Insecticide Basics for the Pest Management Professional

Bulletin Update Outline — Based on Dr. Michael Scharf's GTBOP Presentation (October 18, 2017)

Prepared by: Rich Braman, UGA Cooperative Extension / Center for Urban Agriculture For: Dr. Dan Suiter (UGA) & Dr. Michael Scharf (Purdue University) Purpose: Working outline to facilitate the bulletin revision, reorganizing Dr. Scharf's presentation content into publication-ready sections

Source document: GTBOP_ProseTranscript_2017-10-18_InsecticideMOA.md (corrected and verified from 742-block SRT)

How to Use This Document

This outline restructures the webinar's conversational flow into a logical publication framework. Each section includes:

Content notes summarizing what Dr. Scharf covered on this topic
Key details listing specific facts, products, and examples mentioned
Transcript location pointing to the relevant section of the prose transcript for exact wording
Writing notes flagging areas that may need expansion, updating, or editorial decisions

The webinar naturally covered some topics in a sequence optimized for a live audience. This outline regroups that content into the structure of a reference bulletin, consolidating related material that was spread across different parts of the talk.

PART I: WHY UNDERSTANDING INSECTICIDE MODE OF ACTION MATTERS

Section 1.1 — Safety and Non-Target Toxicity

Content notes: Modern insecticides are dramatically more selective than older chemistries. Some classes (diamides) have mammalian toxicity so low that EPA did not initially require a signal word. The ratio of insecticide placed in the environment to what actually reaches a target site in a pest is on the order of billions to one.

Key details from presentation:

Modern insecticides can be 10,000+ times more toxic to insects than to mammals
Diamides had no signal word required by EPA; manufacturers voluntarily added "Caution"
Organophosphates and carbamates are NOT insect-specific — they work equally well against mammals, hence heavy restrictions

Transcript location: "Why Understanding Mode of Action Matters" section; "Understanding LD50" section

Writing notes: This is a strong opening hook for the bulletin. The 10,000x selectivity figure and the diamide signal word story are compelling for a practitioner audience. May want to update with any newer selectivity data post-2017.

Section 1.2 — Interpreting Trade Literature and Advertising

Content notes: Understanding how insecticides work gives practitioners the knowledge to critically evaluate manufacturer claims. Trade literature is not always technically accurate.

Key details from presentation:

Scharf explicitly noted that advertising and trade literature "isn't always technically accurate"
Knowledge of MOA helps practitioners evaluate product claims independently

Transcript location: "Why Understanding Mode of Action Matters" section

Writing notes: Brief section. Could be expanded with specific examples of misleading claims if Dan and Mike wish.

Section 1.3 — Pollinator Protection

Content notes: Nicotinoids are systemic — they move through plants. Lawn applications can result in uptake by flowering plants in the landscape, exposing pollinators.

Key details from presentation:

Nicotinoids move around in plants (systemic activity)
Lawn applications → flowering landscape plants → pollinator exposure pathway

Transcript location: "Why Understanding Mode of Action Matters" section

Writing notes: This was a brief mention in the webinar but has become a much larger regulatory and public concern since 2017. Strong candidate for significant expansion in the updated bulletin with current EPA actions, label changes, and best practices.

Section 1.4 — Resistance Management

Content notes: Product rotation is key to long-term success. Even combination products need rotation. Resistance is arguably the #1 cause of callbacks in cockroach accounts.

Key details from presentation:

Resistance is "probably the number one cause of callbacks in cockroach accounts"
Cockroaches observed surviving on bait as sole food source for a month
Bedbug pyrethroid resistance is widespread; resistance to chlorfenapyr and nicotinoids emerging
Rotation recommendation: switch active ingredients every 3 months, ideally monthly
Combination products (neonicotinoid + pyrethroid) also need rotation — resistance to both AIs observed in roach populations
Not all active ingredients are compatible in rotation sequences; research is ongoing
IRAC (Insecticide Resistance Action Committee) provides mode of action classifications to guide rotation

Transcript location: "Resistance" subsection under Practical Factors; Q&A sections on combination products and IRAC

Writing notes: This section has substantial content from both the presentation body and the Q&A discussion. The Q&A exchange on combination product resistance is particularly valuable — Dan asked the tough question and Mike confirmed dual resistance. IRAC reference should include current web address and brief explanation of the classification numbering system.

Section 1.5 — Product Sustainability and Customer Communication

Content notes: Each insecticide costs hundreds of millions (potentially billions) to bring to market. Wise use extends market life. Understanding MOA helps practitioners communicate competence to customers.

Key details from presentation:

Development cost: hundreds of millions to billions per product
Urban pest control market is a smaller slice of the pie than agriculture, which affects manufacturer investment in new urban AIs
Knowledge of nine major classes enables better customer communication
Q&A noted the industry is "generic heavy" — flow of new AIs has slowed

Transcript location: "Why Understanding Mode of Action Matters" section; Q&A on new active ingredients

Writing notes: The economics discussion from the Q&A adds good context. The point about urban market size vs. agriculture affecting R&D investment is practical industry knowledge worth including.

PART II: INSECT PHYSIOLOGY — THE FOUNDATION

Section 2.1 — Overview of Insecticide-Relevant Physiology

Content notes: Five key physiological systems are relevant to understanding how insecticides work. Scharf structured this as a compressed physiology primer — translating a semester course into key concepts.

Key systems covered:

Nervous system — controls all body functions; target of most insecticide classes
Cuticle — complex multi-layered barrier; target of IGRs and dehydrating dusts; also a penetration barrier
Digestive system — the gut interior is technically "outside" the body; a penetration barrier for ingested insecticides
Tracheal system — physical tubes delivering air directly to cells (unlike mammalian lungs/hemoglobin); entry route for fumigants
Musculature — controlled by nervous system; contains calcium channels targeted by diamides

Transcript location: "Insect Physiology Overview" section and its subsections

Writing notes: This section works well as a brief, illustrated primer in a bulletin. The tracheal system comparison (physical tubes vs. mammalian lungs/hemoglobin) and the gut-as-exterior concept are accessible explanations that help practitioners understand why different formulations work differently.

Section 2.2 — How the Nervous System Works

Content notes: Detailed explanation of nerve impulse transmission — electrical signals along neurons, chemical transmission across synapses via neurotransmitters, receptor binding.

Key details from presentation:

Nervous system = millions of nerve cells
Central nervous system: brain, subesophageal ganglion, ventral nerve cord
Peripheral nerves extend throughout body
Electrical impulses travel along neurons
Synapses = gaps between neurons
Neurotransmitters (e.g., acetylcholine) carry signal across synapses
Receptors on receiving neuron are specific to neurotransmitter type
Finger-snap analogy for speed of neural transmission

Transcript location: "How the Nervous System Works" section

Writing notes: The finger-snap analogy is effective for a lay audience. The distinction between electrical (along neurons) and chemical (across synapses) transmission is foundational for understanding why different insecticide classes target different locations.

Section 2.3 — Neurophysiology Demonstration

Content notes: Scharf's lab can measure insecticide effects on the cockroach nervous system in real time using electrodes on the ventral nerve cord.

Key details from presentation:

American cockroach dissected to expose ventral nerve cord
Electrode placed on nerve cord to measure electrical activity
Baseline recording (5 minutes) compared to post-treatment
Fipronil application → visible increase in firing rate and magnitude (neuroexcitation)

Transcript location: "Neurophysiology in the Lab" section

Writing notes: This is powerful visual content for a bulletin. If the electrophysiology traces (baseline vs. fipronil-treated) are available as figures, they would be excellent illustrations. Mike may have publication-quality versions of these from his research.

PART III: INSECTICIDE CLASSIFICATION FUNDAMENTALS

Section 3.1 — Chemical Structure and Classification

Content notes: Insecticide classification is based on chemical structure, analogous to how insect taxonomy is based on morphology. Different structures → different functions → different target sites.

Transcript location: "Insecticide Classification and Target Sites" section

Section 3.2 — Target Site and Mode of Action — The Key and Lock

Content notes: The insecticide's chemical structure allows it to interact with a specific protein target in the insect. Modern computational chemistry can model these interactions (similar to drug discovery/design).

Key details from presentation:

Target site = protein, usually with 3D structure
Insecticide "docks" with target protein
Key-and-lock analogy (simplified); actual molecular docking is far more complex
Drug discovery and insecticide design have significant overlap

Transcript location: "The Key and Lock Analogy" section

Section 3.3 — Four Basic Modes of Action

Content notes: All insecticide effects at target sites fall into just four categories. This simplifying framework is how Scharf teaches toxicology at Purdue.

The four modes:

Stimulation — causes target to become more active (e.g., nerve fires more rapidly)
Blockage — shuts target off (e.g., nerve kept from firing)
Modulation — changes the shape/function of target subtly (e.g., pyrethroids)
Inhibition — prevents an enzyme from doing its job (e.g., organophosphates inhibit acetylcholinesterase)

Transcript location: "Four Basic Modes of Action" section

Writing notes: This is a key pedagogical framework for the bulletin. The "only four ways" framing makes the whole topic approachable. A simple table or diagram showing these four categories with one example each would be very effective.

Section 3.4 — Understanding LD50

Content notes: The LD50 concept — the dose that kills 50% of test subjects — is essential for understanding relative toxicity and safety.

Key details from presentation:

LD50 is inverse to toxicity: smaller LD50 = higher toxicity
Modern insecticides have high mammalian LD50s (safe) and low insect LD50s (effective)
Some products are 10,000+ times more toxic to target insects than to mammals
The actual amount of insecticide reaching a target site in a pest is a billionth or less of what's applied

Transcript location: "Understanding LD50" section

PART IV: NEUROTOXIC INSECTICIDES — FIVE CLASSIFICATIONS

Overview: Nine total insecticide classifications — five neurotoxic, four non-neurotoxic. This section covers the five that target the nervous system.

Section 4.1 — Target Site Roadmap

Content notes: Scharf provided a visual roadmap showing where each target site sits on the nerve/muscle junction. This is reference material for the detailed sections that follow.

Target sites on neurons:

Axon sodium channels — the "on switch" for nerve firing (targeted by pyrethroids, indoxacarb, metaflumizone)
Chloride channels — post-synaptic; mellowing/inhibitory function (targeted by fipronil, isoxazolines, avermectins)
Acetylcholine receptors — post-synaptic; carry signal across synapse (targeted by neonicotinoids, spinosyns, sulfoximines)
Acetylcholinesterase enzyme — breaks down acetylcholine in synapse (targeted by organophosphates, carbamates)
Neuromuscular calcium channels — at nerve-muscle junction; control muscle contraction (targeted by diamides)

Transcript location: "Target Site Roadmap" section

Writing notes: This roadmap is the backbone of Part IV. A well-designed figure showing a schematic neuron/synapse/muscle junction with labeled target sites would be the single most valuable illustration in the bulletin. Scharf's presentation slides likely contain a version of this.

Section 4.2 — Sodium Channel Insecticides

Stimulators: Pyrethroids, Pyrethrins, DDT

Stimulate sodium channels → excitation → rapid knockdown
The "on switch" is jammed open
Pyrethroids are highly repellent to insects — "like pepper spray"
Visible effect: immediate incoordination and knockdown

Blockers: Indoxacarb (oxadiazine), Metaflumizone (semicarbazone)

Block sodium channels → inhibition → paralysis
The "on switch" is stuck in the off position
Indoxacarb is a major urban insecticide
Metaflumizone has ectoparasite uses and possible urban applications

Transcript location: "Classification 1: Sodium Channel Insecticides" section; Q&A on repellent vs. non-repellent

Writing notes: The repellent/non-repellent distinction from the Q&A belongs here. Scharf's point that "the real distinction is pyrethroids and everything else" is a clean, practical takeaway. Pyrethroids are the repellent class; most other chemistries are not significantly detected by insects.

Section 4.3 — Chloride Channel Insecticides

Blockers: Fipronil (phenylpyrazole), Isoxazolines (fluralaner, sarolaner)

Chloride normally "mellows" neurons (negative charge dampens activity)
Blocking chloride flow → loss of inhibition → excitation
Fipronil is a major urban market product, now off-patent with consumer products available
Isoxazolines: newer class, primarily veterinary/pet products (flea market); cross-resistance potential with fipronil
Lab demonstration: fipronil application → rapid visible increase in nerve firing rate and magnitude

Stimulators: Avermectins (abamectin)

Stimulate chloride channels → excess inhibition → paralysis
Opposite effect from fipronil at the same target site type
Abamectin is an effective gel bait active ingredient

Transcript location: "Classification 2: Chloride Channel Insecticides" section

Writing notes: The fipronil/abamectin contrast — same target site, opposite effects — is an excellent teaching point. Worth highlighting with a comparison callout or sidebar.

Section 4.4 — Acetylcholine Receptor Insecticides

Stimulators: Neonicotinoids, Sulfoximines (sulfoxaflor), Spinosyns (spinosad)

Stimulate the acetylcholine receptor → excitation
Neonicotinoids: huge current market share
Sulfoximines: newer class, same target site
Spinosyns: relevant for landscape market

Transcript location: "Classification 3: Acetylcholine Receptor Insecticides" section

Writing notes: The Q&A on nicotinoids vs. neonicotinoids is relevant here. Scharf explained: nicotinoids look more like nicotine (e.g., imidacloprid); neonicotinoids have evolved structurally but still target the same receptor (e.g., clothianidin). Dan's anecdote about tobacco killing caterpillars ties back to nicotine as the original insecticide. Also connect back to the pollinator discussion — systemic movement through plants.

Section 4.5 — Acetylcholinesterase Inhibitors

Inhibitors: Organophosphates, Carbamates

Inhibit the enzyme that breaks down acetylcholine in the synapse
Result: acetylcholine accumulates → continuous stimulation → excitation
Not insect-specific — works equally well against mammals/humans
Heavy regulatory restrictions for good reason

Transcript location: "Classification 4: Acetylcholinesterase Inhibitors" section

Writing notes: These are the "legacy" chemistry classes that most experienced practitioners know well. Worth noting their declining role in urban pest management and why (safety profile vs. newer options).

Section 4.6 — Combination Products

Neonicotinoid + Pyrethroid combinations

"All start with tea" (common naming pattern)
Hit two target sites simultaneously: acetylcholine receptor + sodium channels
Potentiation effect: synergy, "one plus one equals three"
Still not immune to resistance — dual resistance observed in cockroach populations
Must still be used in rotation

Transcript location: "Classification 5: Combination Products" section; Q&A on combination product resistance

Writing notes: The Q&A exchange adds important content here. Dan asked directly whether combo products at lower doses risk dual resistance, and Mike confirmed they do — evidence of resistance to both AIs in select roach populations. This is practical, industry-relevant information.

PART V: NON-NEUROTOXIC INSECTICIDES — FOUR CLASSIFICATIONS

Section 5.1 — Muscular Calcium Channel Insecticides (Diamides)

Stimulators: Chlorantraniliprole, Cyantraniliprole

Stimulate neuromuscular calcium channels → muscle contraction → energy depletion → paralysis → death
Timeline: contraction for hours, then paralyzed for days as energy depletes
Extremely safe for mammals — EPA did not initially require signal word
Manufacturers voluntarily added "Caution" signal word
Possibly selective even among insect groups (noted in Q&A re: earthworm question)

Transcript location: "Muscular Calcium Channels (Diamides)" section; Q&A on chlorantraniliprole and earthworms

Writing notes: The safety profile of diamides is a significant selling point and an important counternarrative to public concerns about pesticides. The earthworm question from the Q&A is worth noting — Scharf suspected some effect but noted the molecule's selectivity even among invertebrates.

Section 5.2 — Insect Growth Regulators

Juvenile Hormone Analogs (e.g., pyriproxyfen)

Mimic juvenile hormone → cuticle deformation + extra juvenile stages → population crash (juveniles can't reproduce)
Visible indicator: wing twist in cockroaches
Practical field tip: if you see wing twist in a new account, IGRs are already affecting the population — consider rotating to a different chemistry
Resistance concern with continuous use

Chitin Synthesis Inhibitors

Inhibit the enzyme that forms cuticle during molting → death during molt
Visible indicator in termites: "jackknife effect" (body curling from malformed cuticle)
Effective against molting insects — acts at a very specific developmental window

Background on insect development covered:

Three types of metamorphosis: ametabolous, hemimetabolous (roaches, termites, grasshoppers), holometabolous (flies, mosquitoes, caterpillars)
Complex hormonal control of molting and development
Cuticle tanning process in newly emerged adults (e.g., alate termites)

Transcript location: "Insect Growth Regulators" section

Writing notes: The wing-twist-as-field-indicator tip is highly practical for the target audience. The jackknife effect in termites is similarly useful. These are the kind of applied details that make a bulletin valuable to practitioners.

Section 5.3 — Inhibitors of Energy Production

Target: Mitochondria (cellular respiration)

Universal target — mitochondria exist in all organisms (plants, animals, insects, bacteria)
Different products affect different parts of the respiratory chain

Products mentioned:

Hydramethylnon — cockroach bait active ingredient
Chlorfenapyr — has a food label; relatively safe; resistance potential noted
Sulfuryl fluoride — fumigant
Methyl bromide — fumigant (note: largely phased out since 2017)
Disodium octaborate tetrahydrate (DSOBTH) — wood treatment; disrupts insect respiration
Boric acid — disrupts respiration; also has physical mode of action (abrasive/desiccant effect on gut lining)

Transcript location: "Inhibitors of Energy Production" section

Writing notes: Boric acid's dual mode of action (chemical + physical) is an interesting detail worth highlighting. May need to update re: methyl bromide phase-out status and any newer products in this category since 2017.

Section 5.4 — Cuticle Dehydrating Dusts

Products: Silica gel, Diatomaceous earth (DE)

Physical mode of action — not a chemical toxicant
Abrade the waxy epicuticular layer → water loss → dehydration → death
Diatomaceous earth: ground exoskeletons of diatoms (silicon-based organisms)
Active component: silicon
Effect: lethargy, then death from desiccation

Transcript location: "Cuticle Dehydrating Dusts" section

Writing notes: Brief section. These products are simple in mechanism but important for IPM and for situations requiring non-chemical or minimal-chemical approaches.

PART VI: PRACTICAL FACTORS AFFECTING INSECTICIDE PERFORMANCE

Section 6.1 — Stability, Persistence, and Formulations

Content notes: Raw insecticides are oily, UV-sensitive, and would be unsafe to handle directly. Formulations solve all of these problems.

Key details:

Most insecticides are oily (lipophilic) — helps cross cuticle and membranes but creates handling challenges
UV light degrades raw active ingredients rapidly
Insecticides can move with water despite not dissolving in it

Formulation functions:

Enhance stability and extend longevity
Enhance safety
Ease handling and mixing
Keep AI suspended/dissolved in water

Formulation types mentioned:

Baits, granulars, dusts, aerosols, fumigants
Liquid forms: emulsifiable concentrate (EC), wettable powder (WP), microencapsulated (ME), suspension concentrate (SC)

Transcript location: "Stability, Persistence, and Formulations" section

Section 6.2 — Pest Behavior and Insecticide Delivery

Content notes: Natural pest behaviors can be exploited to enhance insecticide effectiveness. Three examples from the presentation.

Example 1: Cockroach secondary and tertiary kill

Cockroach eats bait → dies → another roach feeds on carcass or feces → secondary kill
Insecticide can pass through two digestive tracts and still cause tertiary kill in a third roach

Example 2: Flea larval exposure

Treated pet → adult fleas defecate insecticide → flea larvae feed on adult feces for nutrition → secondary exposure

Example 3: Social insect transfer (termites, ants)

Trophallaxis (food sharing from mouth and anus) and allogrooming spread insecticides through colony
Slow-acting insecticides preferred → maximize colony penetration before detection

Transcript location: "Pest Behavior" section

Writing notes: These three examples are vivid and practical. The tertiary kill through two roach digestive tracts is a memorable detail. For the social insect section, note that Dave Oi's companion webinar on ants may have additional relevant content.

Section 6.3 — Sanitation and IPM

Content notes: Poor sanitation undermines even the best insecticide programs.

Key points:

Excess food competes with bait placements
Clutter creates untreatable harborage
Dirt and grease physically bind insecticides, reducing contact
IPM mindset essential for maximizing insecticide effectiveness

Transcript location: "Sanitation" section

Section 6.4 — Resistance (expanded from Section 1.4)

Content notes: Detailed resistance section drawing from both the main presentation and the extensive Q&A discussion.

See Section 1.4 above for key details. Consider consolidating here or cross-referencing.

Additional Q&A content for this section:

Resistance is inevitable with overuse — possible to any product
"Appropriate use for lengths of time and intensities of selection" determines outcome
IRAC classification system helps guide rotation decisions
IRAC website updated 1-2 times per year with complete landscape of available chemistries
Research on optimal rotation sequences is ongoing (Scharf lab)

Transcript location: "Resistance" section; all Q&A segments on resistance and IRAC

Section 6.5 — Oral vs. Dermal Toxicity

Content notes: From Q&A — insecticides are almost always more toxic via ingestion than by contact.

Key details:

Insect cuticle: waterproof, multi-layered barrier
Insect gut: thin cell layer, much less resistant to penetration
Mammalian skin: incredibly resistant barrier to insecticides/toxins
Practical implication: ingestion-based delivery (baits) can be highly effective at lower doses

Transcript location: Q&A section "On Oral vs. Dermal Toxicity"

Writing notes: This came up as an audience question but is foundational enough to warrant inclusion in the bulletin body rather than just Q&A.

Section 6.6 — Essential Oils and 25B Products

Content notes: From Q&A — the green revolution in pest management.

Key details:

Consumer demand is the primary driver
25B exempt actives (rosemary, spearmint, cedar) avoid registration costs
Effective as repellents (Dan: "very good repellents — we've done a lot of work with them on ants")
Not necessarily effective as toxicants

Transcript location: Q&A section "On Essential Oils and 25B Products"

Writing notes: This topic has grown considerably since 2017. Worth expanding with current market data and any efficacy research published since.

SUPPORTING REFERENCES

Publications Cited in Presentation

Scharf, M.E. & D.R. Suiter. 2011. "Insecticide Primer and Insecticide Mode of Action." PCT Magazine.
Scharf, M.E. & D.R. Suiter. ~2007. "Insecticide Basics for the Pest Management Professional." UGA Cooperative Extension publication. (The bulletin being updated)

External Resources Mentioned

IRAC (Insecticide Resistance Action Committee) — mode of action classification charts, updated 1-2x annually

EDITORIAL NOTES FOR DAN AND MIKE

Content that may need updating (2017 → present)

Neonicotinoid regulatory landscape (significant EPA and state-level changes since 2017)
Methyl bromide phase-out status
New products in the diamide and isoxazoline classes
Bedbug resistance — current scope of the problem
Essential oils / 25B market growth
Any new IRAC classifications added since 2017
Current status of Scharf lab rotation research (papers published?)
Fipronil patent/generic status update

Structural suggestions

The "nine classifications" framework (5 neurotoxic + 4 non-neurotoxic) is a clean organizing principle
The "four basic modes of action" framework should appear early as a conceptual anchor
Consider a one-page summary table at the end (see companion Reference Compendium)
The neurophysiology figure (target site roadmap) deserves a full-page treatment

Q&A content worth integrating

Several valuable exchanges from the Q&A are better suited to the bulletin body than a standalone Q&A section:

Combination product resistance (Section 4.6)
Nicotinoid vs. neonicotinoid terminology (Section 4.4)
Oral vs. dermal toxicity (Section 6.5)
Repellent vs. non-repellent (Section 4.2)
IRAC as a practitioner resource (Section 6.4)

Prepared from GTBOP webinar archive materials. All content derived exclusively from Dr. Scharf's October 18, 2017 presentation as transcribed and corrected through the GTBOP archive pipeline.