2,4-Dichlorophenoxyacetic acid

2,4-Dichlorophenoxyacetic acid
2,4-Dichlorophenoxyacetic acid
2,4-Dichlorophenoxyacetic acid in 3-D
IUPAC name (2,4-dichlorophenoxy)acetic acid
Other names 2,4-D hedonal trinoxol
style="background: #F8EABA; text-align: center;" colspan="2" | Identifiers
CAS number	94-75-7 Y
PubChem	1486
ChemSpider	1441
SMILES
InChI
InChI key	OVSKIKFHRZPJSS-UHFFFAOYAM
style="background: #F8EABA; text-align: center;" colspan="2" | Properties
Molecular formula	C8H6Cl2O3
Molar mass	221.04 g mol−1
Appearance	white to yellow powder
Melting point	140.5 °C (413.5 K)
Boiling point	160 °C (0.4 mm Hg)
Solubility in water	900 mg/L (25 °C)
style="background: #F8EABA; text-align: center;" colspan="2" | Related compounds
Related compounds	2,4,5-T, Dichlorprop
Y (what is this?)  (verify) Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
Infobox references

2,4-Dichlorophenoxyacetic acid (2,4-D) is a common systemic herbicide used in the control of broadleaf weeds. It is the most widely used herbicide in the world, and the third most commonly used in North America. 2,4-D is actually an important synthetic auxin (plant hormone), and as such it is often used in laboratories for plant research and as a supplement in plant cell culture media such as MS medium.

History

2,4-D was developed during World War II by a British team at Rothamsted Experimental Station, under the leadership of Judah Hirsch Quastel, aiming to increase crop yields for a nation at war. When it was commercially released in 1946, it became the first successful selective herbicide and allowed for greatly enhanced weed control in wheat, maize (corn), rice, and similar cereal grass crop, because it only kills dicots (two seed leaves), leaving behind monocots (one seed leaf).

Mechanism of herbicide action

2,4-D is a synthetic auxin, which is a class of plant hormones. It is absorbed through the leaves and is translocated to the meristems of the plant. Uncontrolled, unsustainable growth ensues, causing stem curl-over, leaf withering, and eventual plant death. 2,4-D is typically applied as an amine salt, but more potent ester versions exist as well.

Manufacture

2,4-D is a member of the phenoxy family of herbicides, which include:

• 2,4,5-Trichlorophenoxyacetic acid (2,4,5-T)
• 2-Methyl-4-chlorophenoxyacetic acid (MCPA)
• 2-(2-Methyl-4-chlorophenoxy)propionic acids (mecoprop, MCPP)
• 2-(2,4-Dichlorophenoxy)propionic acid (dichloroprop, 2,4-DP)
• (2,4-Dichlorophenoxy)butyric acid (2,4-DB)

2,4-D is manufactured from chloroacetic acid and 2,4-dichlorophenol, which is itself produced by chlorination of phenol. Alternatively, it may be produced by the chlorination of phenoxyacetic acid. The production processes creates several contaminants including isomers, monochlorophenol, and other polychlorophenols and their acids.

Dioxin impurities

The powerful defoliant and herbicide Agent Orange, used extensively throughout the Vietnam War, contained 2,4-D. The controversies associated with the use of Agent Orange were associated with a contaminant (dioxin) in the 2,4,5-T component. However, 2,4-D is still contaminated to some extent with dioxins, predominately those with 2 or 3 chlorine atoms. Another form of dioxin, 2,7-dichlorodibenzo-p-dioxin (DCDD), an inevitable by-product of 2,4-D manufacturing, was found to be "equipotent" to dioxin TCDD in its toxic effect on the immunity of mice. TCDD received all the publicity while the DCDD component was largely forgotten. To this day, DCDD is not regulated or monitored by the EPA and PMRA, even though DCDD levels could be at much higher levels than TCDD. The typical smell of 2,4-D is the break-down product 2,4-dichlorophenol, which is a suspected endocrine disrupter and possible carcinogen. 2,4-D is toxic to the liver at small dosages. Increases in liver function tests, jaundice, acute hepatitis, lobular and portal inflammation indicative of a toxic reaction, as well as permanent damage leading to cirrhosis in exposed golfers

Applications

2,4-D is primarily used as a herbicide. It is sold in various formulations under a wide variety of brand names. 2,4-D can be found in lawn herbicide mixtures such as "Weed B Gon MAX", "PAR III", "Trillion", "Tri-Kil", "Killex" and "Weedaway Premium 3-Way XP Turf Herbicide". All of these mixtures typically contain three active ingredients: 2,4-D, mecoprop and dicamba. Over 1,500 herbicide products contain 2,4-D as an active ingredient.

2,4-D is most commonly used for:

• Weed control in lawns and other turf
• No-till burndown
• Control of weeds and brush along fences and highway and railroad rights of way
• Conifer release (control of broad-leaf trees in conifer plantings)
• Grass hayfields and pastures
• Cereal grains
• Corn and sorghum (occasionally)
• As a synthetic auxin analogue

2,4-D continues to be used, where legal, for its low cost. However, where municipal lawn pesticide bylaws exist, such as in Canada, alternatives such as corn gluten meal and vinegar-based products are increasingly being used to combat weeds.

Toxicity

The LD₅₀ determined in an acute toxicity rat study is 639 mg/kg. Single oral doses of 5 and 30 mg/kg body weight did not cause any acute toxic effects in human volunteers. This chemical has been observed to increase the risk of amyotrophic lateral sclerosis (ALS) (see Burns et al. Occup Environ Med. 2001 Jan;58(1):24-30).

The amine salt formulations can cause irreversible eye damage (blindness); ester formulations are considered non-irritating to the eyes.

One study found that occupational exposure to 2,4-D caused male reproductive problems, including dead and malformed sperm.

Cancer risk

Different organizations have taken different stances on 2,4-D's cancer risk. On August 8, 2007, the United States Environmental Protection Agency issued a ruling that stated that existing data does not support a conclusion that links human cancer to 2,4-D exposure. However, the International Agency for Research on Cancer (IARC) has classified 2,4-D among the phenoxy acid herbicides MCPA and 2,4,5-T as a class 2B carcinogen - possibly carcinogenic to humans. A 1995 panel of 13 scientists reviewing studies on the carcinogenicity of 2,4-D had divided opinions, but the predominant opinion was that it is possible that 2,4-D causes cancer in humans.

A 1990 study of farmers in Nebraska, even when adjusting for exposure to other chemicals, found that 2,4-D exposure substantially increased the risk of Non-Hodgkin's lymphoma (NHL). A 2000 study of 1517 former employees of Dow Chemical Company who had been exposed to the chemical in manufacturing or formulating 2,4-D found no significant increase in risk of mortality due to NHL following 2,4-D exposure, but did find an increase in risk of mortality due to amyotrophic lateral sclerosis.

Environmental Behavior

Owing to the longevity and extent of use, 2,4-D is among the most thoroughly studied herbicides with respect to environmental properties. 2,4-D applied at 1.16 lb/acre to bluegrass turf in a laboratory experiment had a half-life of ten days. Other half-life figures for the herbicide in soil are seven days (15-25 degree C with 65% moisture) and ten days in non-sterile soil and 1.5 to 16 days in other studies. Soil microbes are primarily responsible for its disappearance in soil. Studies in Alaska and Canada failed to detect leaching in 22 weeks or from spring to fall , but 2,4-D has been included on the EPA list of compounds that are likely to leach from soil.

In aquatic environments microorganisms readily degrade 2,4-D and breakdown by sunlight is not a major reason for loss. Rates of breakdown increase with increased nutrients, sediment load and dissolved organic carbon. Under oxygenated conditions the half-life can be short, in the order of one week to several weeks. 2,4-D interferes with normal plant growth processes. Uptake of the compound is through leaves, stems and roots; however, it is, in general, nonpersistent. In one study when 2,4-D was applied to grass, there were 80 ppm at day zero, 45 ppm at 14 days, and 6 ppm at 56 days. Breakdown in plants is by a variety of biological and chemical pathways .

A number of 2,4-D-degrading bacteria have been isolated and characterized from a variety of environmental habitats. Metabolic pathways for the compound’s degradation have been available for many years, and genes encoding 2,4-D catabolism have been identified for several organisms. As a result of the extensive metadata on environmental behavior, physiology and genetics, 2,4-D was the first herbicide for which the bacteria actively responsible for in situ degradation was demonstrated. This was accomplished using the technique of DNA-based stable isotope probing, which enables a microbial function (activity), such as degrading a chemical, to be linked with the organism’s identity without the need to culture the organism involved. This advancement has been particularly beneficial for the study of soil microorganisms, since only a very small fraction of the thousands of species present in highly diverse soil bacterial communities can be isolated in pure culture.

Despite its short half-life in soil and in aquatic environments, the compound has been detected in groundwater supplies in at least five States and in Canada . It has also been detected in surface waters throughout the United States at very low concentrations.

Legal issues

2,4-D has been evaluated by the European Union and included on its list of approved herbicides, stating inter alia that "the review [of 2,4-D] has established that the residues arising from the proposed uses, consequent on application consistent with good plant protection practice, have no harmful effects on human or animal health." Concern over 2,4-D is such that it is currently not approved for use on lawns and gardens in Sweden, Denmark, Norway, Kuwait and the Canadian provinces of Québec and Ontario . 2,4-D use is severely restricted in the country of Belize. In 2005, the United States Environmental Protection Agency approved the continued use of 2,4-D. In Canada, the Pest Management Regulatory Agency (PMRA) has placed a condition of registration on 2,4-D such that the 2,4-D registrant(s) must provide the PMRA with a required developmental neurotoxicity study by September 20, 2009. According to the PMRA, the due date of the study has since been extended to early 2010.

External links

Government and academic references:

• 2,4-D Technical Fact Sheet - National Pesticide Information Center
• 2,4-D Pesticide Information Profile - Extension Toxicology Network
• EPA 2,4-D Reregistration Eligibility Decision
• 2,4-D RED Facts
• Biomonitoring Data for 2,4-Dichlorophenoxyacetic Acid in the US and Canada: Interpretation in a Public Health Risk Assessment Context Using Biomonitoring Equivalents, Environmental Health Perspectives online 12. 8. 2009
• Burns et al.: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1740039/?tool=pubmed

Industry website:

• 24d.org

Health and environmental references:

• ChemicalWATCH Factsheet
• Highlights of Major Problems with PMRA's Feb. 21, 2005 Review on 2,4-D Herbicide
• Overview of the toxic effects of 2,4-D
• 2,4-D: The Wrong Symbol for Pesticides

ca:Àcid 2,4-diclorofenoxiacètic