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Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
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Appendix A
Herbicide Selection

Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×

Herbicidea

Classificationb

Haloxyfop (aryloxyphenoxypropionates)

Clethodim (cyclohexanediones)

Pinoxaden (phenylpyrazolines)

ACCase inhibitors (A(1))

Alachlor (chloroacetanilides)

Diphenamid (acetamides)

Flufenacet (oxyacetamides)

Fentrazamide (tetrazolinones)

Mitosis inhibitors (K3(15))

Bensulfuron-methyl (sulfonylureas)

Imazethapyr (imidazolinones)

Cloransulam-methyl (triazolopyrimidines)

ALS inhibitors (B(2))

Atrazine (symmetrical triazines)

Photosynthesis II inhibitors (C1(5))

Dicamba (benzoic acids)

Synthetic auxins (O(4))

Glufosinate (organophosphorus)

Glutamine synthetase inhibitor (H(10))

Glyphosate (organophosphorus)

Enolpyruvyl shikimate-3-phosphate (EPSP) synthase inhibitor (G(9))

*Reference dose.

†Lethal dose.

§Lethal concentration.

Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×

Mode of Actionc

Relative Toxicity

Inhibitor of acetyl coenzyme-A carboxylase (ACCase), a pivotal enzyme in plant fatty acid biosynthesis.

Varies based on specific chemical compound; likely to be carcinogenic to humans according to EPA Proposed EPA Weight-of-the-Evidence Categories (US-EPA, 2009a).

Inhibition of cell division (long-chain fatty acid inhibitor).

Slightly toxic; oral RfD* of 1 × 102 mg/kg-day. Critical effects: hemosiderosis, hemolytic anemia (US-EPA, 2009b).

Inhibition of the acetolactate synthase (ALS) enzyme resulting in cessation of the biosynthesis of essential branched chain amino acids (leucine, valine, and isoleucine).

Varied; generally low acute and chronic toxicity to humans and not likely to be carcinogenic.

Inhibit photosynthesis by binding with a specific protein in the photosystem II complex.

Slightly to moderately toxic; oral RfD of 3.5 × 102 mg/kg-day. Critical effects: decreased body weight gain (other effect: cardiac toxicity and moderate-to-severe dilation of the right atrium (EXTOXNET, 2009a; US-EPA, 2009c)).

The specific mode of action is not well defined, however these herbicides mimic the endogenous auxin indoleacetic acid, a plant hormone that stimulates growth and appears to negatively affect cell wall plasticity and nucleic acid metabolism.

Relatively nontoxic. Acute oral LD50 in rats is 1707 mg/kg, dermal LC50§ in rabbits is >2000 mg/kg. However, eye irritation in rabbit is extreme.

Inhibits the activity of glutamine synthetase, which causes ammonia buildup in the cell. The ammonia destroys cell membranes.

Practically nontoxic by ingestion; some increase in absolute and relative kidney weights in males. No observed carcinogenesis. Oral RfD of 4 × 104 mg/kg-day (NPIC, 2009; US-EPA, 2009d).

Inhibits the EPSP synthase, which leads to depletion of essential aromatic amino acids (tryptophan, tyrosine, and phenylalanine).

Generally nontoxic. Increased incidence of renal tubular dilation in third generation weanlings. Oral RfD of 1 × 101 mg/kg-day (US-EPA, 2009e).

Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×

Herbicidea

Classificationb

Amides, pyridiazinones, pyridines, isoxazoles, pyrazoles, triazoles, triketones, and others

Carotenoid biosynthesis inhibitors

Fluridone (unclassified)

(F1(12))

Mesotrione (triketones)

(F2(28))

Amitrole (triazoles)

(F3(11))

Metribuzin (triazinones, asymmetrical triazines)

Photosynthesis II inhibitors (C1(5))

Dicarboximide herbicides, triazolone herbicides, diphenylethers, N-phenylphthalimides, oxadiazoles, thiadiazoles, triazolinones, and others

Protoporphyrinogen Oxidase (PPO) inhibitors (E(14))

Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×

Mode of Actionc

Relative Toxicity

Inhibit the catabolic degradation of tyrosine to plastoquinones (important for photosynthesis and carotenoid biosynthesis) and tocopherol (vitamin E, which protects biological membranes against oxidative stress and the photosynthetic apparatus against photo-inactivation).

Varied; developmental toxicity, probable human carcinogen, phytotoxic (US-EPA, 2004, 2006, 2009f, 2009g).

Inhibition of phytoene desaturase, an enzyme essential for carotenoid biosynthesis.

 

Inhibition of hydroxyphenylpyruvate dioxygenase (HPPD), an enzyme involved in the synthesis of plastoquinone (PQ) and tocopherol (vitamin E).

 

Target site is generally considered unknown with the exception of amitrole, which inhibits lycopene cyclase and clomazone that is reported to inhibit an early step in the nonmevalonic acid isoprenoid pathway ultimately leading to carotenoid synthesis.

 

Inhibit photosynthesis by binding with a specific protein in the photosystem II complex.

A slightly toxic compound in EPA toxicity class III. Liver and kidney effects, decreased body weight, mortality; no indications of carcinogenic effects. RfD of 2.5 10–2 mg/kg-day (EXTOXNET, 2009b; US-EPA, 2009h).

Inhibits the protoporphyrinogen oxidase (PPO) which is in the chlorophyll synthesis pathway. The PPO inhibition starts a reaction in the cell that ultimately causes the destruction of cell membranes. The leaking cell membranes rapidly dry and disintegrate.

Varied; including compounds having: slight toxicity (EPA category III); classified as a “not likely” human carcinogen to “likely to be a human carcinogen” (US-EPA, 2001).

Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×

Herbicidea

Classificationb

2,4-D (phenoxyacetic herbicide)

Synthetic auxins (O(4))

aHerbicide listed is one example of the herbicide family.

bHerbicide mode of action code according to the Herbicide Resistance Action Committee (HRAC, 2010) and the Weed Science Society of America (WSSA) classification (Senseman and Armbrust, 2007). The capitalized letter is the HRAC classification and the superscript number is the WSSA classification.

cThe indicated herbicide mode of action is from the HRAC and WSSA descriptions as well as other citations.

REFERENCES

EXTOXNET (Extension Toxicology Network). 2009a. Atrazine. Corvallis, OR: Oregon State University. Available online at http://extoxnet.orst.edu/pips/atrazine.htm. Accessed November 14, 2009.

———. 2009b. Metribuzin. Corvallis, OR: Oregon State University. Available online at http://extoxnet.orst.edu/pips/metribuz.htm. Accessed November 14, 2009.

HRAC (Herbicide Resistance Action Committee). 2010. Classification of herbicides according to mode of action. Washington, DC. Available online at http://www.hracglobal.com/Publications/ClassificationofHerbicideModeofAction/tabid/222/Default.aspx. Accessed January 21, 2010.

NPIC (National Pesticide Information Center). 2009. Glufosinate. Corvallis, OR: Oregon State University. Available online at http://extoxnet.orst.edu/pips/atrazine.htm. Accessed November 14, 2009.

Senseman, S.A., and K. Armbrust, eds. 2007. Herbicide handbook. 9th ed., p. 458. Lawrence, KS: Weed Science Society of America.

US-EPA (U.S. Environmental Protection Agency). 2001. Pesticide fact sheet: Flumioxazin. 7501C. Office of Prevention, Pesticides, and Toxic Substances. Washington, DC. Available online at http://www.epa.gov/opprd001/factsheets/flumioxazin.pdf. Accessed January 21, 2010.

———. 2004. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Fluridone. 7508C. Office of Prevention, Pesticides, and Toxic Substances. Washington, DC.Available online at www.epa.gov/oppsrrd1/REDs/fluridone_tred.pdf. Accessed January 21, 2010.

———. 2006. Pesticide fact sheet: 1,2,4-triazole, triazole alanine, triazole acetic acid: Human health aggregate risk assessment in support of reregistration and registration actions for triazole-derivative fungicide compounds. Office of Prevention, Pesticides, and Toxic Substances. Washington, DC. Available online at www.epa.gov/opprd001/factsheets/tetraHHRA.pdf. Accessed January 21, 2010.

———. 2009a. User’s manual for RSEI, version 2.2.0 [1996 - 2006 TRI data]. Office of Prevention, Pesticides, and Toxic Substances. Washington, DC. Available online at http://www.epa.gov/oppt/rsei/pubs/RSEI%20Users%20Manual%20V2.2.0.pdf. Accessed June 24, 2009.

Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×

Mode of Actionc

Relative Toxicity

Mimics a plant growth regulator. The specific mode of action is not well defined, however these herbicides mimic the endogenous auxin indoleacetic acid, a plant hormone that stimulates growth and appears to negatively affect cell wall plasticity and nucleic acid metabolism.

Critical effects include: hematologic, hepatic, and renal toxicity. RfD of 1 × 102 mg/kg-day.

———. 2009b. Alachlor (CASRN 15972-60-8). National Center for Environmental Assessment. Washington, DC. Available online at http://www.epa.gov/ncea/iris/subst/0129.htm. Accessed January 21, 2010.

———. 2009c. Atrazine (CASRN 1912-24-9). National Center for Environmental Assessment. Washington, DC. Available online at http://www.epa.gov/ncea/iris/subst/0209.htm. Accessed January 21, 2010.

———. 2009d. Glufosinate-ammonium (CASRN 77182-82-2). National Center for Environmental Assessment. Washington, DC. Available online at http://www.epa.gov/ncea/iris/subst/0247.htm. Accessed January 21, 2010.

———. 2009e. Glyphosate (CASRN 1071-83-6). National Center for Environmental Assessment. Washington, DC. Available online at http://www.epa.gov/ncea/iris/subst/0057.htm. Accessed January 21, 2010.

———. 2009f. Pesticide fact sheet. Office of Prevention, Pesticides, and Toxic Substances. Washington, DC. Available online at http://www.epa.gov/ncea/iris/subst/0057.htm. Accessed January 21, 2010.

———. 2009g. Tembotrione chemical documents. Office of Prevention, Pesticides, and Toxic Substances. Washington, DC. Available online at http://www.epa.gov/opprd001/factsheets/tembotrione.htm. Accessed January 21, 2010.

———. 2009h. Metribuzin (CASRN 21087-64-9). Office of Prevention, Pesticides, and Toxic Substances. Washington, DC. Available online at http://www.epa.gov/NCEA/iris/subst/0075.htm. Accessed January 21, 2010.

Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×

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Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×
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Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×
Page 238
Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×
Page 239
Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×
Page 240
Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×
Page 241
Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×
Page 242
Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×
Page 243
Suggested Citation:"Appendix A: Herbicide Selection." National Research Council. 2010. The Impact of Genetically Engineered Crops on Farm Sustainability in the United States. Washington, DC: The National Academies Press. doi: 10.17226/12804.
×
Page 244
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Since genetically engineered (GE) crops were introduced in 1996, their use in the United States has grown rapidly, accounting for 80-90 percent of soybean, corn, and cotton acreage in 2009. To date, crops with traits that provide resistance to some herbicides and to specific insect pests have benefited adopting farmers by reducing crop losses to insect damage, by increasing flexibility in time management, and by facilitating the use of more environmentally friendly pesticides and tillage practices. However, excessive reliance on a single technology combined with a lack of diverse farming practices could undermine the economic and environmental gains from these GE crops. Other challenges could hinder the application of the technology to a broader spectrum of crops and uses.

Several reports from the National Research Council have addressed the effects of GE crops on the environment and on human health. However, The Impact of Genetically Engineered Crops on Farm Sustainability in the United States is the first comprehensive assessment of the environmental, economic, and social impacts of the GE-crop revolution on U.S. farms. It addresses how GE crops have affected U.S. farmers, both adopters and nonadopters of the technology, their incomes, agronomic practices, production decisions, environmental resources, and personal well-being. The book offers several new findings and four recommendations that could be useful to farmers, industry, science organizations, policy makers, and others in government agencies.

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