Toxic Effects of Pesticides – Review Flashcards

A comprehensive set of flashcards covering definitions, mechanisms, toxic effects, treatment, environmental issues, and specific examples for major pesticide classes discussed in the lecture.

What is the general definition of a pesticide?

Any substance or mixture intended for preventing, destroying, repelling, or mitigating any pest.

How are pesticides commonly classified?

By target species: insecticides (insects), herbicides (weeds), fungicides (fungi), rodenticides (rodents), etc.

What additional products can fall under regulatory pesticide definitions?

Plant growth regulators, repellents, and attractants.

What two main components make up a pesticide formulation?

The active ingredient and inert ingredients such as emulsifiers or solvents.

Why is a risk–benefit balance important in pesticide use?

Because benefits like crop protection and vector control must be weighed against human-health and environmental risks.

Which pesticide class is generally the most acutely toxic to humans?

Insecticides.

List the three major routes of human pesticide exposure.

Oral, dermal, and inhalation.

Who is at highest risk for pesticide poisoning?

Workers involved in manufacturing, mixing, and application (occupational exposure).

What WHO criterion is used to classify pesticide hazard?

Acute oral or dermal toxicity.

What key feature do all chemical insecticides in current use share regarding their mechanism?

They are neurotoxicants that disrupt nervous-system targets.

Name two major molecular targets of insecticides.

Acetylcholinesterase (AChE) and voltage-gated sodium channels.

Which two insecticide classes inhibit acetylcholinesterase?

Organophosphates and carbamates.

How do pyrethroids affect nerve function?

They delay inactivation of voltage-sensitive sodium channels, leading to hyperexcitability.

Which compound historically controlled malaria in South Africa but raised environmental concerns?

DDT.

What structural feature distinguishes P=S organophosphates from P=O analogs?

P=S compounds (phosphorothioates) require bioactivation by CYPs to the P=O oxon form.

Describe the primary mechanism of organophosphate (OP) acute toxicity.

Irreversible phosphorylation and inhibition of AChE, causing acetylcholine accumulation at cholinergic synapses.

List three hallmark symptoms of acute OP poisoning.

Salivation, bronchoconstriction, muscle twitching (part of cholinergic syndrome).

What two drugs are standard therapy for acute OP poisoning?

Atropine and an oxime such as pralidoxime (2-PAM).

What is the ‘aging’ process in OP poisoning?

Dealkylation of phosphorylated AChE that renders the enzyme irreversibly inhibited and unresponsive to oximes.

What is the intermediate syndrome following OP poisoning?

Marked weakness of respiratory and proximal limb muscles occurring 1–several days after exposure.

Define OP-induced delayed polyneuropathy (OPIDP).

A distal sensorimotor axonopathy appearing 2–3 weeks after exposure, linked to phosphorylation and aging of neuropathy target esterase (NTE).

Why don’t carbamates cause OPIDP?

Carbamylated NTE does not age, preventing the cascade that produces OPIDP.

How does carbamate inhibition of AChE differ from OP inhibition?

Carbamate binding is rapid and reversible; symptoms generally resolve within hours.

What protective role can carbamates play against OPs?

Pretreatment with a carbamate can transiently occupy AChE and prevent irreversible phosphorylation by an OP.

Differentiate Type I and Type II pyrethroid poisoning signs in rats.

Type I (T-syndrome): tremor, whole-body tremors; Type II (CS-syndrome): salivation, choreoathetosis, seizures.

What common occupational effect occurs after dermal exposure to pyrethroids?

Transient paresthesia (tingling/burning) that resolves within 24 hours.

Which vertebrate group is especially sensitive to pyrethroids?

Fish.

What is the main mechanism of action of DDT?

Prolonged activation of sodium channels, similar to Type I pyrethroids.

In which tissue does DDT preferentially accumulate?

Adipose (fat) tissue.

What chronic hepatic effects can DDT produce?

Liver hypertrophy, necrosis, and potent induction of cytochrome P450 enzymes.

Which isomer of DDT is biologically active?

p,p′-DDT.

Give two examples of organochlorine pesticides with notable endocrine-disrupting activity.

o,p′-DDT (estrogenic) and p,p′-DDE (anti-androgenic).

Why do organochlorines persist in the environment?

They are chemically stable, lipid soluble, and slowly metabolized, leading to bioaccumulation and biomagnification.

What receptor subtype do neonicotinoids primarily target in insects?

Nicotinic acetylcholine receptors (nAChRs) in the insect CNS.

Why is mammalian toxicity relatively low for neonicotinoids?

Poor blood–brain-barrier penetration and lower affinity for mammalian nAChRs.

Which ecological concern is prominent for neonicotinoids?

High toxicity to bees, impairing their immune system and survival.

How do rotenoids cause toxicity?

They inhibit mitochondrial complex I, disrupting cellular respiration.

Which insecticide class activates invertebrate glutamate-gated chloride channels?

Avermectins.

What human genetic factor may increase avermectin neurotoxicity?

Polymorphisms that decrease P-glycoprotein efflux at the blood–brain barrier.

Explain the mechanism of Bacillus thuringiensis (Bt) toxins in insects.

Activated toxins form pores in midgut epithelial membranes, disrupting ion balance and destroying cells.

What is the primary mode of action for the repellent DEET?

Interference with mosquito olfactory/antenna receptors that locate hosts.

List two key features a rodenticide should possess.

High efficacy in small dose and lack of bait shyness (palatability).

How do anticoagulant rodenticides such as warfarin cause death?

They inhibit vitamin K epoxide reductase, blocking activation of clotting factors II, VII, IX, and X, leading to internal bleeding.

Name two distinctive clinical signs of anticoagulant rodenticide poisoning.

Hematuria and spontaneous ecchymosis (hematomas).

What is the mechanism of bromethalin toxicity?

Its metabolite desmethylbromethalin uncouples mitochondrial oxidative phosphorylation, causing CNS energy failure and myelin edema.

Which rodenticide is selectively toxic to rats by opening the mitochondrial permeability transition pore?

Norbormide.

What is the hallmark target organ for paraquat toxicity?

The lung, especially Type II alveolar cells.

Describe the biochemical mechanism underlying paraquat-induced lung damage.

Redox cycling generates superoxide radicals, depleting NADPH and causing oxidative stress that injures alveolar epithelium.

How does diquat toxicity differ from paraquat?

Diquat does not accumulate in lung tissue; its chronic targets are GI tract, kidney, and eye (cataracts).

Why are fungicides captan and folpet of toxicological interest?

They are potent eye irritants and mutagenic in vitro, and induce duodenal tumors in mice.

What metabolite of dithiocarbamate fungicides inhibits thyroid hormone synthesis?

Ethylenethiourea (ETU).

Which fungicide class inhibits microtubule assembly and can cause chromosomal aneuploidy?

Benzimidazoles.

Which fungicide resembles disulfiram and may interact with alcohol metabolism?

Dithiocarbamates.

What acute neurologic symptoms are characteristic of methyl bromide exposure?

Headache, seizures, paresthesias, neuropathy, and ataxia.

Why is chloropicrin added to some fumigant formulations?

It has a pungent odor and causes eye/respiratory irritation, serving as a warning agent.

What are the three timing categories used to classify herbicide application?

Preplanting, preemergent, and postemergent.

Which herbicide is notorious for severe pulmonary fibrosis in survivors of poisoning?

Paraquat.

Give one reason why Bt genes are incorporated into crops.

To provide built-in resistance to specific insect pests while maintaining low mammalian toxicity.