2.3 Economic Thresholds, Injury Levels & Pesticide Resistance Management
Key Takeaways
- The Economic Injury Level (EIL) is the lowest pest population density that causes economic damage equal to the total cost of pest control, establishing the economic break-even point.
- The Economic Threshold (ET), or action threshold, is the pest density at which management must be initiated to prevent an increasing pest population from reaching the EIL, providing essential operational lead time.
- Economic thresholds are dynamic: higher crop market values lower the threshold (justifying treatment at lower pest counts), whereas higher pesticide or application costs raise the threshold.
- Pesticide resistance evolves because repeated use of identical chemical modes of action exerts selective pressure that kills susceptible individuals and allows pre-existing resistant biotypes to survive and dominate.
- Resistance management mandates rotating and tank-mixing distinct Mode of Action (MoA) groups (HRAC/WSSA for herbicides, IRAC for insecticides, FRAC for fungicides) and applying full labeled rates rather than sub-lethal doses.
Economic Thresholds, Injury Levels & Pesticide Resistance Management
Sound pest management decisions require balancing the biological dynamics of pest populations against agronomic economics. Applying a pesticide when pest populations are too low to cause meaningful economic yield loss wastes financial capital, damages beneficial insect populations, and accelerates chemical resistance. Conversely, delaying treatment until pest damage is widespread results in irreversible economic injury.
The Economic Injury Level (EIL) and Economic Threshold (ET)
In 1959, entomologists V.M. Stern and colleagues introduced the foundational concepts of the Economic Injury Level and Economic Threshold, providing an objective, quantitative basis for pesticide application decisions.
Economic Injury Level (EIL)
The Economic Injury Level (EIL) is defined as the lowest population density of a pest that will cause economic damage equal to the cost of pest management. At the EIL, the dollar loss caused by the pest exactly equals the total cost of the pesticide and its application. Treating a pest population below the EIL results in a net financial loss.
Mathematically, the EIL is conceptualized through the classic Pedigo formula:
Where:
- $C$ = Cost of management per unit area (chemical cost + application machinery/labor cost per acre, e.g., $18.00/acre)
- $V$ = Market value per unit of yield ($/bushel, $/hundredweight, $/pound)
- $I$ = Injury per pest density (injury unit per pest individual)
- $D$ = Damage per unit injury (yield loss per unit of injury)
- $K$ = Proportionate reduction in pest population achieved by the control measure (efficacy, e.g., 0.90 for 90% control)
Economic Threshold (ET) / Action Threshold
The Economic Threshold (ET), also termed the Action Threshold, is the pest population density at which management action must be initiated to prevent an increasing pest population from reaching the Economic Injury Level.
The ET is always lower than the EIL ($ET < EIL$). This difference provides an essential operational buffer or lead time. Applicators require time to schedule equipment, acquire chemical inventory, wait for suitable weather conditions (avoiding high winds or rain events), and allow the pesticide to achieve control before the pest population expands past the EIL.
graph LR
TimeAxis["Pest Population Growth Over Time"] --> PopRise["Pest Density Rises Toward Threshold"]
PopRise --> ET["ECONOMIC THRESHOLD (ET)<br/>★ Action Initiated Here ★<br/>Accounts for applicator lead time & weather"]
ET --> EIL["ECONOMIC INJURY LEVEL (EIL)<br/>Cost of Treatment = Crop Loss Value<br/>Treating past this point incurs net loss"]
style ET fill:#f0ad4e,color:#000
style EIL fill:#d9534f,color:#fff
Dynamic Nature of EIL and ET
Neither the EIL nor the ET is a fixed, static number. They fluctuate dynamically based on commodity markets and input costs:
- Market Value ($V$): If the market price of the crop rises, the EIL and ET decrease. Because each bushel is worth more, a smaller pest population is required to cause economic loss equal to the treatment cost, justifying chemical intervention at lower pest counts.
- Control Costs ($C$): If the cost of the chemical or custom application increases, the EIL and ET increase. Higher treatment costs require greater pest damage to justify the expense.
- Crop Susceptibility: Thresholds vary across crop growth stages. For example, soybean defoliation thresholds are set at 30% during vegetative stages, but drop to 20% during critical reproductive bloom and pod-fill stages (R1 to R5) when defoliation directly reduces seed set and yield.
Field Scouting Methodologies
Deciding whether a pest population has reached the Economic Threshold requires rigorous, objective field scouting. Biased or haphazard sampling leads to misjudging pest pressure.
Scouting Patterns and Eliminating Edge Bias
Field borders and headlands frequently support higher pest densities due to pests migrating from ditches, shelterbelts, or neighboring crops. Walking only field edges provides an inaccurate overestimation of whole-field pest pressure. Applicators must sample using systematic interior walking patterns—such as a "W"-pattern, "Z"-pattern, or inverted "M"-pattern—to inspect representative locations across the entire acreage.
Exception: Perimeter-targeted scouting is appropriate for pests that exhibit strict field-edge aggregation during initial colonization, such as grasshoppers migrating out of drying roadside ditches or two-spotted spider mites moving into soybean field borders during drought.
Standardized Sampling Tools
- Sweep Netting: Standard 15-inch diameter sweep nets are swung through the top of the crop canopy in 180-degree pendulum sweeps. Insect counts are averaged per 10 or 20 sweeps. Widely used for scouting alfalfa weevil larvae, lygus bugs in canola, and potato leafhoppers.
- Quadrant and Row Counts: Using a 1-square-foot or 1-square-meter frame (or evaluating 1/1,000th of an acre) tossed randomly to quantify weed seedling densities, soil-dwelling cutworms, or wireworms.
- Degree-Day (Thermal Unit) Modeling: Because insects are poikilothermic (cold-blooded), their rate of development depends on ambient temperature. Applicators utilize Growing Degree Days (GDD) calculated from daily minimum and maximum temperatures above a base developmental threshold ($T_{base}$):
Degree-day models accurately forecast peak adult flight, egg hatch, and larval emergence for pests like the wheat midge (Sitodiplosis mosellana), European corn borer, and sugarbeet root maggot (Tetanops myopaeformis), allowing scouting to be timed to critical pest life stages.
The Evolution of Pesticide Resistance
Pesticide resistance is the inherited ability of a pest biotype to survive an application of a pesticide that would normally kill a wild-type population. Resistance occurs across all pest classes: weeds (herbicide resistance), insects (insecticide resistance), and plant pathogens (fungicide resistance).
The Selection Pressure Mechanism
Applicators must recognize a critical biological reality: Pesticides do not cause genetic mutations to create resistance.
Instead, rare, naturally occurring genetic mutations or polymorphisms exist at extremely low background frequencies (e.g., 1 in 1,000,000) within genetically diverse, wild pest populations. When an applicator applies the same pesticide (or chemistries within the same Mode of Action) repeatedly, the chemical acts as a powerful selection agent:
- The pesticide kills 99.9% of the susceptible individuals.
- The rare, naturally resistant individuals survive the treatment.
- The surviving resistant biotypes reproduce, passing their inherited resistance genes to their offspring.
- Over successive generations, the proportion of resistant individuals increases until the pesticide fails to provide acceptable control.
flowchart TD
Gen1["Generation 1:<br/>Diverse Population (99.9% Susceptible, 0.1% Rare Resistant Biotype)"] --> Spray1["Pesticide Applied (Mode of Action X)"]
Spray1 --> Surv1["Selective Kill:<br/>Susceptible pests die; Resistant biotype survives"]
Surv1 --> Gen2["Generation 2:<br/>Resistant biotypes reproduce; Resistance frequency expands"]
Gen2 --> Spray2["Repeated Application of Same Mode of Action X"]
Spray2 --> Gen3["Generation 3+:<br/>POPULATION DOMINATED BY RESISTANT BIOTYPES<br/>Complete Field Control Failure"]
style Gen1 fill:#2d5a87,color:#fff
style Surv1 fill:#f0ad4e,color:#000
style Gen3 fill:#d9534f,color:#fff
- Cross-Resistance: A pest biotype with a single resistance mechanism (e.g., an altered enzyme target site) exhibits resistance to two or more chemically related active ingredients within the same Mode of Action group.
- Multiple Resistance: A pest biotype possesses two or more distinct resistance mechanisms, conferring resistance to multiple, chemically unrelated Mode of Action groups (e.g., kochia biotypes in North Dakota exhibiting resistance to Group 2, Group 4, and Group 9 herbicides simultaneously).
Mode of Action (MoA) Classification Systems
To standardize resistance management, global technical committees established numbered Mode of Action (MoA) classification codes. Under EPA labeling standards, these MoA group numbers appear prominently in bold boxes on the front panel of pesticide labels (e.g., GROUP 9 HERBICIDE).
Herbicide Groups (HRAC / WSSA)
- Group 1 (ACCase Inhibitors): Post-emergence grass herbicides ("dims" and "fops" like clethodim, quizalofop). Inhibits acetyl-CoA carboxylase, preventing lipid synthesis. High resistance risk in wild oat (Avena fatua) and green foxtail.
- Group 2 (ALS Inhibitors): Sulfonylureas, imidazolinones (imazamox, rimsulfuron). Inhibits acetolactate synthase, halting branched-chain amino acid synthesis. Widespread resistance across North Dakota in kochia, Palmer amaranth, and waterhemp.
- Group 4 (Synthetic Auxins): Growth regulators (2,4-D, dicamba, clopyralid). Mimics indole-3-acetic acid (IAA), causing rapid, abnormal cell division, epinasty, stem twisting, and vascular collapse. Auxin resistance is expanding in kochia.
- Group 9 (EPSPS Inhibitor): Glyphosate. Inhibits 5-enolpyruvylshikimate-3-phosphate synthase, halting aromatic amino acid synthesis. Widespread resistance in kochia and pigweed complexes across the Northern Plains.
- Group 14 (PPO Inhibitors): Cell membrane disruptors (fomesafen, sulfentrazone, flumioxazin). Inhibit protoporphyrinogen oxidase, generating toxic reactive oxygen radicals. Crucial for pre-emergence residual weed control.
- Group 27 (HPPD Inhibitors): Pigment synthesis bleaching herbicides (mesotrione, isoxaflutole). Inhibit 4-hydroxyphenylpyruvate dioxygenase, causing newly formed plant tissues to emerge pure white.
Insecticide Groups (IRAC)
- Group 1A & 1B (Acetylcholinesterase Inhibitors): Carbamates (1A) and Organophosphates (1B: malathion, dimethoate). Inhibit the enzyme acetylcholinesterase, leading to continuous nervous excitation.
- Group 3A (Sodium Channel Modulators): Synthetic pyrethroids (bifenthrin, lambda-cyhalothrin). Keep nerve axonic sodium channels open, causing paralysis. Pyrethroid resistance is documented in soybean aphids.
- Group 4A (Nicotinic Acetylcholine Receptor Agonists): Neonicotinoids (imidacloprid, thiamethoxam). Disrupt insect nerve transmissions; widely used as systemic seed treatments.
- Group 28 (Ryanodine Receptor Modulators): Diamides (chlorantraniliprole). Open ryanodine calcium channels in muscle tissue, causing lethargy and paralysis.
Fungicide Groups (FRAC)
- Group 3 (DMI / Triazoles): Inhibit sterol biosynthesis in fungal cell walls. Medium resistance risk; critical for managing Fusarium head blight in wheat.
- Group 7 (SDHI): Succinate dehydrogenase inhibitors (boscalid, fluxapyroxad). Inhibit fungal mitochondrial respiration complex II.
- Group 11 (QoI / Strobilurins): Inhibit fungal mitochondrial respiration complex III (azoxystrobin, pyraclostrobin). High resistance risk; a single genetic mutation (e.g., G143A) confers complete resistance, as observed in Cercospora beticola in North Dakota sugarbeets.
- Group M (Multi-Site Contact Fungicides): Copper, mancozeb, chlorothalonil. Inhibit multiple biochemical sites simultaneously. Extremely low resistance risk; indispensable tank-mix partners.
Proactive Resistance Management Strategies
- Rotate Mode of Action Groups: Never apply pesticides belonging to the same MoA group consecutively in the same field. Rotate across distinct group numbers between seasons and during sequential treatments within a single season.
- Tank-Mix Multiple Effective Modes of Action: Apply mixtures of two or more chemistries from different MoA groups that are both active and effective against the target pest. The statistical probability of a single pest individual carrying natural resistance to two entirely different chemical classes simultaneously is exponentially lower than for a single MoA.
- Apply Full Labeled Rates: Never apply sub-lethal or reduced chemical rates. Cut rates allow individuals with partial, polygenic metabolic resistance to survive, accumulate resistance traits, and produce fully resistant progeny. Always apply the labeled rate calibrated to the target pest size.
- Incorporate Cultural and Mechanical Controls: Integrate crop rotations, narrow row spacing, inter-row cultivation, and certified seed to reduce overall pest numbers. Suppressing total weed populations reduces the raw number of individuals exposed to chemical selection pressure.
- Clean Equipment: Prevent the physical movement of resistant weed seeds (such as Palmer amaranth) by power-washing combines and tillage machinery between fields.
If the market price of spring wheat increases from $6.00 to $10.00 per bushel while pesticide product and application costs remain constant, how does this economic shift alter the Economic Injury Level (EIL)?
An agricultural producer notices that an ALS-inhibiting herbicide (Group 2) that formerly provided 99% control of kochia now leaves scattered patches of healthy, seed-bearing plants despite proper application timing, nozzle selection, and spray volumes. What biological mechanism explains this field failure?
Which application practice significantly accelerates the evolution of metabolic pesticide resistance across insect and weed populations?