2.1 Types of Pesticides and Modes of Action

2.1 Types of Pesticides and Modes of Action

A "pesticide" is any substance or mixture intended to prevent, destroy, repel, or mitigate a pest, together with plant regulators, defoliants, and desiccants. That definition is deliberately broad, and the exam expects you to place any product you are handed into the right family, know what it kills, and know roughly how it kills. Mode of action is not academic trivia: it drives antidote selection when someone is poisoned, resistance-rotation planning, and the choice between a contact and a systemic product on a given job.

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1. Classification by Target Organism

The suffix -cide comes from the Latin caedere, "to kill." The prefix tells you the target:

Four more categories are legally pesticides even though they do not kill anything:

• Plant growth regulators slow or redirect plant growth (trinexapac-ethyl on turf).
• Defoliants cause leaves to drop; desiccants dry plant tissue — both used to prepare crops for harvest.
• Repellents drive pests away rather than killing them (DEET, deer repellents).
• Attractants draw pests to a trap or bait (pheromone lures).

A fumigant is defined by physical state rather than target: it is a pesticide that acts as a gas, penetrating soil, structures, or commodities. Fumigants are among the most hazardous products an applicator handles and are heavily restricted.

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2. Classification by Chemical Origin

"Natural" does not mean low-hazard. Nicotine and rotenone are botanicals with severe mammalian toxicity, and a botanical origin says nothing about signal word or restricted-use status.

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3. Four Behavioral Distinctions That Change Your Product Choice

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|                 FOUR AXES OF PESTICIDE BEHAVIOR                         |
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|  SELECTIVE ......... kills certain pests, spares others                 |
|  NONSELECTIVE ...... kills nearly everything it contacts                |
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|  CONTACT ........... kills on contact; stays where it lands             |
|  SYSTEMIC .......... absorbed and translocated inside the organism      |
+-------------------------------------------------------------------------+
|  RESIDUAL .......... remains active for days to months after use        |
|  NON-RESIDUAL ...... breaks down quickly; little or no lasting activity |
+-------------------------------------------------------------------------+
|  PRE-EMERGENCE ..... applied before weed seedlings emerge               |
|  POST-EMERGENCE .... applied to weeds already growing                   |
+-------------------------------------------------------------------------+

• Selective vs. nonselective. 2,4-D controls broadleaf weeds while leaving turfgrass standing; glyphosate does not discriminate. Selectivity can also come from placement — a shielded directed spray makes a nonselective product behave selectively.
• Contact vs. systemic. A contact insecticide must physically reach the pest, so coverage is everything. A systemic moves through the plant's xylem (upward, with water) or phloem (with sugars, including downward to roots), so a soil drench can protect new growth the sprayer never touched. Systemic herbicides like glyphosate translocate to rhizomes and kill perennial weeds that a contact burndown only tops off.
• Residual vs. non-residual. Residual activity is an asset for pre-emergent weed control and a liability near sensitive rotational crops or water. Residual is why a plant-back interval exists on many herbicide labels.
• Pre- vs. post-emergence. A pre-emergent herbicide forms a chemical barrier in the top layer of soil and does nothing to weeds already up; applying prodiamine to visible crabgrass in July wastes the application.

For insecticides, one more distinction matters: stomach poisons must be eaten (baits, Bt), while contact poisons penetrate the cuticle. Insect mouthparts therefore determine product choice — see section 8.1.

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4. Modes of Action Worth Knowing by Name

Insecticides

Herbicides — grouped by site of action: ALS inhibitors, EPSP synthase inhibitors (glyphosate), photosystem II inhibitors (atrazine, simazine), synthetic auxins (2,4-D, dicamba), ACCase inhibitors, microtubule assembly inhibitors (prodiamine, pendimethalin), and HPPD inhibitors (mesotrione).

Fungicides — multi-site protectants (chlorothalonil, mancozeb) coat the leaf surface and must be present before infection, and carry low resistance risk. Single-site systemics (DMI, QoI, and SDHI chemistries) move into the plant and can act after infection, but carry high resistance risk.

Rodenticides — anticoagulants block vitamin K epoxide reductase, disabling clotting factor synthesis; first-generation products (warfarin, chlorophacinone, diphacinone) require multiple feedings, while second-generation products (brodifacoum, bromadiolone, difethialone) are lethal from a single feeding and pose greater secondary poisoning risk to raptors, cats, and dogs. Non-anticoagulants work differently: bromethalin uncouples oxidative phosphorylation, cholecalciferol causes fatal hypercalcemia, and zinc phosphide releases phosphine gas in the stomach — and vitamin K1 is useless against all three.

[!IMPORTANT] Why mode of action is on the exam. It answers three separate questions at once: which antidote the emergency room needs (section 3.3), which products may be rotated against each other without inviting cross-resistance (section 8.4), and whether a product will reach a pest that the spray never physically touched.