G2066 Index: Crops, Insects, & Pests

Issued 2011, revised June 2016

Insecticide Mode of Action Classification for Nebraska Field Crops

Robert J. Wright, Extension Entomology Specialist

Insecticides differ in their modes of action, or how they act against a target pest. This NebGuide discusses insect resistance management and provides modes of action for insecticides used for Nebraska field crops.

Insecticide resistance is becoming an increasing problem worldwide; over 500 insects are documented to be resistant to one or more insecticides. Although we often think of insecticide resistance as a problem in tropical areas, or in greenhouses where insects can produce many generations in a year, Nebraska also has had problems with insecticide resistance.

Western corn rootworms have developed resistance to insecticides twice: in the 1950s to persistent soil insecticides such as aldrin, dieldrin, and heptachlor and more recently, in the 1990s to foliar insecticides such as methyl parathion and carbaryl that were used to control adult corn rootworms in central Nebraska. Also, some greenbug populations are resistant to chlorpyrifos. We now have a greater diversity of types of insecticides labeled for use on Nebraska field crops than in the past. Understanding available modes of action of these insecticides and not repeatedly using products with the same mode of action can play an important role in reducing future problems with insecticide resistance.

Insecticide Resistance

Pesticide resistance may be defined as a decreased response of a population of animals or plants to a pesticide or control agent as a result of previous exposure to the pesticide. Resistance is different from “tolerance,” which is the innate ability to survive a given toxicant dose without prior exposure and evolutionary change.

Insecticide resistance can be thought of as “accelerated evolution” or a population responding to an intense selective pressure and survival of those individuals that possess genes conferring resistance. Insecticide resistance occurs as a response to insect management practices over multiple years.

Resistance develops as a result of random mutations, producing a small number of individuals which possess traits that allow survival of normally lethal doses of insecticides. The insecticide itself does not produce a genetic change.

Insecticide Resistance Action Committee (IRAC)

IRAC is an international industry consortium providing a coordinated response to prevent or delay the development of resistance in insect and mite pests. Its website (www.irac-online.org) has a great deal of additional information. The following text from the IRAC website has been modified with permission.

Mode of Action, Target Site Resistance and Cross-Resistance

In most cases, not only does resistance render the selecting compound ineffective, it often also confers cross-resistance to other chemically related compounds. This is because compounds within a specific chemical group usually share a common target site within the pest, and thus share a common mode of action. For example, both carbamates such as Furadan® and Sevin® and organophosphates such as Lorsban® and Counter®, are acetylcholine inhibitors. Carbamates and organophosphates are subgroups with a similar mode of action.

It is common for resistance to develop based on a genetic modification of this target site. When this happens, the selecting compound’s interaction with its target site is impaired and the pesticide loses its pesticidal efficacy. Because all compounds within the chemical subgroup share a common mode of action, there is a high risk that the resistance that has developed will automatically confer cross-resistance to all the compounds in the same subgroup. It is this concept of cross-resistance within chemically related insecticides or acaricides that is the basis of the IRAC mode of action classification.

Effective IRM Strategies Use Alternations or Sequences of Different Modes of Action

The objective of successful Insecticide Resistance Management (IRM) is to prevent or delay the evolution of resistance to insecticides, or to help regain susceptibility in insect pest populations in which resistance has already arisen. Effective IRM is an important element in maintaining the efficacy of valuable insecticides. It is important to recognize that it is usually easier to proactively prevent resistance from occurring than it is to reactively regain susceptibility.

Experience has shown that all effective insecticide or acaricide resistance management strategies seek to minimize the selection for resistance from any one type of insecticide or acaricide. In practice, alternations, sequences, or rotations of compounds from different mode of action groups provide a sustainable and effective approach to IRM. This ensures that selection from compounds in any one mode of action group is minimized. The IRAC mode of action classification is provided as an aid to insecticide selection for these types of IRM strategies.

The following IRM principles are recommended and endorsed by IRAC:

  • Consider options for minimizing insecticide use by selecting early maturing or pest- tolerant varieties of crop plants.
  • Include effective cultural and biological control practices that work in harmony with effective IRM programs. Adopt all nonchemical techniques known to control or suppress pest populations, including biological sprays (Bts), resistant varieties, within-field refuges (untreated areas), and crop rotation.
  • Where possible, select insecticides and other pest management tools that preserve beneficial insects.
  • Use products at their full, recommended doses. Reduced (sublethal) doses quickly select populations with average levels of tolerance, while doses that are too high may impose excessive selection pressures.
  • Apply insecticides with appropriate, well-maintained equipment and use recommended water volumes, spray pressures, and optimal temperatures to obtain optimal coverage.
  • Where larval stages are being controlled, target younger larval instars where possible because these are usually much more susceptible and therefore much more effectively controlled by insecticides than older stages.
  • Use appropriate local economic thresholds and spray intervals.
  • Where there are multiple applications per year or growing season, use alternate products with different mode of action classes.
  • In the event of a control failure, do not reapply the same insecticide. Change the class of insecticide to one having a different mode of action and to which there is no locally known cross-resistance.

The Mode of Action Classification

This classification was developed and endorsed by IRAC and is based on the best available evidence of the mode of action of available insecticides. IRAC companies have agreed to the classification details and internationally recognized industrial and academic insect toxicologists and biochemists have approved the classification.

Table I. Mode of action of insecticides

Main Group and Primary Site of Action Chemical Subgroup or Exemplifying Active Ingredient Active Ingredient (Representative Trade Names®)

1. Acetylcholine esterase inhibitors

1A Carbamates

Aldicarb (Temik®)

Carbaryl (Sevin®, others)

Carbofuran (Furadan®)

Methomyl (Lannate®)

Oxamyl (Vydate®)

Thiodicarb (Larvin®)

1B Organophosphates

Acephate (Orthene®)

Chlorethoxyfos (Fortress®)

Chlorpyrifos (Lorsban®, others)

Dimethoate (Dimethoate, others)

Ethoprop (Mocap®)

Malathion (Fyfanon®, others)

Methamidophos (Monitor®)

Methidathion (Supracide®)

Methyl parathion (Penncap-M®)

Phorate (Thimet®)

Phosmet (Imidan®)

Tebupirimphos (Aztec®)

Terbufos (Counter®)

2. GABA-gated chloride channel antagonists

2A Cyclodiene organochlorines

Endosulfan (Thionex®, others)

2B Phenylpyrazoles (fiproles)

Fipronil (Regent®)

3. Sodium channel modulators

3A Pyrethroids Pyrethrins

Permethrin (Ambush®, Pounce®)

Bifenthrin (Capture®, others)

Beta-cyfluthrin (Baythroid®)

Deltamethrin (Decis®)

Esfenvalerate (Asana®)

Zeta-cypermethrin (Mustang® MAX)

Gamma-cyhalothrin (Proaxis™)

Lambda-cyhalothrin (Warrior)

Tefluthrin (Force®)

3B DDT Methoxychlor

4. Nicotinic acetylcholine receptor agonists

4A Neonicotinoids

Thiamethoxam (Cruiser®)

Imidacloprid (Gaucho®)

Clothianidin (Poncho™)

4B Nicotine

4C Sulfoximes

Sulfoxaflor (Transform®)

4D Butenolides

Flupyradifurone (Sivanto®)

5. Nicotinic acetylcholine receptor allosteric activators

Spinosyns

Spinosad (Entrust™, Success®, Tracer®)

Spinetoram (Radiant®)

6. Chloride channel activators

Avermectins Milbemycins

7. Juvenile hormone mimics

7A Juvenile hormone analogues

7B Fenoxycarb

7C Pyriproxyfen

8. Miscellaneous nonspecific (multi-site) inhibitors

9. Selective homopteran feeding blockers

9B Pymetrozine

Pymetrozine (Fulfill®)

9C Flonicamid

10. Mite growth inhibitors

10A Clofentezine Hexythiazox (Onager®)

Hexythiazox (Onager)

10B Etoxazole

Etoxazole (Zeal®)

11. Microbial disruptors of insect midgut membranes

Bacillus thuringiensis or Bacillus sphaericus and the insecticidal proteins they produce

Cry proteins used in Bt corn hybrids, Dipel®, and others

12. Inhibitors of mitochondrial ATP synthase

12A Diafenthiuron

12B Organotin miticides

12C Propargite

Propargite (Comite® II)

12D Tetradifon

13. Uncouplers of oxidative phosphorylation via disruption of the proton gradient

Chlorfenapyr DNOC

14. Nicotinic acetylcholine receptor channel blockers

Nereistoxin analogues

15. Inhibitors of chitin biosynthesis, type 0, Lepidopteran

Benzoylureas

Diflubenzuron (Dimilin®)

16. Inhibitors of chitin biosynthesis, type 1, Homopteran

Buprofezin

17. Moulting disruptor, Dipteran

Cyromazine

18. Ecdysone receptor agonists

Diacylhydrazines

Methoxyfenozide (Intrepid®)

19. Octopamine receptor agonists

Amitraz

20. Mitochondrial complex III electron transport inhibitors (Coupling site II)

20A Hydramethylnon

20B Acequinocyl

20C Fluacrypyrim

21. Mitochondrial complex I electron transport inhibitors

21A METI acaricides

Fenpyroximate (Portal®)

21B Rotenone

22. Voltage-dependent sodium channel blockers

22A Indoxacarb

Indoxacarb (Steward®)

22B Metaflumizone

23. Inhibitors of acetyl CoA carboxylase

Tetronic and Tetramic acid derivatives

Spiromesifen (Oberon®)

24. Mitochondrial complex IV electron transport inhibitors

24A Phosphine

24B Cyanide

25.

26.

27.

28. Ryanodine receptor modulators

Diamides

Flubendiamide (Belt™) Rynaxypyr (Coragen®)

Un Compounds of unknown or uncertain mode of action

Azadirachtin

Azadirachtin (Azatin® XL Plus)

Benzoximate

Bifenazate

Chinomethionat

Cryolite

Dicofol

Pyridalyl

Based on information obtained from www.irac-online.org, IRAC (Insecticide Resistance Action Committee) Mode of Action Classification Version 8.1, issued April 2016.

Disclaimer

Reference to commercial products or trade names is made with the understanding that no discrimination is intended of those not mentioned and no endorsement by University of Nebraska–Lincoln Extension is implied for those mentioned.

This publication has been peer reviewed.

UNL Extension publications are available online at extensionpubs.unl.edu.

Extension is a Division of the Institute of Agriculture and Natural Resources at the University of Nebraska–Lincoln cooperating with the Counties and the United States Department of Agriculture.

© 2011–2016, The Board of Regents of the University of Nebraska on behalf of the University of Nebraska–Lincoln. All rights reserved.

University of Nebraska–Lincoln Extension educational programs abide with the nondiscrimination policies of the University of Nebraska–Lincoln and the United States Department of Agriculture.