2,4-D is one of the oldest and most widely available herbicides and defoliants in the world, having been commercially available since 1945, and is now produced by many chemical companies since the patent on it has long since expired. It can be found in numerous commercial lawn herbicide mixtures, and is widely used as a weedkiller on cereal crops, pastures, and orchards. Over 1,500 herbicide products contain 2,4-D as an active ingredient.
2,4-D was first reported in 1944 by Franklin D-Jones at the C. B. Dolge Company in Connecticut.[5] The biological activity of 2,4-D as well as the similar hormone herbicides 2,4,5-T, and MCPA were discovered during World War II, a case of multiple discovery by four groups working independently under wartime secrecy in the United Kingdom and the United States: William G. Templeman and associates at Imperial Chemical Industries (ICI) in the UK; Philip S. Nutman and associates at Rothamsted Research in the UK; Franklin D. Jones and associates at the American Chemical Paint Company; and Ezra Kraus, John W. Mitchell, and associates at the University of Chicago and the United States Department of Agriculture. All four groups were subject to wartime secrecy laws and did not follow the usual procedures of publication and patent disclosure. In December 1942, following a meeting at the Ministry of Agriculture the Rothamsted and ICI workers pooled resources and Nutman moved to Jealott's Hill to join the ICI effort.[6] The first scientific publication describing the 2,4-D structure and plant growth regulating activity was by Percy W. Zimmerman and Albert E. Hitchcock at the Boyce Thompson Institute,[7] who were not the original inventors. The precise sequence of early 2,4-D discovery events and publications has been discussed.[8]
William Templeman found that when indole-3-acetic acid (IAA), a naturally-occurring auxin, was used at high concentrations, it could stop plant growth. In 1940, he published his finding that IAA killed broadleaf plants within a cereal field.[9] MCPA was discovered at about that time by his ICI group.[6][10]:Sec 7.1
In the USA, a similar search for an acid with a longer half life, i.e., a metabolically and environmentally more stable compound, led to 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), both phenoxy herbicides and analogs of IAA. Robert Pokorny, an industrial chemist for the C.B. Dolge Company in Westport, Connecticut, published their synthesis in 1941.[11]
2,4-D was not used as a chemical warfare agents during the war.[10]:Sec 7.1 Britain and the United States were looking for a chemical to starve Germany and Japan into submission by killing their potato and rice crops, but 2,4-D was found to be ineffective for that purpose, because both crops tolerate it. Within a year after the war ended, 2,4-D was commercially released as an herbicide to control broadleaf weeds in grain crops such as rice and wheat,[12] and in the 1950s it was registered in the United States to control size and enhance skin color in potatoes without affecting yields.[13]
The first publication of 2,4-D's use as a selective herbicide came in 1944.[14][15] The ability of 2,4-D to control broadleaf weeds in turf was documented soon thereafter, in 1944.[16] Starting in 1945, the American Chemical Paint Company brought 2,4-D to market as an herbicide called "Weedone". It revolutionized weed control, as it was the first compound that, at low doses, could selectively control dicotyledons (broadleaf plants), but not most monocotyledons— narrowleaf crops, such as wheat, maize (corn), rice, and similar cereal grass crops.[10] At a time when labor was scarce and the need for increased food production was large, it literally "replaced the hoe".[10]:Sec 7.1
In the 2000s, Dow AgroSciences developed a new cholinesalt version of 2,4-D (2,4-D choline) that Dow included in its "Enlist Duo" herbicide along with glyphosate and an agent that reduces drift; the choline salt form of 2,4-D is less volatile than 2,4-D.[20][21][22]
2,4-D is a synthetic auxin that induces uncontrolled growth and eventually death in susceptible plants.[24][25][26] 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 aminesalt, but more potent ester versions exist, as well.[27]
2,4-D is primarily used as a selective herbicide that kills many terrestrial and aquatic broadleaf weeds, but not grasses. 2,4-D can be found in commercial lawn herbicide mixtures, which often contain other active ingredients including mecoprop and dicamba. Over 1,500 herbicide products contain 2,4-D as an active ingredient.[28]
Estimated use of 2,4-D in the USA to 2019
A variety of sectors use products containing 2,4-D to kill weeds and unwanted vegetation. In agriculture, it was the first herbicide for selective killing of weeds but not crops. It has been used since 1945[29] to control broad-leafed weeds in pastures, orchards, and cereal crops such as corn, oats, rice, and wheat.[30] Cereals, in particular, have excellent tolerance to 2,4-D when it is applied before planting. 2,4-D is the cheapest way for farmers to control winter annual weeds by spraying in the fall, often at the lowest recommended rate. This is particularly effective before planting beans, peas, lentils, and chickpeas.[31] The estimated use of 2,4-D in US agriculture is mapped by the US Geological Survey. In 2019, the latest date for which figures are available, this reached 45,000,000 pounds (20,000,000kg) annually.[32]
In domestic lawn and garden maintenance, 2,4-D is commonly used. In forestry, it is used for stump treatment, trunk injection, and selective control of brush in conifer forests. Along roadways, railways, and power lines, it is used to control weeds and brush which might interfere with safe operation and damage equipment. Along waterways, it is used to control aquatic weeds that might interfere with boating, fishing, and swimming or clog irrigation and hydroelectric equipment. It is often used by government agencies to control the spread of invasive, noxious, and non-native weed species and prevent them from crowding out native species, and also to control many poisonous weeds such as poison ivy and poison oak.[33]:35–36[34]
A 2010 monitoring study conducted in the US and Canada found that "current exposures to 2,4-D are below applicable exposure guidance values."[35]
2,4-D has been used in laboratories for plant research as a supplement in plant cell culture media such as MS medium since at least 1962.[36] 2,4-D is used in plant cell cultures as a dedifferentiation (callus induction) hormone. It is classified as an auxin plant hormone derivative.[37]
Men who work with 2,4-D are at risk for abnormally shaped sperm and thus fertility problems; the risk depends on the amount and duration of exposure and other personal factors.[38]
Acute toxicity
According to the U.S. Environmental Protection Agency, "The toxicity of 2,4-D depends on its chemical forms, including salts, esters, and an acid form. 2,4-D generally has low toxicity for humans, except certain acid and salt forms can cause eye irritation. Swimming is restricted for 24 hours after application of certain 2,4-D products applied to control aquatic weeds to avoid eye irritation."[39]As of 2005[update] the median lethal dose or LD50 determined in acute toxicity rat studies was 639mg/kg.[40]
On August 8, 2007, the EPA issued a ruling that existing data do not support a link between human cancer and 2,4-D exposure.[47]
A 1995 panel of 13 scientists reviewing studies on the carcinogenicity of 2,4-D had divided opinions. None of the scientists thought the weight of the evidence indicated that 2,4-D was a "known" or "probable" cause of human cancer. The predominant opinion indicated that it is possible that 2,4-D can cause cancer in humans, although not all of the panelists believed the possibility was equally likely: one thought the possibility was strong, leaning toward probable, and five thought the possibility was remote, leaning toward unlikely. Two panelists believed it unlikely that 2,4-D can cause cancer in humans.[48]
In a prior 1987 report the IARC classified some chlorphenoxy herbicides including 2,4-D, MCPA and 2,4,5-T as a group as class 2B carcinogens - "possibly carcinogenic to humans".[49]
2,4-D has been linked to lymphoma and bladder cancer in dogs.[50]
Contaminants
A July 2013 Four Corners investigation found elevated levels of dioxins in a generic version of 2,4-D, one of Australia's most widely used herbicides. Samples imported from China had "one of the highest dioxin readings for 2,4-D in the last 10 to 20 years, and could pose potential health risks."[51]
Metabolism
When radioactively labeled 2,4-D was fed to livestock, 90% or more of the total radioactive residue (TRR) was shed in urine unchanged or as conjugated forms of 2,4-D. A relatively small portion of 2,4-D was metabolized into dichlorophenol, dichloroanisole, 4-chlorophenoxyacetic acid (6.9% of the TRR in milk), and 2,4-dichlorophenol (5% of the TRR in milk; 7.3% of the TRR in eggs and 4% of the TRR in chicken liver). Residue levels in kidney were the highest.[33]:21
Environmental behavior
Owing to the longevity and extent of use, 2,4-D has been evaluated several times by regulators and review committees.[52][53][54]
2,4-D amine salts and esters are not persistent under most environmental conditions.[18] The degradation of 2,4-D is rapid (half life of 6.2 days) in aerobic mineral soils.[40]:54 2,4-D is broken down by microbes in soil, in processes that involve hydroxylation, cleavage of the acid side-chain, decarboxylation, and ring opening. The ethyl hexyl form of the compound is rapidly hydrolyzed in soil and water to form the 2,4-D acid.[18] 2,4-D has a low binding affinity in mineral soils and sediment, and in those conditions is considered intermediately to highly mobile, and therefore likely to leach if not degraded.[18]
In aerobic aquatic environments, the half life is 15 days. In anaerobic aquatic environments 2,4-D is more persistent, with a half life of 41 to 333 days.[55] 2,4-D has been detected in streams and shallow groundwater at low concentrations, in both rural and urban areas. Breakdown is pH dependent.[18] Some ester forms are highly toxic to fish and other aquatic life.[17]
"The ester forms of 2,4-D can be highly toxic to fish and other aquatic life. 2,4-D generally has moderate toxicity to birds and mammals, is slightly toxic to fish and aquatic invertebrates, and is practically nontoxic to honeybees" per EPA.[39][datemissing]
Microbial breakdown
A number of 2,4-D-degrading bacteria have been isolated and characterized from a variety of environmental habitats.[56][57] 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 situdegradation were demonstrated.[58] 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.[59]
Regulation
Maximum residue limits were first set in the EU in 2002 and re-evaluated in 2011 by the European Food Safety Authority, which concluded that the codex maximum residue limits were "not expected to be of concern for European consumers".[33]:26 The total chronic exposure represented less than 10% of the acceptable daily intake (ADI).[33]:28 2,4-D is currently not approved for use on lawns and gardens in Denmark, Norway, Kuwait, and the Canadian provinces of Québec[60] and Ontario.[61][failed verification] 2,4-D use is severely restricted in the country of Belize. In 2008, Dow AgroScience, LLC, sued the Canadian government for allowing Quebec to ban 2,4-D, but settled in 2011.[62]
In 2012, EPA denied the petition filed November 6, 2008, by the Natural Resources Defense Council to revoke all tolerances and to cancel all registrations of 2,4-D. EPA stated that new study and EPA's comprehensive review confirmed EPA's previous finding that the 2,4-D tolerances are safe at anticipated exposure.[54][63][64] The estimated annual use of 2,4-D in US agriculture is mapped by the US Geological Service.[65]
In October 2014, the US EPA registered Enlist Duo, an herbicide containing the less volatile 2,4-D choline salt, glyphosate, and an antidrift agent, for use in six states: Illinois, Indiana, Iowa, Ohio, South Dakota, and Wisconsin.[20] In November 2015, the EPA attempted to withdraw its own approval of Enlist Duo, as a result of legal actions against both the agency and Dow by two U.S. groups. However, while it was implied that the approval was "gone" because of the action, in fact, Enlist Duo was still approved pending a decision by the courts. On January 25, 2016, the US Ninth Circuit Court of Appeals denied EPA's motion to vacate its Enlist Duo registration. Dow stated the product would be available in 15 US states and Canada for the 2016 crop season.[66][67]
On 21 August 2013, the Australian Pesticides and Veterinary Medicines Authority (APVMA) banned selected 2,4-D high volatile ester (HVE) products due to their environmental hazards. HVE 2,4-D products had already been banned in Europe and North America for 20 years; low volatile ester products continue to be available in Australia and worldwide.[68] In July 2013 APVMA published their report findings.[69]
Genetically modified crops
In 2010, Dow published that it had created genetically modified soybeans made resistant to 2,4-D by insertion of a bacterial aryloxyalkanoate dioxygenase gene, aad1.[70][71][72]:1 Dow intended it to be used as an alternative or complement to Roundup Ready crops due to the increasing prevalence of glyphosate-resistant weeds.[73]
As of April 2014, genetically modified maize and soybeans resistant to 2,4-D and glyphosate have been approved in Canada.[21] In September 2014, the USDA also approved Dow's maize and soybeans, and in October, the EPA registered the "Enlist Duo" herbicide containing 2,4-D and glyphosate.[20][71][74]
Herbicides, also commonly known as weed killers, are substances used to control undesired plants, also known as weeds. Selective herbicides control specific weed species while leaving the desired crop relatively unharmed, while non-selective herbicides kill plants indiscriminately. The combined effects of herbicides, nitrogen fertilizer, and improved cultivars has increased yields of major crops by 3x to 6x from 1900 to 2000.
Roundup is a brand name of herbicide originally produced by Monsanto, which Bayer acquired in 2018. Prior to the late-2010s formulations, it used broad-spectrum glyphosate-based herbicides. As of 2009, sales of Roundup herbicides still represented about 10 percent of Monsanto's revenue despite competition from Chinese producers of other glyphosate-based herbicides. The overall Roundup line of products represented about half of Monsanto's yearly revenue in 2009. The product is marketed to consumers by Scotts Miracle-Gro Company. In the late-2010s other non-glyphosate containing herbicides were also sold under the Roundup brand.
Operation Ranch Hand was a U.S. military operation during the Vietnam War, lasting from 1962 until 1971. Largely inspired by the British use of chemicals 2,4,5-T and 2,4-D during the Malayan Emergency in the 1950s, it was part of the overall herbicidal warfare program during the war called "Operation Trail Dust". Ranch Hand involved spraying an estimated 19 million U.S. gallons (72,000 m3) of defoliants and herbicides over rural areas of South Vietnam in an attempt to deprive the Viet Cong of food and vegetation cover. Areas of Laos and Cambodia were also sprayed to a lesser extent. According to the Vietnamese government, the chemicals caused 400,000 deaths. The United States government has described these figures as unreliable.
Glyphosate is a broad-spectrum systemic herbicide and crop desiccant. It is an organophosphorus compound, specifically a phosphonate, which acts by inhibiting the plant enzyme 5-enolpyruvylshikimate-3-phosphate synthase (EPSP). It is used to kill weeds, especially annual broadleaf weeds and grasses that compete with crops. Its herbicidal effectiveness was discovered by Monsanto chemist John E. Franz in 1970. Monsanto brought it to market for agricultural use in 1974 under the trade name Roundup. Monsanto's last commercially relevant United States patent expired in 2000.
A defoliant is any herbicidal chemical sprayed or dusted on plants to cause their leaves to fall off. Defoliants are widely used for the selective removal of weeds in managing croplands and lawns. Worldwide use of defoliants, along with the development of other herbicides and pesticides, allowed for the Green Revolution, an increase in agricultural production in mid-20th century. Defoliants have also been used in warfare as a means to deprive an enemy of food crops and/or hiding cover, most notably by the United Kingdom during the Malayan Emergency and the United States in the Vietnam War. Defoliants were also used by Indonesian forces in various internal security operations.
Alachlor is an herbicide from the chloroacetanilide family. It is an odorless, white solid. The greatest use of alachlor is for control of annual grasses and broadleaf weeds in crops. Use of alachlor is illegal in the European Union and no products containing alachlor are currently registered in the United States.
2,4,5-Trichlorophenoxyacetic acid, a synthetic auxin, is a chlorophenoxy acetic acid herbicide used to defoliate broad-leafed plants. It was developed in the late 1940s, synthesized by reaction of 2,4,5-Trichlorophenol and chloroacetic acid. It was widely used in the agricultural industry until being phased out, starting in the late 1970s due to toxicity concerns. Agent Orange, a defoliant used by the British in the Malayan Emergency and the U.S. in the Vietnam War, was equal parts 2,4,5-T and 2,4-D. 2,4,5-T itself is toxic with a NOAEL of 3 mg/kg/day and a LOAEL of 10 mg/kg/day. Agent Pink contained 100% 2,4,5-T. Additionally, the manufacturing process for 2,4,5-T contaminates this chemical with trace amounts of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). TCDD is a carcinogenic persistent organic pollutant with long-term effects on the environment. With proper temperature control during production of 2,4,5-T, TCDD levels can be held to about .005 ppm. Before the TCDD risk was well understood, early production facilities lacked proper temperature controls and individual batches tested later were found to have as much as 60 ppm of TCDD.
Phenoxy herbicides are two families of chemicals that have been developed as commercially important herbicides, widely used in agriculture. They share the part structure of phenoxyacetic acid.
Fenoprop, also called 2,4,5-TP, is the organic compound 2-(2,4,5-trichlorophenoxy)propionic acid. It is a phenoxy herbicide and a plant growth regulator, an analog of 2,4,5-T in which the latter's acetic acid sidechain is replaced with a propionate group (with an extra CH3). The addition of this extra methyl group creates a chiral centre in the molecule and useful biological activity is found only in the (2R)-isomer. The compound's mechanism of action is to mimic the auxin growth hormone indoleacetic acid (IAA). When sprayed on plants it induces rapid, uncontrolled growth. As with 2,4,5-T, fenoprop is toxic to shrubs and trees.
Dicamba is a selective systemic herbicide first registered in 1967. Brand names for formulations of this herbicide include Dianat, Banvel, Diablo, Oracle and Vanquish. This chemical compound is a chlorinated derivative of o-anisic acid. It has been described as a "widely used, low-cost, environmentally friendly herbicide that does not persist in soils and shows little or no toxicity to wildlife and humans."
Dichlorprop is a chlorophenoxy herbicide similar in structure to 2,4-D that is used to kill annual and perennial broadleaf weeds. It is a component of many common weedkillers. About 4 million pounds of dichlorprop are used annually in the United States.
There is a high use of pesticides in New Zealand due predominantly to the large agricultural industry.
This is an index of articles relating to pesticides.
Saflufenacil is the ISO common name for an organic compound of the pyrimidinedione chemical class used as an herbicide. It acts by inhibiting the enzyme protoporphyrinogen oxidase to control broadleaf weeds in crops including soybeans and corn.
The Enlist Weed Control System is an agricultural system that includes seeds for genetically modified crops that are resistant to Enlist and the Enlist herbicide; spraying the herbicide will kill weeds but not the resulting crop. The system was developed by Dow AgroSciences, part of Dow Chemical Company. In October 2014 the system was registered for restricted use in Illinois, Indiana, Iowa, Ohio, South Dakota and Wisconsin by the US Environmental Protection Agency. In 2013, the system was approved by Canada for the same uses.
Glyphosate-based herbicides are usually made of a glyphosate salt that is combined with other ingredients that are needed to stabilize the herbicide formula and allow penetration into plants. The glyphosate-based herbicide Roundup was first developed by Monsanto in the 1970s. It is used most heavily on corn, soy, and cotton crops that have been genetically modified to be resistant to the herbicide. Some products include two active ingredients, such as Enlist Duo which includes 2,4-D as well as glyphosate. As of 2010, more than 750 glyphosate products were on the market. The names of inert ingredients used in glyphosate formulations are usually not listed on the product labels.
Cyanazine is a herbicide that belongs to the group of triazines. Cyanazine inhibits photosynthesis and is therefore used as a herbicide.
Ohio River Park is a Superfund Site located in Neville Island, Pennsylvania. Between the 1920s-1970s, the Site was used for municipal waste, pesticide manufacturing, coke sludge disposal, cement manufacturing disposal, and pesticide waste. In 1977, Neville Land Company donated the Site to Allegheny County who started developing the Site as a community park. In 1979, Allegheny County found various hazardous contaminants on the Site. On August 30, 1990, the Site was determined to be a Superfund Site due to VOCs, SVOCs, inorganics, and pesticides being present in the surface soil, subsurface soil, surface water, river sediment, and groundwater. Soil remediation began in February 1998 and ended in September 1999. Today, Ohio River Park has the Robert Morris University Island Sports Center and Coraopolis Bridge on top of it. Additionally, benzene continues to be monitored because it is still present in the Site's groundwater.
Fluazifop is the common name used by the ISO for an organic compound that is used as a selective herbicide. The active ingredient is the 2R enantiomer at its chiral centre and this material is known as fluazifop-P when used in that form. More commonly, it is sold as its butyl ester, fluazifop-P butyl with the brand name Fusilade.
Indaziflam is a preemergent herbicide especially for grass control in tree and bush crops.
↑ Pokorny R (1941). "New Compounds. Some Chlorophenoxyacetic Acids". Journal of the American Chemical Society. 63 (6): 1768. doi:10.1021/ja01851a601.
1 2 Allen H, etal. (1978). "Chapter 5: Selective herbicides". In Peacock F (ed.). Jealott's Hill: Fifty years of Agricultural Research 1928-1978. Imperial Chemical Industries Ltd. pp.35–41. ISBN0901747017.
↑ Zimmerman PW, Hitchcock AE (1942). "Substituted phenoxy and benzoic acid growth substances and the relation of structure to physiological activity". Contrib. Boyce Thompson Institute. 12: 321–343.
↑ Templeman WG, Marmoy CJ (November 1940). "The effect upon the growth of plants of watering with solutions of plant-growth substances and of seed dressings containing these materials". Annals of Applied Biology. 27 (4): 453–471. doi:10.1111/j.1744-7348.1940.tb07517.x.
↑ Pokorny R (June 1941). "New Compounds. Some Chlorophenoxyacetic Acids". Journal of the American Chemical Society. 63 (6): 1768. doi:10.1021/ja01851a601.
↑ "Weed Control Methods Handbook: 2,4-D"(PDF). invasive.org. University of Georgia Center for Invasive Species and Ecosystem Health. April 2001. Retrieved 2015-11-01.
↑ Chlorphenoxy Herbicides (Group 2B) in IARC monographs on the evaluation of carcinogenic risks to humans: An updating of IARC Monographs volumes 1 to 42. Supplement 7, WHO, Lyon, France 1987.
↑ Islam F, Wang J, Farooq MA, Khan MS, Xu L, Zhu J, Zhao M, Muños S, Li QX, Zhou W (2018). "Potential impact of the herbicide 2,4-dichlorophenoxyacetic acid on human and ecosystems". Environment International. 111: 332–351. doi:10.1016/j.envint.2017.10.020. PMID29203058.
↑ Cavalca, L., A. Hartmann, N. Rouard, and G. Soulas. 1999. Diversity of tfdC genes: distribution and polymorphism among 2,4-dichlorophenoxyacetic acid degrading soil bacteria. FEMS Microbiology Ecology 29: 45-58.
This page is based on this Wikipedia article Text is available under the CC BY-SA 4.0 license; additional terms may apply. Images, videos and audio are available under their respective licenses.
