcinogenicity which are sufficient to classify the agent into one of the other categories.

TLV Basis - Critical Effect(s): URT and skin irr
Molecular Weight: 221.04

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

AIHA WEEL Values for CAS94-75-7 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS94-75-7 (National Institute for Occupational Safety and Health, 2007):

Listed as: 2,4-D
REL:

TWA: 10 mg/m(3)
STEL:
Ceiling:
Carcinogen Listing: (Not Listed) Not Listed
Skin Designation: Not Listed
Note(s):

IDLH:

IDLH: 100 mg/m3
Note(s): Not Listed

OSHA PEL Values for CAS94-75-7 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Listed as: 2,4-D (Dichlorophenoxyacetic acid)
Table Z-1 for 2,4-D (Dichlorophenoxyacetic acid):

8-hour TWA:

ppm:

Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

mg/m3: 10

Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

Ceiling Value:
Skin Designation: No
Notation(s): Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS94-75-7 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS94-75-7 (U.S. Environmental Protection Agency, 2010):

Listed as: 2,4-D (D016)
Final Reportable Quantity, in pounds (kilograms):

100 (45.4)

Additional Information: Unlisted Hazardous Wastes Characteristic of Toxicity
Listed as: Acetic acid, (2,4-dichlorophenoxy)-, salts & esters
Final Reportable Quantity, in pounds (kilograms):

100 (45.4)

Additional Information:
Listed as: 2,4-D Acid
Final Reportable Quantity, in pounds (kilograms):

100 (45.4)

Additional Information:
Listed as: 2,4-D, salts and esters
Final Reportable Quantity, in pounds (kilograms):

100 (45.4)

Additional Information:

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS94-75-7 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS94-75-7 (U.S. Environmental Protection Agency, 2010b):

Listed as: Acetic acid, (2,4-dichlorophenoxy)-, salts & esters
P or U series number: U240
Footnote:
Listed as: 2,4-D, salts & esters
P or U series number: U240
Footnote:
Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

EPA SARA Title III, Extremely Hazardous Substance List for CAS94-75-7 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA SARA Title III, Community Right-to-Know for CAS94-75-7 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Listed as: 2,4-D [Acetic acid, (2,4-dichlorophenoxy)-]
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

DOT List of Marine Pollutants for CAS94-75-7 (49 CFR 172.101 - App. B, 2005):

Not Listed

EPA TSCA Inventory for CAS94-75-7 (EPA, 2005):

Listed as: Acetic acid, (2,4-dichlorophenoxy)-

SHIPPING REGULATIONS

SURFACE

DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):

Not Listed

ICAO International Shipping Name (ICAO, 2002):

Not Listed

LABELS

NFPA

NFPA Hazard Ratings for CAS94-75-7 (NFPA, 2002):

Not Listed

-HANDLING AND STORAGE

SUMMARY

INDUSTRIAL CHEMICALS

Chemical material containing 2,4-D should be stored in a secure, dry location that is temperature-controlled or refrigerated and protected from moisture and light. Storage in the original container is recommended. Due to fire and explosion hazards, it should be kept away from oxidizing materials and, if possible, stored in an inert atmosphere. Workers may experience serious eye and skin irritation if protective clothing and equipment are not used during handling and use. Appropriate precautions should be taken to prevent contamination and exposure (EXTOXNET, 2002; Hartley & Kidd, 1990; Meister & 2002, 2002; NTP , 2001).

HANDLING

2,4-D is considered an eye and skin irritant, and it presents a toxicity hazard through ingestion, inhalation, eye contact, and dermal exposure (EXTOXNET, 2002; Lewis, 2001; NTP , 2001).

Appropriate protective clothing should be worn to prevent repeated or prolonged contact. This will vary by formulation, although long-sleeved shirt, long pants, shoes and socks, chemical-resistant or rubber gloves, eye protection, and an apron should be worn during handling. Eye and respiratory protection, such as a full-face respirator or safety glasses and a filter mask, are also recommended (ITI, 1995; Meister & 2002, 2002; OHM/TADS , 2002; Sittig, 1991).

The material should be carefully handled so as not to contaminate water, food, or animal feed during storage, use, or disposal. Spray equipment contaminated with 2,4-D should be thoroughly cleaned if it is to be used for any other purposes (Meister & 2002, 2002).

STORAGE

CONTAINER

Store in a tightly-closed container, preferably in the original container. The product material of 2,4-D may be stored in bags, drums, one gallon cans, and in 4,000 or 8,000 gallon tank cars. After use, containers can be rinsed with a 5% solution of sodium bicarbonate (Hartley & Kidd, 1990; HSDB , 2002; Meister & 2002, 2002; OHM/TADS , 2002; Sittig, 1991).

ROOM/CABINET RECOMMENDATIONS

Chemical material should be stored in a refrigerated or cool and well-ventilated environment, protected from moisture and light. It will decompose in sunlight. The material is corrosive to metals. It should be kept away from oxidizing materials and if possible stored in an inert atmosphere (Hartley & Kidd, 1990; NTP , 2001; Pohanish & Greene, 1997; Sittig, 1991).
2,4-D should not be stored near other agrochemicals, food, feed, or seeds (Meister & 2002, 2002).

INCOMPATIBILITIES

2,4-D is incompatible with strong oxidizers. It is also corrosive to metals (Hartley & Kidd, 1990; OHM/TADS , 2002; Pohanish & Greene, 1997; Sittig, 1991).

-PERSONAL PROTECTION

SUMMARY

RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (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.

Appropriate protective clothing should be worn to prevent repeated or prolonged contact. This will vary by formulation, although long-sleeved shirt, long pants, shoes and socks, chemical-resistant or rubber gloves, eye protection, and an apron should be worn during handling. Eye and respiratory protection, such as a full-face respirator or safety glasses and a filter mask, are also recommended (ITI, 1995; Meister & 2002, 2002; OHM/TADS , 2002; Sittig, 1991).

EYE/FACE PROTECTION

Eye protection, such as safety glasses or a face shield with the use of a respirator, should be used to prevent the likelihood of eye contact (ITI, 1995; Sittig, 1991)

RESPIRATORY PROTECTION

Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.

A filter-mask can be used during handling and a full face-respirator is recommended when large spills are being managed (ITI, 1995; Meister & 2002, 2002; OHM/TADS , 2002; Sittig, 1991).

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 94-75-7.

Specific recommendations and test data for this chemical were not found in the available manufacturers' product literature. A complete list of consulted manufacturers and references is presented below.

ENGINEERING CONTROLS

In case of a spill, the areas should be well ventilated. HEPA or charcoal filters can be used to minimize exhaust emissions (HSDB , 2002).

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

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 151 (ERG, 2004)
- Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes.
- Containers may explode when heated.
- Runoff may pollute waterways.
2,4-D is considered a stable compound, and the solid form is not combustible. However, contact with strong oxidizers may cause fire and explosions. In addition, liquid solutions formulated with organic carrier solvents may be flammable. Although 2,4-D powder is considered nonflammable, toxic gases and vapors may be released in a fire involving 2,4-D. Fire can be extinguished with dry chemical,carbon dioxide, water spray, or foam extinguishing agents. Personal protective clothing and eye and respiratory protection should be used in fire-fighting activities (ACGIH, 2001; (NIOSH , 2002; OHM/TADS , 2002; Pohanish & Greene, 1997; Sittig, 1991) WHO, et al., 2002).

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS94-75-7 (NFPA, 2002):

Not Listed

INITIATING OR CONTRIBUTING PROPERTIES

The acid and salts of 2,4-D are nonflammable, but commercial formulations of 2,4-D acid may have a flash point minimum of 88 degrees C (Cleveland open cup). 2,4-D can react with strong oxidizers, presenting a potential fire or explosion hazard. Liquid formulations of 2,4-D may contain flammable organic carrier solvents that would increase the fire hazard of the material. Ignition sources should be removed in the event of a spill (ACGIH, 2001; (NIOSH , 2002; NTP , 2001; HSDB , 2002).

FIRE CONTROL/EXTINGUISHING AGENTS

SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Dry chemical, CO2 or water spray.

LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (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 151 (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 CAS94-75-7 (NFPA, 2002):

Not Listed

If it is involved in a fire, use dry chemical, carbon dioxide, Halon, water spray, or foam as a fire extinguishing agent. Personal protective clothing including a self-contained breathing apparatus (SCBA), rubber gloves, hat, suit, and boots must be worn. Highly toxic fumes will be present when 2,4-D is involved in a fire and respiratory protection should be used (NTP , 2001; OHM/TADS , 2002; Sittig, 1991).

COMBUSTION TOXICITY

Toxic fumes of carbon monoxide, hydrogen chloride, and phosgene may be emitted when 2,4-D is involved in a fire or when it is heated to decomposition (ACGIH, 2001; (NTP , 2001).

EXPLOSION HAZARD

2,4-D is a stable compound and is not combustible. However, contact with strong oxidizers may cause fire and explosions. In addition, liquid solutions formulated with organic solvents may be flammable (ACGIH, 2001; (OHM/TADS , 2002; Pohanish & Greene, 1997).

DUST/VAPOR HAZARD

The material has corrosive properties and, as such, is an irritant to the eyes, skin , and respiratory tract. In a fire or when heated to decomposition, 2,4-D emits toxic fumes of hydrogen chloride, carbon monoxide, and phosgene. (ACGIH, 2001; (Lewis, 2000) WHO, et al., 2002).

REACTIVITY HAZARD

It is incompatible with strong oxidizers; contact may cause fire and explosions. The material is also corrosive to metals (ACGIH, 2001; (Hartley & Kidd, 1990; Pohanish & Greene, 1997).

EVACUATION PROCEDURES

SUMMARY

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 151 (ERG, 2004)

Increase, in the downwind direction, as necessary, the isolation distance of at least 25 to 50 meters (80 to 160 feet) in all directions.

FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (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 151 (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:

CANUTEC:

613-996-6666 (Collect calls are accepted);
*666 cellular (in Canada only).

UNITED STATES:

CHEMTREC®:

1-800-424-9300 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
703-527-3887 for calls originating elsewhere (Collect calls are accepted).

CHEM-TEL, INC.:

1-800-255-3924 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
813-248-0585 for calls originating elsewhere (Collect calls are accepted).

INFOTRAC:

1-800-535-5053 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
352-323-3500 for calls originating elsewhere (Collect calls are accepted).

3E COMPANY:

1-800-451-8346 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
760-602-8703 for calls originating elsewhere (Collect calls are accepted).

NATIONAL RESPONSE CENTER (NRC):

1-800-424-8802 - (24 hours) (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
202-267-2675 for calls in the District of Columbia.

MILITARY SHIPMENTS:

703-697-0218 - Explosives/ammunition incidents (Collect calls are accepted);
1-800-851-8061 - All other dangerous goods incidents.

NATIONWIDE POISON CONTROL CENTER (United States only):

1-800-222-1222 (Toll-free in the U.S.).

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.

Workers should be removed from the area that is affected by a spill. Toxic fumes of carbon monoxide, hydrogen chloride, and phosgene may be emitted when 2,4-D is involved in a fire or when it is heated to decomposition (ACGIH, 2001; (NTP , 2001; Sittig, 1991).

AIHA ERPG Values for CAS94-75-7 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS94-75-7 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Dichlorophenoxy acetic acid, 2,4- (2,4- D salts and esters)
TEEL-0 (units = mg/m3): 10
TEEL-1 (units = mg/m3): 10
TEEL-2 (units = mg/m3): 40
TEEL-3 (units = mg/m3): 100
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 CAS94-75-7 (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):

Not Listed

NIOSH IDLH Values for CAS94-75-7 (National Institute for Occupational Safety and Health, 2007):

IDLH: 100 mg/m3
Note(s): Not Listed

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
- 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 151 (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.
The area of a spill should be ventilated and workers in the area should be evacuated. All sources of ignition should be removed. Responders to cleanup should utilize protective clothing and equipment and contain the spill. Liquid solutions may be absorbed on clay or vermiculite. Solid spill material can be dampened with 60%-70% ethanol. Absorbent towels dampened with the ethanol solution can be used to wipe up any remaining solid material. Spill material should be placed in an appropriate container for disposal if material is not reusable. Contaminated towels and clothing should be placed in airtight bag for disposal (HSDB , 2002; NTP , 2001; Sittig, 1991).
The spill area and all contaminated surfaces should be washed with a 60%-70% ethanol solution and then a soap and water solution. The area should not be reentered until a safety officer or another responsible person has verified cleanup (NTP , 2001; Sittig, 1991).
Disposal methods for wastes containing 2,4-D equal to or greater than 100 kg/month must conform to EPA hazardous waste regulations. Farms are allowed to destroy up to 10 kg if necessary, and this can be accomplished by chemical treatment with chloride of lime or sodium bicarbonate and using appropriate safety precautions during handling (HSDB , 2002).
When handling any carcinogenic waste materials, certain precautions are recommended. For example, waste liquids should be placed in proper containers that are properly labeled and tightly closed. Bottles used to store waste should be placed in a sealed and labeled plastic bag to prevent contamination of the bottle surface (HSDB , 2002).
Recommended disposal method is incineration. It is not recommended that material containing 2,4-D be discharged to sewer (HSDB , 2002).

SMALL LEAK/SPILL

When a small spill occurs, the area should be ventilated and the material swept onto paper or other suitable material and reused or placed in an appropriate container for disposal. Avoid dust generation. The spill area and all contaminated surfaces should be washed with a 60%-70% ethanol solution and then a soap and water solution (HSDB , 2002; NTP , 2001).

LARGE LEAK/SPILL

In instances of a large spill, the area should be ventilated and workers in the area of a spill should be evacuated. Responders to cleanup should utilize protective clothing and equipment. Liquid solutions may be absorbed on clay or vermiculite and placed in a suitable disposal container. Solid material should be collected and may be reclaimed. The spill area and all contaminated surfaces should be washed with a 60%-70% ethanol solution and then a soap and water solution (HSDB , 2002; NTP , 2001; Sittig, 1991).

WASTE TREATMENT OPTIONS

RECYCLING/RECLAMATION

Large spills that are appropriately contained and collected can be reclaimed (Meisterpro, 2002).
Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.

CHEMICAL TREATMENT

To assist in the collection of 2,4-D, soluble calcium or magnesium salts can be added to solutions of 2,4-D (or its salts) to obtain an insoluble solid calcium or magnesium salt. The product maintains its herbicide capabilities (HSDB , 2002).
2,4-D can be detoxified by chemical treatment with chloride of lime or sodium bicarbonate. Farms are allowed to destroy up to 10 kg if necessary. Containers can be rinsed with a 5% solution of sodium bicarbonate (HSDB , 2002).
Water treatment of 2,4-D solution can be implemented using coagulation and complete water treatment by ozonation. This process removed only 17% of the 2,4-D, however. The use of activated charcoal in filtering solution or exhausts is also an effective treatment technique. Wastewater treatment technologies that have been evaluated for 2,4-D and related herbicides include a concentration process using resin absorption (HSDB , 2002).

BIOREMEDIATION

Biological treatment facilities will achieve degradation of 2,4-D (HSDB , 2002).

PHYSICAL TREATMENT

Incineration of phenoxys is reported to be effective utilizing a straight combustion process or catalytic combustion. Incineration at high temperatures with adequate residence time will lead to complete detoxification of 2,4-D. It is considered the most environmentally-acceptable method of disposal. Incinerability data provides a thermal stability ranking of hazardous organic compounds for 2,4-D as rank 211 on a scale of 1 (highest stability) to 320 (lowest stability). Incineration should be at high temperatures or PCDDs may be formed (HSDB, 2002: Sittig, 1991; Verschueren, 2000).
When landfilling is considered, 2,4-D is nonpersistent, although it may last in dry areas up to a year. Because it is not persistent and readily biodegrades, small quantities could be buried in non-crop areas away from water supplies (HSDB , 2002).

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

2,4-D is one of the most extensively used systemic herbicides, and its use in agricultural applications is the primary source of environmental release. Over 1500 registered products contain 2,4-D as an active ingredient. It may further enter the environment from spills, disposal of unused product, and washing of equipment, or as a result of production and disposal of 2,4-D or its by-products, such as in discharge of industrial effluents or wastes. It is also a hydrolysis product of 2,4-D esters and can appear where formulations containing esters were released to the environment (Howard, 1991; NPTN , 2002; (EPA, 2002)).

In 1993, it was estimated that more than 25 million pounds of active ingredient (2,4-D) were used from various formulations. The EPA estimates that 12 to 15 million pounds of active ingredient are used annually for nonagricultural applications (Harbison, 1998).

Human exposure to 2,4-D is through direct contact during product use and will primarily be associated with workers involved in its manufacture and use. Exposure may occur to persons who work or live near areas treated with the chemical, as spray applications can drift up to a few kilometers. Exposure may also result from ingestion of contaminated food products or drinking water (EPA, 1990; Bingham et al, 2001; (EPA, 2002)).

Concentrations in environmental media were reported as 2,4-D equivalents (Howard, 1991):

In sediment at TVA (Tennessee Valley Authority) reservoirs, concentrations were 0.95 to 56 ppm, 96 hours after application, 0.14 to 33.6 ppm after 42 days, and 0.3 to 0.49 ppm nine months later. Comparable levels were detected in sediment of Florida and Georgia ponds at 0.6 ppm one day after treatment and at trace to nondetectable amounts after 56 days (Howard, 1991).
A four-year water sampling effort of midwestern U.S. streams found 2,4-D in 18 of 20 streams at concentrations from 0.02 to 0.99 ppb. Application of 4.48 kg/ha acid equivalent in a Florida wildlife refuge followed by water sampling found concentrations of 0.037 ppm and 0.001 to 0.004 ppm one and after 56 days, respectively. During a national groundwater survey of pesticides, 2,4-D was detected in five of 50 states at a mean of 1.2 ppb and a maximum concentration of 49.5 ppb (Howard, 1991).
Airborne concentrations in urban areas were measured from 1.5 to 4 ng/m(3), and a rural location had a level of 1.151 ng/m(3) (Howard, 1991).

Residues measured after herbicide spraying (Verschueren, 2001):

lingonberry - <0.05 to 7.0 ppm, 2-13 weeks after spraying
wild mushroom (NE Finland) - <0.05 to 1.2 ppm, 2-13 weeks after spraying
birch and aspen foliage - 0.15 to 31 ppm, 13-43 weeks after spraying.

Groundwater quality well data for 150 investigations in the U.S. up to 1988 provided a median concentration of 1.4 mcg/L for all positive detections for all studies. The maximum reported concentration was 50 mcg/L(Verschueren, 2000).

ENVIRONMENTAL FATE AND KINETICS

Atmospheric degradation is mostly abiotic through vapor phase reaction with hydroxyl radicals (half-life of 1 day), direct photooxidation, and possibly photolysis. 2,4-D absorption is within the wavelength range 288 to greater than 290 nm, indicating susceptibility to photolysis. Absorption greater than 290 nm indicates that direct photooxidation could be an important atmospheric fate process. The photooxidaton half-life in air was determined to be from 1.8 to 18 hours (Howard, 1991; Howard et al, 1991).
Airborne 2,4-D results from spray applications, and spray drifting can travel up to a few kilometers. In the air, 2,4-D can undergo photooxidation by reaction with hydroxyl radicals (estimated half-life of one day) or direct photooxidation. Direct photooxidation may be important as 2,4-D absorbs light at wavelengths greater than 290 nm. Due to its significant water solubility, atmospheric removal by gravitational settling of aerosol and rainout may also be important (Howard, 1991).
Based on estimated reaction with photochemically produced hydroxyl radicals, the estimated half-life of vapor phase 2,4-D in the atmosphere is 23.9 hours (Howard, 1991).
The photooxidation half-life in air was estimated to be 1.8 to 18 hours (Howard et al, 1991).

WATER

SURFACE WATER
- In an aquatic environment, 2,4-D will be lost primarily due to biodegradation. Typical half-lives for this process are 10 days to greater than 50 days. It readily undergoes biodegradation with rates increased by high nutrients, sediment load, and dissolved organic carbon. Biodegradation is further influenced by chemical concentration, temperature, availability of oxygen, and microbial acclimation associated with a prior history of 2,4-D or other phenoxyacetic acid contamination. In sediments, adsorption is not anticipated to be considerable and degradation is rapid (half-life less than 1 day). Volatilization and hydrolysis from aquatic systems will be negligible ((EPA, 2002); EXTOXNET, 2002; Howard, 1991).
- Photolysis will contribute to the degradation of 2,4-D in water. Half-lives of 2 to 4 days are reported for UV photolysis in water. Miceller solubilization and photosensitization by certain adjuvants may improve photolysis in aqueous solution ((EPA, 2002); Howard, 1991).
- The functional groups of 2,4-D are generally resistant to hydrolysis although this form of abiotic degradation may become important at pH greater than 8 (Howard, 1991).
- 2,4-D will be more persistent in oligotrophic waters or where high concentrations have been released ((EPA, 2002)).
- Mineralization:
- Half-Lives in Water:
GROUND WATER
- The likelihood of 2,4-D contaminating groundwater by leaching from soil is limited by the rapid degradation in soil and by its uptake by target plants. Residues detected in groundwater were mostly associated with point sources such as mixing, loading, and disposal (EPA, 1990).
- The half-life in groundwater ranges from 20 days to 6 months based on estimated unacclimated aqueous aerobic and anaerobic biodegradation half-lives (Howard et al, 1991).

SOIL

TERRESTRIAL
- 2,4-D is not persistent in soil, lasting for 30 days at its highest application rate, though it has been reported that 2,4-D can have an effect on susceptible plants for up to 4 weeks following application. It will be taken up from the soil by the targeted plants where metabolism is usually slow and varies among plant species. Soil microbes are responsible for its eventual disappearance from soil, and biodegradation is a very important fate mechanism in most soil types. Rapid degradation by soil microorganisms occurs, with rates affected by contaminant concentration, water content, temperature, organic content of the soil, and prior exposure of the local soil microbes to 2,4-D or its esters (EXTOXNET, 2002; Hartley & Kidd, 1990; Howard, 1991; NPTN , 2002; OHM/TADS , 2002; USDA , 2002).
- Adsorption to soil organic matter can occur over time; however, in general, soil adsorption is not expected to be significant, especially at basic pHs. Adsorption will depend on soil type and organic content, increasing with higher soil organic content and lower soil pH. Desorption can occur in mineral soils, but not high organic content soil. EPA reports that 2,4-D is mobile to highly mobile in five soil types and aged residues are only slightly mobile. Migration to groundwater will be significant in course-grained sandy soils of low organic content or in very basic soils (EPA, 1990; Howard, 1991; USDA , 2002; (EPA, 2002)).
- Volatilization from soil systems is considered to be negligible based on the extremely low Henry's Law constant. Hydrolysis is also considered negligible in soil systems (Howard, 1991; (EPA, 2002)).
- In soil, the primary transport mechanism of 2,4-D is through percolation. Diffusion will occur only within short distances. However, 2,4-D can move upward in the soil when the surface soil dries or if rapid evaporation takes place. The chemical can thus concentrate at the soil surface where it may undergo photolysis, airborne transport, or again leach downward ((EPA, 2002)).
- Residual activity of 2,4-D in soil may exist for one to six weeks (USDA , 2002).
- Experimental Koc values are 19.6 and 109.1 ((EPA, 2002)).
- 2,4-D, 2,4,5-T, dichlorophenol, and 2,4,5-trichlorophenol all showed similar adsorption and desorption diffusion coefficients for volcanic soil, as measured by Freundlich type isotherms (Susarla et al, 1993).
- Half-Lives in Soil:

OTHER

OTHER
- A laboratory study was conducted to determine the effect of hydrogen peroxide and iron ions on the decomposition of 2,4-D and 2,4,5-T. The process resulted in 40% to 70% conversion to carbon dioxide and quantitative dechlorination. The reaction was irradiated using visible light with a small UV component. The photo-assisted conversion to carbon dioxide proceeded to completion in less than 2 hours, with hydrogen peroxide to herbicide molar ratios as low as 5 (Pignatello, 1992).
- A laboratory study was conducted to determine the rate constants for degradation of herbicides by ozone. The half-life for removal of 2,4-D at pH 7.5 and in the presence of bicarbonate ions was 39.5 minutes at a dissolved ozone concentration of 10 micromolar. The addition of a second herbicide did not affect the relative degradation rate (Xiong & Graham, 1992).
- The oxidation of 2,4-D by Fenton-type reagents in the near-UV is enhanced by several photochemical reactions involving Fe(+3) ions. This oxidation works well in the presence of hydrogen peroxide (H2O2) and provides the basis for a waste treatment system. Hydroxyl radical reactions convert nearly 40% of ring and carbonyl carbons to carbon dioxide and initiate dechlorination reactions. The remaining 60% of carbon is mineralized by photolysis/decarboxylation of Fe(+3) complexes of degradation intermediates. Oxalic acid was identified as an intermediate (Sun & Pignatello, 1993).
- Two organo-clays, decylammonium-montmorillonite (C10M) and decylammonium-vermiculite (C10V), were evaluated as sorbents for the weak acid herbicide 2,4-D. Langmuir and Freundlich adsorption parameters indicated an increased adsorption capacity after treatment with decylammonium. The C10V material produced a higher and stronger sorption capacity (Hermosin & Cornejo, 1992).

ABIOTIC DEGRADATION

In the environment, uptake of 2,4-D occurs in targeted plants. Soil or aquatic microbes will biodegrade remaining 2,4-D levels in soil and water. Biodegradation is an important mechanism, and is influenced by chemical concentration, organic content, water content, nutrients, temperature, and microbial acclimation. Adsorption in soil or sediment is not significant, but it can occur in soil over time. Percolation through soil may impact groundwater, although this migration pathway is influenced by soil type. Rapid degradation in soil and plant uptake will limit soil leaching. Losses from volatilization or hydrolysis in water and soil sytems are negligible. Atmospheric degradation is primarily abiotic, by reaction with hydroxyl radicals, direct photooxidation, or photolysis. Its solubility may also contribute to atmospheric removal processes (EPA, 1990; Hartley & Kidd, 1990; Howard, 1991; (EPA, 2002); EXTOXNET, 2002; NPTN , 2002; OHM/TADS , 2002; USDA , 2002).

In the evaluation of first-order hydrolysis half-life, the result was reported as 'no hydrolyzable groups' and the rate constant at neutral pH was stated to be zero (Howard et al, 1991).

BIODEGRADATION

A variety of microorganisms in soil, freshwater, and marine ecosystems are capable of degrading 2,4-D, with the rate depending on presence of acclimated organisms, nutrient levels, temperature, and contaminant concentrations (Howard, 1991; (EPA, 2002)).

In most soil, biodegradation will be the most important fate mechanism. Microbial degradation in soil will involve hydroxylation, decarboxylation, cleavage of the acid side-chain, and ring opening. Biodegradation rates are influenced by chemical concentration, soil moisture content, soil organic content, temperature, and pre-exposure of the soil to 2,4-D acid or its esters. Half-lives will range from less than one day to several weeks, with longer periods of biodegradation more likely in dry or sandy, low organic content soils. It degrades rapidly in aerobic silty clay and loam soil systems. Fastest degradation was observed in muck soils (EPA, 1990; Hartley & Kidd, 1990; Howard, 1991; USDA , 2002).

Degradation products from microbial degradation have been evaluated in various environmental media. In soil, microbial metabolism can occur in stages, producing 2,4-dichlorophenol, 4-chlorophenol, other hydroxylic aromatics, and then innocuous metabolites. 2,4-D in anaerobic sediment was reported to form 2,4-dichlorophenol. In aquatic environments, microbial biodegradation products include 2,4-dichlorophenol, other hydroxylic aromatics, and polymeric acids (Howard, 1991; USDA , 2002).

A mixture of microorganisms from activated sludge, soil, and sediments produced half-lives of 1.8 to 3.1 days under aerobic conditions and 69 to 135 days under anaerobic conditions. However, anaerobic biodegradation was not observed when primary digester sludge was tested under methanogenic conditions for 60 days (Howard, 1991).

Rapid biodegradation in sediments and lake mud is expected. Reported half-lives are less than one day. Lake bottom mud showed oxidation of 81-85% 2,4-D in 24 hours based on BOD (Howard, 1991).

Biodegradation in anoxic habitats maintained in a dark environment (% substrate disappearance after 3 months) (Verschueren, 2001):

Sewage sludge (at 37 degrees C) - 100%
Pond sediment (at 20 degrees C) - 100%
Methanogenic aquifer (at 20 degrees C) - 99%
Sulfate reducing aquifer (at 20 degrees C) - 0%
Detected metabolites in sewage sludge, pond sediment, and methanogenic aquifer: 2,4-dichlorophenol, 4-chlorophenol, and phenol.

Samples of solid waste material from a fertilizer manufacturing plant containing 1.5% 2,4-D were leached in a mineral salts solution. Up to 90% of the total 2,4-D was dissolved in the aqueous solution within three days. The solution was subsequently inoculated with cultures of herbicide-degrading bacteria taken from a holding pond, a liquid waste bioreactor, and soil adjacent to the plant. Nearly complete biodegradation of 2,4-D occurred in 8 to 32 days; pH control was critical in reducing the degradation time (Oh & Tuovinen, 1994).

Degradation of 2,4-D and 2-methyl-4-chlorophenoxyacetic acid (MCPA) was compared in two soil types. In spiked, noncontaminated soil, three bacterial isolates (Xanthomonas maltophilia SB5, Pseudomonas species SB9, and Rhodococcus globerulus SA(2)) degraded an average of 91% 2,4-D and 99% MCPA in 28 days. In contaminated soil, the degradation was 48% of 2,4-D and 61% of MCPA. Degradation significantly increased in both soil types when a combined nitrogen/phosphorus/potassium fertilizer was added; degradation was inhibited in both with the addition of lime (to raise soil pH). After 8 weeks, there was significant degradation of the herbicides in both soil types when amended with nitrogen only or phosphorus only. There was no significant difference in degradation when amended with potassium only or in the soils with no amendment (Mcghee & Burns, 1995).

An experimental study was done to evaluate the biodegradability of 2,4-D by two isolated bacteria and adsorbed in low and high carbon containing soils. Results showed the solution phase chemical was metabolized preferentially, and that rates in the high organic matter soil were lower than the lesser carbon-containing soils (Greer & Shelton, 1992).

Pseudomonas cepacia degraded 2,4-D in liquid cultures of non-sterile soil. Each log increase in inoculum density reduced the time for complete degradation of 2,4-D by 0.5 days. The in-soil degradation required an acclimation period for cell induction and diffusion of 2,4-D and added bacteria in the soil matrix (Comeau et al, 1993).

Surface adsorption of 2,4-D on sediment (soil) was found to inhibit the degradation process, while 2,4-D in solution was degraded by the microbes, Pseudomonas sp, in solution or on the solid surface. This result suggests moisture plays an important role in the 2,4-D degradation process (Zou et al, 1992).

Soils with and without a history of 2,4-D exposure exhibited as much as a 7-log increase in the number of 2,4-D metabolizing organisms after four amendments of 400 ppm of 2,4-D (Holben et al, 1992).

BIOACCUMULATION

HUMANS

Biotransformation of phenoxy herbicides is rare in mammals. More than 95% of a 2,4-D dose to humans evaluated was excreted unchanged in urine within five days (ILO , 1998).
Workers using 2,4-D may absorb approximately 0.1 mg 2,4-D/kg body weight/day on the average. Absorption will be influenced by occupational hygiene practices. The urinary excretion rate of 2,4-D was 0.4 to 6.3 mcg/kg body weight/day in an evaluation of 45 lawn care workers who sprayed the material for at least 3 weeks (Howard, 1991).

FISH

A half-life of less than 2 days is reported for fish and oysters based on limited studies. EPA reports that available data indicate a low potential for 2,4-D to accumulate in fish (EPA, 1990; EXTOXNET, 2002).
After intravascular or oral administration of 2,4-D (10 mg/kg of body weight) in channel catfish, the fish were monitored via pharmacokinetics, tissue distribution and level of excretion. The plasma concentration exhibited a rapid decline after intravascular dose with a half-life of 0.76 hours. The half-life after the oral dose was 1.5 hours and the chemical was available in several tissues. Nearly 90% of the dose was excreted in the urine within 24 hours. There was a low potential for accumulation in the edible portions of the fish (Plakas et al, 1992).
There is no evidence of bioaccumulation of 2,4-D in aquatic organisms (Bingham et al, 2001).

BIRDS

Eggs are not affected by high doses of 2,4-D. Chickens fed moderate quantities of 2,4-D in drinking water from birth to maturity had very low levels in eggs (EXTOXNET, 2002; NPTN , 2002).

PLANTS

AQUATIC
- In plants, 2,4-D will be absorbed through the plant leaves, stems, and roots and it tends to accumulate principally at the rapid growth regions of shoots and roots (EPA, 1990; NPTN , 2002).
- Plant concentrations were examined in two plankton samples taken from a TVA reservoir. After application of 20 to 40 lbs/acre, concentrations, reported as 2,4-D equivalents and as calculated percents of 2,4-D in plankton, were as follows (Howard, 1991):
TERRESTRIAL
- 2,4-D is absorbed through plant leaves, stems, and roots and tends to accumulate principally at the rapid growth regions of shoots and roots (EPA, 1990; NPTN , 2002).
- Uptake by plants defined by cuticle-water distribution coefficient (log Kcw) (Verschueren, 2001).

MAMMALS

Evidence does not exist that accumulation occurs in mammals or other organisms to significant levels. Rats dosed at 1 mg/kg showed no peak concentrations in blood, liver, kidney, lungs, and spleen after 6 to 8 hours, and no detectable residues were found after 24 hours. Six days following exposure, only traces of 2,4-D were found in milk of lactating animals (EXTOXNET, 2002).
2,4-D has been shown to pass through the placenta in pigs and rats, with 20% detected in the uterus, placenta, fetus, and amniotic fluid (EXTOXNET, 2002).

BIOCONCENTRATION FACTOR

EPA states that there is no evidence that bioconcentration of 2,4-D occurs through the food chain, citing large-scale monitoring of residues in soils, foods, feedstuffs, wildlife, and humans and examinations of degradation and metabolism activities in ecosystems. It does not tend to bioconcentrate in aquatic organisms (Howard, 1991; (EPA, 2002)).
BCFs of 0.003 to 7 are reported for various fish and aquatic plants ((EPA, 2002))
Bluegill sunfish and channel catfish BCF = 1 x 10(-05) (pH not given) (Howard, 1991)
Frog tadpole BCF = 2 x 10 (-03) (Howard, 1991)
BCF for three seaweeds: 0.001 to 0.003 (pH 7.8, using carbon14 ring-labeled 2,4-D) (Howard, 1991)
BCF = 6 for algae, Chlorella fusca (wet weight; pH not given, using carbon14 ring-labeled 2,4-D) (Howard, 1991; Verschueren, 2001)

ENVIRONMENTAL TOXICITY

At recommended field application rates, 2,4-D does not affect microorganisms. Higher levels can inhibit nitrogen-fixing algae and soil fungi (USDA , 2002).

2,4-D is highly toxic to numerous nontarget plants. It is phytotoxic to most broad-leafed crops, particularly cotton, vines, tomatoes, ornamentals, fruit tress, oilseed rape, and beet (EXTOXNET, 2002; Hartley & Kidd, 1990; USDA , 2002).

2,4-D is slightly toxic to wildfowl and slightly to moderately toxic to birds (EXTOXNET, 2002).

Toxicity to fish and aquatic invertebrates will depend on the formulation of 2,4-D. Some compounds are highly toxic while others are less toxic (EXTOXNET, 2002; USDA , 2002).

Depending on the formulation, the LC50 is between 1.0 and 100 mg/L in cutthroat trout (EXTOXNET, 2002)
Channel catfish experienced less than 10% mortality at 10 mg/L for 48 hours (EXTOXNET, 2002)
Green sunfish exposed to 110 mg/L for 41 hours showed no effect on swimming response (EXTOXNET, 2002)
Brown shrimp exhibited a slight increase in mortality at 2 mg/L for 48 hours (EXTOXNET, 2002)
Survival rates were not adversely affected in adult dungeness crabs at concentrations of 10 mg/L for 85 days. The immature crabs experienced slight toxicity with a 96-hour LC50 greater than 10 mg/L (EXTOXNET, 2002)
A half-life of less than 2 days is reported for fish and oysters based on limited studies (EXTOXNET, 2002)

Synergistic effects may occur on aquatic organisms when 2,4-D is combined with picloram (Harbison, 1998).

EPA characterizes 2,4-D as moderately toxic to practically nontoxic to avian species on an acute basis (EPA, 1990).

EPA has stated that there is sufficient information to characterize 2,4-D as relatively nontoxic to honeybees when bees are exposed to direct treatment. However, a study cited by EXTOXNET provided information that moderate doses were shown to severely impair honeybee brood production, but at lower exposure levels the exposed bees lived significantly longer than control bees. Oral and contact LD50 study values for 2,4-D were >100 mcg/bee (EPA, 1990; Bingham et al, 2001; EXTOXNET, 2002).

The EPA notes that it has been determined that certain uses of 2,4-D may jeopardize the continued existence of endangered species or the critical habitat of certain endangered species (EPA, 1990).

A 15-year study was done to evaluate the long term effects of using 2,4-D on soil microbial population and biochemical processes. Both amine and ester formulations were used at the rate of 0.95 kg/hectare two times a year. The results indicated the ester formulation interferes with nutritional cycling to a greater extent than does the amine formulation. Microbial respiration tended to temporarily increase and dehydrogenase activity increased when using the amine, while both decreased with application of the ester formulation (Rai, 1992).

2,4-D was found to be nearly half as toxic to lake fish and cutthroat trout at pH 8.5 versus pH 6.5 (HSDB, 2004).

Toxicity for freshwater Ectoprocta bacterium: no appreciable effect at 2.5 mg/L for 84 hour exposure (Verschueren, 2000).

Blue green algae (Anabaenopsis raciborskii): 2,4-D at 10 mg/L stimulated growth and nitrogen fixation. At 100 mg/L there was no significant inhibition of growth, and at 1,000 mg/L there was complete inhibition of growth (Verschueren, 2001).

WORMS (Tubifex tubifex): 2,4-D toxic at 80 mg/L. The risk to earthworms from the use of 2,4-D is low (Bingham et al, 2001; Verschueren, 2001).

The following is a list of aquatic plants that 2,4-D is effective in controlling ((USACE, 2002)):

Alternanthera philoxeroides (Mart.) Griseb. (Alligatorweed)
Brasenia schreberi J.F. Gmel. (Water-Shield)
Ceratophyllum demersum L. (Coontail)
Eichhornia crassipes (Mart.) Solms (Waterhyacinth)
Justicia americana (L.) Vahl (Waterwillow)
Ludwigia peploides (Kunth) Raven (Floating Primrose Willow)
Ludwigia uruguayensis (Camb.) Hara (Uruguayan Primrose Willow)
Lythrum salicaria L. (Purple Loosestrife)
Mikania scandens (L.) Willd. (Climbing Hempweed)
Myriophyllum aquaticum (Vell.) Verdc. (Parrotfeather)
Myriophyllum heterophyllum Michx. (Variable-Leaf Milfoil)
Myriophyllum sibiricum Komarov (Northern Watermilfoil)
Myriophyllum spicatum L. (Eurasian Watermilfoil)
Nelumbo lutea Willd. (American Lotus)
Nuphar lutea (L.) Sm. (Spatter-Dock)
Nymphaea odorata Ait. (Fragrant Water-Lily)
Polygonum arifolium L. (Tearthumb)
Polygonum hydropiperoides Michx. (Smartweed)
Trapa natans L. (Water Chestnut)
Typha spp. (Cattails)
Utricularia spp. (Bladderwort)

ECOTOXICITY VALUES:

EC50 - ALGAE (Chlorococcum sp.): 50-60 mg/L for 10D (Verschueren, 2001)
EC50 - ALGAE (Dunaliella tertiolecta): 75-90 mg/L for 10D (Verschueren, 2001)
EC50 - ALGAE (Isochrysis galbana): 50-60 mg/L for 10D (Verschueren, 2001)
EC50 - ALGAE (Phaeodactylum tricornutum): 50-60 mg/L for 10D (Verschueren, 2001)
EC50 - MICROORGANISM (Trichoderma viride): 350 mg/L -- growth inhibition (Verschueren, 2001)
EC50 - MICROORGANISM (Saprolegnia parasitica): 220 mg/L -- growth inhibition (Verschueren, 2001)
EC50 - MICROORGANISM (Mortierall isabellina): >400 mg/L -- growth inhibition (Verschueren, 2001)
EC50 - MICROORGANISM (Chlorella vulgaris): 19 mg/L -- growth inhibition (Verschueren, 2001)
EC50 - MICROORGANISM (Chlorella pyrenoidosa): 56 mg/L -- growth inhibition (Verschueren, 2001)
EC50 - MICROORGANISM (Arthrobacter globiformis): 270 mg/L -- growth inhibition (Verschueren, 2001)
EC50 - MICROORGANISM (Psuedomonas pictorum): 490 mg/L -- growth inhibition (Verschueren, 2001)
LC50 - AMPHIBIANS (Unspecified): 8->346 ppm (USDA, 2002)
LC50 -BLUEGILL: 0.9 ppm for 48H (Verschueren, 2001)
LC50 - BIRDS (Unspecified): 472->2000 mg/kg (USDA, 2002)
LC50 - FIDDLE CRAB: 5000 ppm for 96H (OHM/TADS, 2002)
LC50 -FISH (Unspecified): >250 ppm (Meisterpro, 2002)
LC50 -FISH (Unspecified): 0.3-2840 ppm (USDA, 2002)
LC50 - INVERTEBRATES (Unspecified): 0.1->100 ppm (USDA, 2002)
LC50 - MALLARD DUCK and BOBWHITE QUAIL: >5620 ppm (Meisterpro, 2002)
LC50 - MAMMALS (Unspecified): 639 - >5000 mg/kg (USDA, 2002)
LC50 - LAKE TROUT (Salvelinus namaycush): 45 mg/L for 96H (HSDB, 2004)
LC50 - CUTTHROAT TROUT (Salmo clarki): 64 mg/L for 96H (HSDB, 2004)
LC50 - RAINBOW TROUT: 2.2 ppm for 48H (OHM/TADS, 2002)
LC50 - RAINBOW TROUT: 1.1 ppm for 48H (OHM/TADS, 2002)
LC50 - RAINBOW TROUT: 1.1 ppm for 48H (OHM/TADS, 2002)
LC50,S - STRIPED BASS: 70 mg/L for 96H (Verschueren, 2001)
LC50,S - BANDED KILLFISH: 27 mg/L for 96H (Verschueren, 2001)
LC50,S - PUMPKINSEED FISH: 95 mg/L for 96H (Verschueren, 2001)
LC50,S - WHITE PERCH: 40 mg/L for 96H (Verschueren, 2001)
LC50,S - AMERICAN EEL: 300 mg/L for 96H (Verschueren, 2001)
LC50,S - CARP: 96.5 mg/L for 96H (Verschueren, 2001)
LC50,S - GUPPY: 70.7 mg/L for 96H (Verschueren, 2001)
LD50 - (ORAL) CHORUS FROG, Tadpole: 100 ppm (OHM/TADS, 2002)
LD50 - (ORAL) CHUKAR (Alectoris chukar), Male and Female, 4 mo.: 200-400 mg/kg (HSDB, 2004)
LD50 - (ORAL AND CONTACT) HONEYBEE: >100 mcg/bee (Bingham, et al., 2001)
LD50 - (ORAL) JAPANESE QUAIL (Coturnix japonica), Male, 2 mo.: 668 mg/kg (HSDB, 2004)
LD50 - (ORAL) JAPANESE QUAIL (Coturnix japonica), Male and Female, 14D: >5000 ppm (HSDB, 2004)
LD50 - (ORAL) MALLARD (Anas platyrhynchos), Female, 3-5 mo.: >1000 mg/kg (HSDB, 2004)
LD50 - (ORAL) MALLARD (Anas platyrhynchos), Male, 4 mo.: >2000 mg/kg (HSDB, 2004)
LD50 - (ORAL) MULE DEER (Odocoileus hemionus hemionus), Male and Female, 8-11 mo.: 400-800 mg/kg (HSDB, 2004)
LD50 - (ORAL) ROCK DOVE (Columba livia), Male and Female: 668 mg/kg (HSDB, 2004)
LD50 - (ORAL) PHEASANT (Phasianus colchicus), Female: 472 mg/kg, 3-4 mo. (HSDB, 2004)

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

221.04

DESCRIPTION/PHYSICAL STATE

2,4-D is odorless, white crystalline, nonflammable powder or crystals. It may have a phenolic odor and yellowish color due to impurities. Forms of 2,4-D include the acid or parent compound, esters, amines, and salts. It may be found in emulsions, aqueous solutions, or as the dry compound. 2,4-D may decompose on exposure to light, and it degrades rapidly in water (ACGIH, 2001; (EXTOXNET, 2002; Lewis, 2001; Lewis, 2000; NTP , 2001).

Carrier solvents that are used in the miscellaneous commercial formulations of 2,4-D may change the physical properties (WHO, et al., 2002)

2,4-D is a weak acid; Ka = 2.3 x 10(-3) (HSDB , 2002; ILO , 1998).

VAPOR PRESSURE

8.25 x 10 (-05) mmHg (at 25 degrees C) (ACGIH, 2001; (HSDB , 2002)

0.02 mPa (at 25 degrees C) (EXTOXNET, 2002)

1.05 x 10(-2) mmHg (at 25 degrees C) (Howard, 1991)

2.4 x 10(-5) mmHg (estimated; based on water solubility of 682 mg/L and a Henry's Law constant of 1.02 x 10(-8) atm-m(3)/mol) (Howard, 1991)

6 x 10(-7) mmHg (unspecified T) (Howard, 1991)

53 Pa (at 160 degrees C) (Hartley & Kidd, 1990)

0.02 mPa (at 25 degrees C) (EXTOXNET, 2002)

0.4 mmHg (at 160 degrees C) (EPA, 1990)

SPECIFIC GRAVITY

OTHER TEMPERATURE AND/OR PRESSURE

1.563 (at 20 degrees C (solid)) (CHRIS, 2005)

FREEZING/MELTING POINT

MELTING POINT

135-142 degrees C (EPA, 1990)
138 degrees C(ACGIH, 2001; Budavari, 2000; (EPA, 2002); ILO, 1998; Lewis, 2001a)
140.5 degrees C (Hartley & Kidd, 1990a; Howard, 1991a)
141 degrees C (Lewis, 2000a)

BOILING POINT

160 degrees C (at 0.4 mmHg) (ACGIH, 2001; (Budavari, 2000; EPA, 1990; Howard, 1991; ILO , 1998; Lewis, 2001; Lewis, 2000)

FLASH POINT

The acid and salts of 2,4-D are nonflammable, but commercial formulations of 2,4-D acid may have a flash point minimum of 88 degrees C (Cleveland open cup) (HSDB , 2002).

SOLUBILITY

IN WATER

2,4-D does not easily dissolve and is nearly insoluble in water (Budavari, 2000; Lewis, 2001).
Slightly soluble in water (ACGIH, 2001).
2,4-D in acid form, the oil-soluble amine salt, and the low volatile ether do not dissolve well in water. Other amine salts dissolve very well in water (USDA , 2002).
682 mg/L (at 25 degrees C) (Howard, 1991)
620 mg/L (at 20 degrees C) (Harbison, 1998; Hartley & Kidd, 1990)
677 ppm at 25 degrees C (HSDB , 2002)
540 ppm (at 20 degrees C) (HSDB , 2002)
0.09 g/100 g at 25 degrees C (HSDB , 2002)

IN ORGANIC SOLVENTS

2,4-D is soluble in alcohol and other organic solvents (ACGIH, 2001; (Budavari, 2000; Lewis, 2001).
In ethanol, 1250 g/kg (at 20 degrees C) (Hartley & Kidd, 1990)
85.0 g/100 g acetone (at 25 degrees C) (HSDB , 2002)
1.07 g/100 g benzene (at 28 degrees C) (HSDB , 2002)
0.5 g/100 g carbon disulfide (at 29 degrees C) (HSDB , 2002)
0.10 g/100 g carbon tetrachloride at (25 degrees C) (HSDB , 2002)
0.4 g/100 g ortho-dichlorobenzene (at 25 degrees C) (HSDB , 2002)
0.10 - 0.35 g/100 g diesel oil and kerosene (at 25 degrees C) (HSDB , 2002)
In diethyl ether, 243 g/kg (at 20 degrees C) (Hartley & Kidd, 1990)
78.5 g/100 g dioxane (at 31 degrees C) (HSDB , 2002)
10.3 g/100 g ethanol (50%) (at 25 degrees C) (HSDB , 2002)
In ethanol, 1250 g/kg (at 20 degrees C) (Hartley & Kidd, 1990)
130.0 g/100 g ethyl alcohol (95%) (at 25 degrees C) (HSDB , 2002)
27.0 g/100 g ethyl ether (at 25 degrees C) (HSDB , 2002)
In n-heptane, 1.1 g/kg (at 20 degrees C) (Hartley & Kidd, 1990)
31.6 g/100 g isopropanol (at 31 degrees C) (HSDB , 2002)
31.27 g/100 g methyl isobutyl ketone (at 25 degrees C) (HSDB , 2002)
0.067 g/100 g toluene (at 25 degrees C) (HSDB , 2002)
In toluene, 6.7 g/kg (at 20 degrees C) (Hartley & Kidd, 1990)
In xylene, 5.8 g/kg (at 20 degrees C) (Hartley & Kidd, 1990)

OTHER

The material is not easily dissolved in oils (Lewis, 2001).
Insoluble in petroleum oils (HSDB , 2002).

OCTANOL/WATER PARTITION COEFFICIENT

log 2.81 (at 20 degrees C) (Howard, 1991)
log 2.50/2.81 at 20 degrees C (Verschueren, 2001)

HENRY'S CONSTANT

1.37x10(-10) atm-m(3)/mol (Howard, 1991)

1.02x10(-8) atm-m(3)/mol (estimated by bond method) (Howard, 1991)

7.5x10(-8) atm-m(3)/mol (Ehrenfeld et al, 1986)

SPECTRAL CONSTANTS

2221 (Coblentz Society Spectral Collection) (HSDB , 2002)

3427 (Sadtler Research Laboratories Spectral Collection) (HSDB , 2002)

MASS

4511 (National Bureau of Standards EPA-NIH Mass Spectra Data Base, NSRDS-NBS-63) (HSDB , 2002)

OTHER/PHYSICAL

ORGANIC CARBON PARTITION COEFFICIENT

Experimental Koc = 19.6 and 109.1 (EPA, 2002).

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Information to evaluate chemical incidents

Information to evaluate chemical incidents

Information to evaluate chemical incidents