Herbicide

From Wikipedia, the free encyclopedia - View original article

 
Jump to: navigation, search
Weeds killed with herbicide

Herbicides, also commonly known as weedkillers, are pesticides used to kill unwanted plants.[1] 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 not 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; such action of natural herbicides, and other related chemical interactions, is called allelopathy.

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

Contents

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.[2] It was first commercialized by the paint company Sherwin-Williams 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 other 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 use either an amine salt (often 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, 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, more recently developed herbicides achieve higher levels of selectivity than 2,4-D.

The triazine family of herbicides, which includes atrazine, were introduced in the 1950s; they have the 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 nonselective weed control. It is now a major herbicide in selective weed control in growing crop plants due to the development of resistant crop plants. 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.

Health and environmental effects

Herbicides have widely variable toxicity. In addition to acute toxicity from high exposure levels, there is concern of possible carcinogenicity,[3] 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. 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 preharvest 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 has suggested such contamination results in a small rise in cancer risk after exposure to these herbicides.[4] Triazine exposure has been implicated in a likely relationship to increased risk of breast cancer, although a causal relationship remains unclear.[5]

Herbicide manufacturers have at times made 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.[6] Roundup is toxic and has resulted in death after being ingested in quantities ranging from 85 to 200 ml, although it has also been ingested in quantities as large as 500 ml with only mild or moderate symptoms.[7] The manfucturer of Tordon 101 (Dow AgroSciences, owned by the Dow Chemical Company) has claimed Tordon 101 has no effects on animals and insects,[8] in spite of evidence of strong carcinogenic activity of the active ingredient[9] Picloram in studies on rats.[10]

The risk of Parkinson's disease has been shown to increase with occupational exposure to herbicides and pesticides.[11] The herbicide paraquat is suspected to be one such factor.[12]

All commercially sold, organic and nonorganic herbicides must be extensively tested prior to approval for sale and labeling by the Environmental Protection Agency. However, because of the large number of herbicides in use, concern regarding health effects is significant. 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.[13] One study also found Roundup caused genetic damage, but the damage was not caused by the active ingredient.[14]

Ecological effects

Commercial 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.[15] Most observed effects are due not to toxicity, but to habitat changes and the decreases in abundance of species on which birds rely 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 which have low toxicity to birds are used, they decrease the abundance of many types of vegetation on which the birds rely.[16] 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.[17] 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.[18]

Scientific uncertainty

The health and environmental effects of many herbicides is unknown, and even the scientific community often disagrees 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 2,4-D causes cancer in humans.[19] As of 1992, studies on phenoxy herbicides were too few 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 lymphoma.[3]

Resistance

Scientists generally agree 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.[20]

Classification

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

By activity:

By use:

  1. Preplant 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. Pre-emergent herbicides are applied to the soil before the crop emerges and prevent germination or early growth of weed seeds.
  3. Postemergent 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:

Bipyridinium herbicides (such as diquat and paraquat) hit the "Fe-S - Fdx step" while diphenyl ether herbicide (such as nitrofen, nitrofluorfen, and acifluorfen) hit the "Fdx - NADP step".[clarification needed][21]

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. Commercially sold organic herbicides are expensive and may not be affordable for commercial farming.[citation needed] Depending on the application, they may be less effective than synthetic herbicides and are generally used along with cultural and mechanical weed control practices.

Homemade organic herbicides include:

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 long booms, of 60 to 80 feet (18 to 24 m) with flat-fan nozzles spaced about every 20 inches (510 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 the application of herbicides to fields late in the weeds' growing season greatly reduces their seed production, and therefore fewer weeds will return the following season. 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.[28]

Weed-wiping may also be used, where a wick wetted with herbicide is suspended from a boom and dragged or rolled across the tops of the taller weed plants. This allows treatment of taller grassland weeds by direct contact without affecting related but desirable plants in the grassland sward beneath.

Misapplication

Herbicide volatilisation or drift may result in herbicide affecting neighboring fields or plants, particularly in windy conditions. Sometimes, the wrong field or plants may be sprayed due to error.

Terminology

In current use

Historical interest: 2,4,5-T

See also

References

  1. ^ a b 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. ^ Gale E. Peterson (1967). "The Discovery and Development of 2,4-D". Agricultural History 41 (3): 243–254.
  3. ^ a b Howard I. Morrison, Kathryn Wilkins, Robert Semenciw, Yang Mao, Don Wigle (1992). "Herbicides and Cancer". Journal of the National Cancer Institute 84 (24): 1866–1874. doi:10.1093/jnci/84.24.1866. PMID 1460670. http://jnci.oxfordjournals.org/cgi/content/abstract/84/24/1866.
  4. ^ 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.
  5. ^ 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.
  6. ^ "MONSANTO PULLS ROUNDUP ADVERTISING IN NEW YORK", Wichita Eagle, Nov. 27, 1996.
  7. ^ 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).
  8. ^ "Complaints halt herbicide spraying in Eastern Shore", CBC News, June 16, 2009.
  9. ^ "Tordon 101: picloram/2,4-D", Ontario Ministry of Agriculture Food & Rural Affairs, Reviewed Jan. 21, 2008.
  10. ^ Reuber, MD (1981). "Carcinogenicity of Picloram". Journal of Toxicology and Environmental Health 7 (2): 207–222. doi:10.1080/15287398109529973. PMID 7014921. http://md1.csa.com/partners/viewrecord.php?requester=gs&collection=ENV&recid=227419&q=Picloram+cancer&uid=787347064&setcookie=yes.
  11. ^ 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.
  12. ^ R.J. Dinis-Oliveira, F. Remião, H. Carmo, J.A. Duarte, A. Sánchez 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.
  13. ^ 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.
  14. ^ Peluso M, Munnia A, Bolognesi C, Parodi S. Environ Mol Mutagen. 1998 31:55-9 PMID 9464316
  15. ^ 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.
  16. ^ 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.
  17. ^ 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.
  18. ^ 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."
  19. ^ 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 (1991). "Weight of the evidence on the human carcinogenicity of 2,4-D". Environ Health Perspect 96: 213–222. PMC 1568222. PMID 1820267. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1568222/.
  20. ^ "Marestail Jumps Glyphosate Fence", Corn and Soybean Digest, Jan 1, 2002.
  21. ^ a b Stryer, Lubert (1995). Biochemistry, 4th Edition. W.H. Freeman and Company. pp. 670. ISBN 0-7167-2009-4.
  22. ^ American Journal of Alternative Agriculture (2000), 15: 189-191
  23. ^ Spray Weeds With Vinegar?
  24. ^ Weed Management in Landscapes
  25. ^ Organic Weed Management in Vineyards
  26. ^ Kolberg, Robert L., and Lori J. Wiles. 2002. Effect of steam application on cropland weeds. Weed Technology. Vol. 16, No. 1. p. 43–49
  27. ^ Flame weeding for vegetable crops
  28. ^ "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.
  29. ^ http://www.herbiguide.com.au/Descriptions/hg_Fluazifop.htm
  30. ^ http://pnwhandbooks.org/weed/agrichemicals/imazamox

Further reading

External links

General Information
Regulatory policy