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Weeds killed with herbicide

An herbicide, commonly known as a weedkiller, is a substance used to kill unwanted plants. Selective herbicides kill specific targets while leaving the desired crop relatively unharmed. Some of these act by interfering with the growth of the weed and are often synthetic "imitations" of plant hormones. Herbicides used to clear waste ground, industrial sites, railways and railway embankments are non-selective and kill all plant material with which they come into contact. Smaller quantities are used in forestry, pasture systems, and management of areas set aside as wildlife habitat.

Some plants produce natural herbicides, such as the genus Juglans (walnuts), or the tree of heaven; the study of such natural herbicides, and other related chemical interactions, is called allelopathy.

Herbicides are widely used in agriculture and in landscape turf management. In the U.S., they account for about 70% of all agricultural pesticide use.[1]


[edit] History

Prior to the widespread use of chemical herbicides, cultural controls, such as altering soil pH, salinity, or fertility levels, were used to control weeds. Mechanical control (including tillage) was also (and still is) used to control weeds.

The first widely used herbicide was 2,4-dichlorophenoxyacetic acid, often abbreviated 2,4-D. It was first commercialized by the Sherwin-Williams Paint company and saw use in the late 1940s. It is easy and inexpensive to manufacture, and kills many broadleaf plants while leaving grasses largely unaffected (although high doses of 2,4-D at crucial growth periods can harm grass crops such as maize or cereals). The low cost of 2,4-D has led to continued usage today and it remains one of the most commonly used herbicides in the world. Like other acid herbicides, current formulations utilize either an amine salt (usually trimethylamine) or one of many esters of the parent compound. These are easier to handle than the acid.

2,4-D exhibits relatively good selectivity, meaning, in this case, that it controls a wide number of broadleaf weeds while causing little to no injury to grass crops at normal use rates. A herbicide is termed selective if it affects only certain types of plants, and nonselective if it inhibits a very broad range of plant types. Other herbicides have been more recently developed that achieve higher levels of selectivity than 2,4-D.

The 1950s saw the introduction of the triazine family of herbicides, which includes atrazine, which have current distinction of being the herbicide family of greatest concern regarding groundwater contamination. Atrazine does not break down readily (within a few weeks) after being applied to soils of above neutral pH. Under alkaline soil conditions atrazine may be carried into the soil profile as far as the water table by soil water following rainfall causing the aforementioned contamination. Atrazine is thus said to have carryover, a generally undesirable property for herbicides.

Glyphosate, frequently sold under the brand name Roundup, was introduced in 1974 for non-selective weed control. It is now a major herbicide in selective weed control in growing crop plants due to the development of crop plants that are resistant to it. The pairing of the herbicide with the resistant seed contributed to the consolidation of the seed and chemistry industry in the late 1990s.

Many modern chemical herbicides for agriculture are specifically formulated to decompose within a short period after application. This is desirable as it allows crops which may be affected by the herbicide to be grown on the land in future seasons. However, herbicides with low residual activity (i.e., that decompose quickly) often do not provide season-long weed control.

[edit] Health and environmental effects

Herbicides have widely variable toxicity. In addition to acute toxicity from high exposures there is concern of possible carcinogenicity[2] as well as other long-term problems such as contributing to Parkinson's Disease.

Some herbicides cause a range of health effects ranging from skin rashes to death[citation needed]. The pathway of attack can arise from intentional or unintentional direct consumption, improper application resulting in the herbicide coming into direct contact with people or wildlife, inhalation of aerial sprays, or food consumption prior to the labeled pre-harvest interval. Under extreme conditions herbicides can also be transported via surface runoff to contaminate distant water sources. Most herbicides decompose rapidly in soils via soil microbial decomposition, hydrolysis, or photolysis.

Phenoxy herbicides are often contaminated with dioxins such as TCDD; research suggested that such contamination results in a small rise in cancer risk after exposure to these herbicides.[3] Triazine exposure has been implicated in a likely relationship to increased risk of breast cancer, although a causal relationship remains unclear.[4]

Herbicide manufacturers have made bold and false or misleading claims about the safety of their products. Chemical manufacturer Monsanto Company agreed to change its advertising after pressure from New York attorney general Dennis Vacco; Vacco complained about misleading claims that its spray-on glyphosate based herbicides, including Roundup, were safer than table salt and "practically non-toxic" to mammals, birds, and fish.[5] Roundup is toxic and has resulted in death after being ingested in quantities ranging from 85-200 ml, although it has also been ingested in quantities as large as 500ml with only mild or moderate symptoms.[6] The manfucturer of Tordon 101 (Dow AgroSciences, owned by the Dow Chemical Company) has claimed that Tordon 101 has no effects on animals and insects[7], in spite of evidence of strong carcinogenic activity of the active ingredient[8] Picloram in studies on rats.[9]

The risk of Parkinson's Disease has been shown to increase with occupational exposure to herbicides and pesticides.[10] The herbicide paraquat is suspected to be one environmental factor causing Parkinson's disease.[11]

All organic and non-organic herbicides must be extensively tested prior to approval for commercial sale and labeling by the Environmental Protection Agency. However, because of the large number of herbicides in use, there is significant concern regarding health effects. In addition to health effects caused by herbicides themselves, commercial herbicide mixtures often contain other chemicals, including inactive ingredients, which have negative impacts on human health. For example, Roundup contains adjuvants which, even in low concentrations, were found to kill human embryonic, placental, and umbilical cells in vitro.[12]. One study also found that roundup caused genetic damage, but found that the damage was not caused by the active ingredient.[13]

Some herbicides may have therapeutic uses. There is current research into the use of herbicides as an anti-malaria drug that targets the plant-like apicoplast plastid in the malaria-causing parasite Plasmodium falciparum.[citation needed]

[edit] Ecological effects

Herbicide use generally has negative impacts on bird populations, although the impacts are highly variable and often require field studies to predict accurately. Laboratory studies have at times overestimated negative impacts on birds due to toxicity, predicting serious problems that were not observed in the field.[14] Most observed effects are due not to toxicity but to habitat changes and the decrease in abundance of species birds rely on for food or shelter. Herbicide use in silviculture, used to favor certain types of growth following clearcutting, can cause significant drops in bird populations. Even when herbicides are used which have low toxicity to birds, the herbicides decrease the abundance of many types of vegetation which the birds rely on.[15] Herbicide use in agriculture in Britain has been linked to a decline in seed-eating bird species which rely on the weeds killed by the herbicides.[16] Heavy use of herbicides in neotropical agricultural areas has been one of many factors implicated in limiting the usefulness of such agricultural land for wintering migratory birds.[17]

[edit] Scientific uncertainty

The health and environmental effects of many herbicides is unknown, and even within the scientific community there is often disagreement on the risk. For example, a 1995 panel of 13 scientists reviewing studies on the carcinogenicity of 2,4-D had divided opinions on the likelihood that 2,4-D causes cancer in humans.[18] As of 1992 there were too few studies on phenoxy herbicides to accurately assess the risk of many types of cancer from these herbicides, even though evidence was stronger that exposure to these herbicides is associated with increased risk of soft tissue sarcoma and non-Hodgkin's Lymphoma.[2]

[edit] Resistance

Scientists generally agree that selection pressure applied to weed populations for a long enough period of time eventually leads to resistance. Plants have developed resistance to Atrazine and to ALS-inhibitors, and more recently, to glyphosate herbicides. Marestail is one weed that has developed glyphosate resistance.[19]

[edit] Classification of herbicides

Herbicides can be grouped by activity, use, chemical family, mode of action, or type of vegetation controlled.

By activity:

  • Contact herbicides destroy only the plant tissue in contact with the chemical. Generally, these are the fastest acting herbicides. They are less effective on perennial plants, which are able to regrow from rhizomes, roots or tubers.
  • Systemic herbicides are translocated through the plant, either from foliar application down to the roots, or from soil application up to the leaves. They are capable of controlling perennial plants and may be slower acting but ultimately more effective than contact herbicides.

By use:

  • Soil-applied herbicides are applied to the soil and are taken up by the roots and/or hypocotyl of the target plant. There are three main types of soil-applied herbicides:
  1. Pre-plant incorporated herbicides are soil applied prior to planting and mechanically incorporated into the soil. The objective for incorporation is to prevent dissipation through photodecomposition and/or volatility.
  2. Preemergent herbicides are applied to the soil before the crop emerges and prevent germination or early growth of weed seeds.
  3. Post-emergent herbicides are applied after the crop has emerged.

Their classification by mechanism of action (MOA) indicates the first enzyme, protein, or biochemical step affected in the plant following application. The main mechanisms of action are:

  • ACCase inhibitors are compounds that kill grasses. Acetyl coenzyme A carboxylase (ACCase) is part of the first step of lipid synthesis. Thus, ACCase inhibitors affect cell membrane production in the meristems of the grass plant. The ACCases of grasses are sensitive to these herbicides, whereas the ACCases of dicot plants are not.
  • ALS inhibitors: the acetolactate synthase (ALS) enzyme (also known as acetohydroxyacid synthase, or AHAS) is the first step in the synthesis of the branched-chain amino acids (valine, leucine, and isoleucine). These herbicides slowly starve affected plants of these amino acids which eventually leads to inhibition of DNA synthesis. They affect grasses and dicots alike. The ALS inhibitor family includes sulfonylureas (SUs), imidazolinones (IMIs), triazolopyrimidines (TPs), pyrimidinyl oxybenzoates (POBs), and sulfonylamino carbonyl triazolinones (SCTs). ALS is a biological pathway that exists only in plants and not in animals thus making the ALS-inhibitors among the safest herbicides.
  • EPSPS inhibitors: The enolpyruvylshikimate 3-phosphate synthase enzyme EPSPS is used in the synthesis of the amino acids tryptophan, phenylalanine and tyrosine. They affect grasses and dicots alike. Glyphosate (Roundup) is a systemic EPSPS inhibitor but inactivated by soil contact.
  • Synthetic auxin inaugurated the era of organic herbicides. They were discovered in the 1940s after a long study of the plant growth regulator auxin. Synthetic auxins mimic this plant hormone. They have several points of action on the cell membrane, and are effective in the control of dicot plants. 2,4-D is a synthetic auxin herbicide.
  • Photosystem II inhibitors reduce electron flow from water to NADPH2+ at the photochemical step in photosynthesis. They bind to the Qb site on the D1 protein, and prevent quinone from binding to this site. Therefore, this group of compounds cause electrons to accumulate on chlorophyll molecules. As a consequence, oxidation reactions in excess of those normally tolerated by the cell occur, and the plant dies. The triazine herbicides (including atrazine) and urea derivatives (diuron) are photosystem II inhibitors.[20]
  • Photosystem I inhibitors steal electrons from the normal pathway through FeS - Fdx - NADP leading to direct discharge of electrons on Oxygen. As result ROS (reactive oxygen species) are produced and oxidation reactions in excess of those normally tolerated by the cell occur leading to plant death.

Bipirydiums herbicides (like Diquat and Paraquat) hit "Fe-S - Fdx step". Diphenilethers herbicides (like Nitrofen , Nitrofluorfen, Acifluoren) hit "Fdx - NADP step".[20]

[edit] Organic herbicides

Almost all herbicides in use today are considered "organic" herbicides in that they contain carbon as a primary molecular component. A notable exception would be the arsenical class of herbicides. Sometimes they are referred to as synthetic organic herbicides. Recently the term "organic" has come to imply products used in organic farming. Under this definition an organic herbicide is one that can be used in a farming enterprise that has been classified as organic. Organic herbicides are expensive and may not be affordable for commercial production.[citation needed] They are much less effective than synthetic herbicides and are generally used along with cultural and mechanical weed control practices.[citation needed]

Organic herbicides include:

  • Spices are now effectively used in patented herbicides.
  • Vinegar[21] is effective for 5-20% solutions of acetic acid with higher concentrations most effective but mainly destroys surface growth and so respraying to treat regrowth is needed. Resistant plants generally succumb when weakened by respraying.
  • Steam has been applied commercially but is now considered uneconomic and inadequate.[22][23][24] It kills surface growth but not underground growth and so respraying to treat regrowth of perennials is needed.
  • Flame is considered more effective than steam but suffers from the same difficulties.[25]
  • D-limonene (citrus oil). D-limonene (citrus oil) is a natural degreasing agent that strips the waxy skin or cuticle from weeds, causing dehydration and ultimately death.

[edit] Application

Most herbicides are applied as water-based sprays using ground equipment. Ground equipment varies in design, but large areas can be sprayed using self-propelled sprayers equipped with a long boom, of 60 to 80 feet (20 to 25 m) with flat fan nozzles spaced about every 20 in (500 mm). Towed, handheld, and even horse-drawn sprayers are also used.

Synthetic organic herbicides can generally be applied aerially using helicopters or airplanes, and can be applied through irrigation systems (chemigation).

A new method of herbicide application involves ridding the soil of its active weed seed bank rather than just killing the weed. Researchers at the Agricultural Research Service have found that applying herbicides to fields late in the weed's growing season greatly reduces its seed production, and therefore fewer weeds will return the following season. If herbicides are applied at the correct stage in the weed's growing season, then the weed's presence in the soil seed bank will greatly be reduced. Because most weeds are annual grasses, their seeds will only survive in soil for a year or two, so this method will be able to 'weed out' the weed with only a few years of herbicide application.[26]

[edit] Terminology

  • Control is the destruction of unwanted weeds, or the damage of them to the point where they are no longer competitive with the crop.
  • Suppression is incomplete control still providing some economic benefit, such as reduced competition with the crop.
  • Crop Safety, for selective herbicides, is the relative absence of damage or stress to the crop. Most selective herbicides cause some visible stress to crop plants.

[edit] Major herbicides in use today

  • 2,4-D, a broadleaf herbicide in the phenoxy group used in turf and in no-till field crop production. Now mainly used in a blend with other herbicides that allow lower rates of herbicides to be used, it is the most widely used herbicide in the world, third most commonly used in the United States. It is an example of synthetic auxin (plant hormone).
  • aminopyralid is a broadleaf herbicide in the pyridine group, used to control broadleaf weeds on grassland, such as docks, thistles and nettles. Notorious for its ability to persist in compost.
  • atrazine, a triazine herbicide used in corn and sorghum for control of broadleaf weeds and grasses. Still used because of its low cost and because it works extrodinarily well on a broad spectrum of weeds common in the U.S. corn belt, Atrazine is commonly used with other herbicides to reduce the over-all rate of atrazine and to lower the potential for groundwater contamination, it is a photosystem II inhibitor.
  • clopyralid is a broadleaf herbicide in the pyridine group, used mainly in turf, rangeland, and for control of noxious thistles. Notorious for its ability to persist in compost. It is another example of synthetic auxin.
  • dicamba, a post-emergent broadleaf herbicide with some soil activity, used on turf and field corn. It is another example of a synthetic auxin.
  • Glufosinate ammonium, a broad-spectrum contact herbicide and is used to control weeds after the crop emerges or for total vegetation control on land not used for cultivation.
  • Fluroxypyr, a systemic, selective herbicide used for the control of broad-leaved weeds in small grain cereals, maize, pastures, range land and turf. It is a synthetic auxin. In cereal growing, fluroxypyr's key importance is control of cleavers, Galium aparine. Other key broad-leaved weeds are also controlled.
  • Glyphosate, a systemic non-selective (it kills any type of plant) herbicide used in no-till burndown and for weed control in crops that are genetically modified to resist its effects. It is an example of an EPSPs inhibitor.
  • Imazapyr a non-selective herbicide used for the control of a broad range of weeds including terrestrial annual and perennial grasses and broadleaved herbs, woody species, and riparian and emergent aquatic species.
  • Imazapic, a selective herbicide for both the pre- and post-emergent control of some annual and perennial grasses and some broadleaf weeds. Imazapic kills plants by inhibiting the production of branched chain amino acids (valine, leucine, and isoleucine), which are necessary for protein synthesis and cell growth.
  • Linuron is a non-selective herbicide used in the control of grasses and broadleaf weeds. It works by inhibiting photosynthesis.
  • Metolachlor is a pre-emergent herbicide widely used for control of annual grasses in corn and sorghum; it has displaced some of the atrazine in these uses.
  • Paraquat, a non-selective contact herbicide used for no-till burndown and in aerial destruction of marijuana and coca plantings. More acutely toxic to people than any other herbicide in widespread commercial use.
  • Pendimethalin, a pre-emergent herbicide widely used to control annual grasses and some broadleaf weeds in a very wide range of crops, including corn, soybeans, wheat, cotton, many tree and vine crops, and many turfgrass species.
  • Picloram, a pyridine herbicide mainly used to control unwanted trees in pastures and edges of fields. It is another synthetic auxin.
  • Sodium chlorate, a non-selective herbicide, considered phytotoxic to all green plant parts. It can also kill through root absorption.
  • Triclopyr, a systemic, foliar herbicide in the pyridine group. It is used to control broadleaf weeds while leaving grasses and conifers unaffected.

[edit] Herbicides of historical interest

  • 2,4,5-Trichlorophenoxyacetic acid (2,4,5-T) was a widely used broadleaf herbicide until being phased out starting in the late 1970s. While 2,4,5-T itself is of only moderate toxicity, 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 extremely toxic to humans. 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. Individual batches tested later were found to have as much as 60 ppm of TCDD.
  • 2,4,5-T was withdrawn from use in the USA in 1983, at a time of heightened public sensitivity about chemical hazards in the environment. Public concern about dioxins was high, and production and use of other (non-herbicide) chemicals potentially containing TCDD contamination was also withdrawn. These included pentachlorophenol (a wood preservative) and PCBs (mainly used as stabilizing agents in transformer oil). Some feel[who?] that the 2,4,5-T withdrawal was not based on sound science. 2,4,5-T has since largely been replaced by dicamba and triclopyr.
  • Agent Orange was a herbicide blend used by the U.S. military in Vietnam between January 1965 and April 1970 as a defoliant. It was a 50/50 mixture of the n-butyl esters of 2,4,5-T and 2,4-D. Because of TCDD contamination in the 2,4,5-T component, it has been blamed for serious illnesses in many veterans and Vietnamese people who were exposed to it. However, research on populations exposed to its dioxin contaminant have been inconsistent and inconclusive. Agent Orange often had much higher levels of TCDD than 2,4,5-T used in the US. The name Agent Orange is derived from the orange color-coded stripe used by the Army on barrels containing the product. It is worth noting that there were other blends of synthetic auxins at the time of the Vietnam War whose containers were recognized by their colors, such as Agent Purple and Agent Pink.

[edit] See also

[edit] References

  1. ^ Kellogg RL, Nehring R, Grube A, Goss DW, and Plotkin S (February 2000), Environmental indicators of pesticide leaching and runoff from farm fields. United States Department of Agriculture Natural Resources Conservation Service. Retrieved on 2010-08-26.
  2. ^ a b Howard I. Morrison, Kathryn Wilkins, Robert Semenciw, Yang Mao, Don Wigle, "Herbicides and Cancer", Journal of the National Cancer Institute, Vol. 84, No. 24, 1866-1874, Dec. 16, 1992.
  3. ^ Manolis Kogevinas, Heiko Becher, Trevor Benn, Pier Alberto Bertazzi, Paolo Boffetta, H. Bas Bueno-de-Mesqurta, David Coggon, Didier Colin, Dieter Flesch-Janys, Marilyn Fingerhut, Lois Green, Timo Kauppinen, Margareta Littorin, Elsebeth Lynge, John D. Mathews, Manfred Neuberger, Neil Pearce, Rodolfo Saracci, "Cancer Mortality in Workers Exposed to Phenoxy Herbicides, Chlorophenols, and Dioxins An Expanded and Updated International Cohort Study", American Journal of Epidemiology, Vol. 145, No. 12, pp. 1061-1075.
  4. ^ M K Kettles, S R Browning, T S Prince, and S W Horstman, "Triazine herbicide exposure and breast cancer incidence: an ecologic study of Kentucky counties.", Environ Health Perspect, Nov. 1977, Vol. 105, No. 11, pp. 1222'1227.
  5. ^ "MONSANTO PULLS ROUNDUP ADVERTISING IN NEW YORK", Wichita Eagle, Nov. 27, 1996.
  6. ^ Alan Ronald Talbot, Mon-Han Shiaw, Jinn-Sheng Huang, Shu-Fen Yang, Tein-Shong Goo, Shur-Hueih Wang, Chao-Liang Chen, Thomas Richard Sanford, "Acute Poisoning with a Glyphosate-Surfactant Herbicide ('Roundup'): A Review of 93 Cases", Human & Experimental Toxicology, Vol. 10, No. 1, 1-8 (1991).
  7. ^ "Complaints halt herbicide spraying in Eastern Shore", CBC News, June 16, 2009.
  8. ^ "Tordon 101: picloram/2,4-D", Ontario Ministry of Agriculture Food & Rural Affairs, Reviewed Jan. 21, 2008.
  9. ^ Reuber, MD, " Carcinogenicity of Picloram", Journal of Toxicology and Environmental Health, Vol. 7, no. 2, pp. 207-222. 1981.
  10. ^ J. M. Gorell, MD, C. C. Johnson, PhD, B. A. Rybicki, PhD, E. L. Peterson, PhD and R. J. Richardson, ScD, "The risk of Parkinson's disease with exposure to pesticides, farming, well water, and rural living", Neurology, 1998;50:1346-1350.
  11. ^ R.J. Dinis-Oliveira, F. Remião, H. Carmo, J.A. Duarte, A. S�¡nchez Navarro, M.L. Bastos and F. Carvalho, "Paraquat exposure as an etiological factor of Parkinson's disease", NeuroToxicology, Vol. 27, No. 6, Dec. 2006, pp. 1110-1122.
  12. ^ Benachour, Nora; Gilles-Eric Séralini (December 23, 2008). "Glyphosate Formulations Induce Apoptosis and Necrosis in Human Umbilical, Embryonic, and Placental Cells". Chemical Research in Toxicology 22 (1): 97'105. doi:10.1021/tx800218n. PMID 19105591. http://pubs.acs.org/doi/abs/10.1021/tx800218n. 
  13. ^ Peluso M, Munnia A, Bolognesi C, Parodi S. Environ Mol Mutagen. 1998 31:55-9 PMID 9464316
  14. ^ Lawrence J. Blus, Charles J. Henny, "FIELD STUDIES ON PESTICIDES AND BIRDS: UNEXPECTED AND UNIQUE RELATIONS", Ecological Applications, Vol. 7, No. 4, pp. 1125-1132.
  15. ^ D. S. MacKinnon and B. Freedman, "Effects of Silvicultural Use of the Herbicide Glyphosate on Breeding Birds of Regenerating Clearcuts in Nova Scotia, Canada", Journal of Applied Ecology, Vol. 30, No. 3 (1993), pp. 395-406.
  16. ^ Ian Newton, "The recent declines of farmland bird populations in Britain: an appraisal of causal factors and conservation actions", Ibis, Vol. 146, No. 4, pp. 579-600.
  17. ^ C.S. Robbins, B.A. Dowell, D.K. Dawson, J.A. Colon, R. Estrada, A. Sutton, R. Sutton, D. Weyer, "Comparison of Neotropical migrant landbird populations wintering in tropical forest, isolated forest fragments, and agricultural habitats."
  18. ^ M. A. Ibrahim, G. G. Bond, T. A. Burke, P. Cole, F. N. Dost, P. E. Enterline, M. Gough, R. S. Greenberg, W. E. Halperin, E. McConnell, I. C. Munro, J. A. Swenberg, S. H. Zahm, and J. D. Graham, "Weight of the evidence on the human carcinogenicity of 2,4-D", Environ Health Perspect., 1991 December; 96: 213'222.
  19. ^ "Marestail Jumps Glyphosate Fence", Corn and Soybean Digest, Jan 1, 2002.
  20. ^ a b Stryer, Lubert (1995). Biochemistry, 4th Edition. W.H. Freeman and Company. pp. 670. ISBN 0-7167-2009-4. 
  21. ^ Spray Weeds With Vinegar?
  22. ^ Weed Management in Landscapes
  23. ^ Organic Weed Management in Vineyards
  24. ^ Kolberg, Robert L., and Lori J. Wiles. 2002. Effect of steam application on cropland weeds. Weed Technology. Vol. 16, No. 1. p. 43'49
  25. ^ Flame weeding for vegetable crops
  26. ^ "A New Way to Use Herbicides: To Sterilize, Not Kill Weeds". USDA Agricultural Research Service. May 5, 2010. http://www.ars.usda.gov/is/pr/2010/100505.htm. 

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