How does carbofos kill bedbugs?

How does carbofos kill bedbugs? - briefly

Carbofos is an organophosphate that blocks acetylcholinesterase, causing excess acetylcholine, uncontrolled nerve impulses, paralysis, and eventual respiratory failure. The insect dies within minutes to hours after sufficient contact.

How does carbofos kill bedbugs? - in detail

Carbofos, an organophosphate compound, eliminates bedbugs by disrupting neural transmission. The active ingredient binds irreversibly to acetylcholinesterase (AChE), the enzyme responsible for hydrolyzing acetylcholine in synaptic clefts. Inhibition of AChE prevents breakdown of the neurotransmitter, leading to excessive accumulation of acetylcholine at cholinergic synapses.

The resulting overstimulation of nicotinic and muscarinic receptors produces continuous depolarization of nerve and muscle cells. Bedbugs experience uncontrolled muscular contractions, loss of coordinated movement, and eventual paralysis. Respiratory muscles cease functioning, causing asphyxiation and death within minutes to hours, depending on dose and exposure route.

Key stages of the toxic action:

  • Contact absorption: cuticular penetration allows carbofos to enter the hemolymph.
  • Systemic distribution: the compound circulates through the hemocoel, reaching the central nervous system.
  • Enzyme inhibition: covalent bonding with the serine hydroxyl group of AChE blocks its active site.
  • Neurotransmitter buildup: acetylcholine levels rise dramatically, sustaining excitatory signaling.
  • Physiological collapse: sustained muscle contraction, loss of coordination, respiratory failure.

Lethal concentrations for Cimex lectularius are reported in the range of 0.2–0.5 µg per insect when applied directly. Sublethal exposure can impair feeding behavior and reproduction, contributing to population suppression.

Resistance mechanisms observed in some populations involve mutations in the AChE gene that reduce binding affinity, or enhanced detoxification by esterases. Monitoring susceptibility and rotating with non‑organophosphate agents mitigates resistance development.

Safety considerations include dermal and inhalation toxicity to humans and non‑target organisms. Proper personal protective equipment and adherence to label instructions minimize occupational risk. Environmental persistence is limited by hydrolysis; carbofos degrades to less toxic metabolites within days under typical indoor conditions.